ࡱ> * >bjbjO O 4-a-a 0NNNNNbbb8\ ' b6z4T;;;$<<443qL(ԩ֩֩֩֩֩֩$S:N<<NN;$<׫DDDN;N$<ԩDԩDD;@``+@F0:?@X?T?NpPDD? : Hospitals &Asylums Cardiology HA-20-4-13 By Anthony J. Sanders  HYPERLINK "mailto:sanderstony@live.com" sanderstony@live.com Hawthorne is the supreme herb for the heart (Elvin-Lewis 77:192)(Gladstar 12) Your heart matters.Above all else, guard your heart, for it is the wellspring of life (Proverbs 4:23) Though the strong eat whatever they want, the weak eat only vegetables (Romans 14:2) Test your servants for 10 days. Give us nothing but vegetables to eat and water to drink (Daniel 1:12)  HYPERLINK \l "an" Anatomy and Physiology  HYPERLINK \l "her" Heart and Valves  HYPERLINK \l "lymph" Blood Vessels, Marrow, Lymph, Spleen and Kidneys  HYPERLINK \l "blood" Blood  HYPERLINK \l "heartd" Cardiovascular Conditions  HYPERLINK \l "angina" Ischemic heart disease  HYPERLINK \l "cad" Arteriosclerosis   HYPERLINK \l "endo" Endocarditis  HYPERLINK \l "valv" Valvulitis  HYPERLINK \l "rhythm" Arrhythmia  HYPERLINK \l "chf" Congestive Heart Failure  HYPERLINK \l "hypertension" Hypertension  HYPERLINK \l "kid" Kidney Disease  HYPERLINK \l "anemia" Anemia and Bleeding Disorders  HYPERLINK \l "leuk" Leukopenia, Lymphoma, Leukemia, Myeloma, and Splenitis  HYPERLINK \l "vasneo" Vascular Neoplasm  HYPERLINK \l "con" Congenital Defects  HYPERLINK \l "treat" Treatment  HYPERLINK \l "tox" Toxicology  HYPERLINK \l "dia" Diagnostic Tests  HYPERLINK \l "surgery" Surgery  HYPERLINK \l "medi" Medicine  HYPERLINK \l "diet" Vegan Diet  HYPERLINK \l "basic" Basic Training Charts I.1.1  HYPERLINK \l "hex" Heart Exterior I.1.2  HYPERLINK \l "hi" Heart Interior I.2.1  HYPERLINK \l "circ" Circulatory System I.2.2  HYPERLINK \l "lymphant" Anterior View of the Lymphatic System I.3.1  HYPERLINK \l "cbcwbc" CBC, Coagulation Tests and WBC Differential Values I.3.2  HYPERLINK \l "abo" Properties of ABO Blood Typing II.1.1  HYPERLINK \l "heartmuscle" Heart With Muscle Damage and a Blocked Artery II.1.2  HYPERLINK \l "cadrug" Drugs used to treat coronary artery disease II.2.1  HYPERLINK \l "ather" Atherosclerosis II.2.2  HYPERLINK \l "stent" Placementof an Endovascular Stent Graft II.3.1  HYPERLINK \l "rh" Rheumatic Heart Disease on Autopsy II.4.1  HYPERLINK \l "pul" Pulmonary, Tricuspid, Aortic and Mitral Valves II.5.1  HYPERLINK \l "ecgread" Electrocardiogram (ECG) Reading II.5.2  HYPERLINK \l "comhar" Common heart rhythm (antiarrhythmic) medication and their effects II.6.1  HYPERLINK \l "chfclass" The New York Heart Association classification of congestive heart failure II.6.2  HYPERLINK \l "hfd" Heart Failure Drugs II.7.2  HYPERLINK \l "sphyg" Blood Pressure Sphygmomanometry Reading II.7.2  HYPERLINK \l "hypermed" Prescription Medicine for the Treatment of Hypertension II.9.1  HYPERLINK \l "dyscracia" Common Laboratory Features of Plasma Cell Dyscracias and Myelomas II. 9.2  HYPERLINK \l "nhl" Non-Hodgkin's Lymphomas II.9.3  HYPERLINK \l "difleuk" Differential Diagnosis of Leukemias III.1.1  HYPERLINK \l "bp" Categories for Blood Pressure Levels in Adults (in mmHg) III.1.2  HYPERLINK \l "ecg" Electrocardiogram (ECG) Reading III.1.3 HYPERLINK \l "lip"Lipid Profile III.1.4  HYPERLINK \l "cbcdif" CBC, Coagulation Tests and WBC Differential III.2.1  HYPERLINK \l "endovascular" Placement of an Endovascular Stent III.4.1  HYPERLINK \l "haw" Hawthorne in bloom III.4.2  HYPERLINK \l "cardiovas" Cardiovascular and Hypertensive Drugs III.4.3  HYPERLINK \l "adverse" Adverse Effects of Hypertensive Drugs III.4.4  HYPERLINK \l "chemo" Chemotherapy Approved for Plasma Cell Myeloma, Leukemias and Lymphomas III.5.1  HYPERLINK \l "veg" Vegetable Calories and Macro-Nutrients III.5.1  HYPERLINK \l "vit" Vitamins and Minerals Essential to Cardiovascular Health III.5.2  HYPERLINK \l "height" Height Weight Tables for Prior and Non-Prior Service III.6.1  HYPERLINK \l "mar" Marine Corp Age Adjusted Physical Fitness Requirements III.6.2  HYPERLINK \l "warm" Army warm up and cool down exercises Bibliography Anatomy and Physiology Heart and Valves The heart is a four-chambered muscular structure. It is about the size of a fist but can get much larger with disease. An adult weighing 160 pounds has about 5 quarts (4.7 liters) of blood in their circulatory system. The heart beats at a rate of 60 to 100 times per minute. It pumps 1,500 gallons of blood each day. It beats about 100,000 times per day and 36 million times per year. In a 70-year lifetime, an average human heart beats more than 2.5 billion times. Heart muscle does not usually regenerate. Expected heart weight varies with height and skeletal structure; it averages approximately 250 to 300 grams (gm) in females and 300 to 350 gm in males. Normally the thickness of the free wall of the right ventricle is 0.3 to 0.5 centimeters (cm) and that of the left ventricle 1.3 to 1.5 cm. Greater weight or ventricular thickness indicates hypertrophy and enlarged chamber size implies dilatation. Increased weight or size of the heart is known cardiomegaly (Schoen 94: 517). The heart pumps blood continuously through the circulatory system (Cohen 10). As the cardiac muscle contracts it pushes blood through the chambers and into the vessels. Nerves connected to the heart regulate the speed with which the muscle contracts. When running, the heart pumps more quickly. When asleep, the heart pumps more slowly. Located in the middle of the chest behind the breastbone, between the lungs, the heart rests in a moistened chamber called the pericardial cavity, which is surrounded by the ribcage. The diaphragm, a tough layer of muscle, lies below. As a result, the heart is a well-protected organ. The heart has four chambers.Connected to the heart are some of the main blood vesselsarteries and veinsthat make up the blood circulatory system. The ventricle on the right side of the heart pumps blood from the heart to the lungs. When air is breathed in, oxygen passes from the lungs through blood vessels where its added to the blood. Carbon dioxide, a waste product, is passed from the blood through blood vessels to the lungs and is removed from the body when the air is breathed out. The atrium on the left side of the heart receives oxygen-rich blood from the lungs. The pumping action of the left ventricle sends this oxygen-rich blood through the aorta (a main artery) to the rest of the body (Sanders 08). Heart Exterior  Credit: American Heart Association On the right side of the heart are the superior and inferior vena cava. These veins are the largest veins in the body. They carry used (oxygen-poor) blood to the right atrium of the heart. Used blood has had its oxygen removed and used by the bodys organs and tissues. The superior vena cava carries used blood from the upper parts of the body, including the head, chest, arms, and neck. The inferior vena cava carries used blood from the lower parts of the body.The used blood from the vena cava flows into the hearts right atrium and then on to the right ventricle. From the right ventricle, the used blood is pumped through the pulmonary arteries to the lungs. Here, through many small, thin blood vessels called capillaries, the blood picks up oxygen needed by all the areas of the body.The oxygen-rich blood passes from the lungs back to your heart through the pulmonary veins.Oxygen-rich blood from the lungs enters the left atrium and is pumped into the left ventricle. From the left ventricle, the blood is pumped to the rest of the body through the aorta (Sanders 08).  Credit: Lucile Salter Packard Children's Hospital Like all organs, the heart needs blood rich with oxygen. This oxygen is supplied through the coronary arteries as its pumped out of the hearts left ventricle. The coronary arteries are located on the hearts surface at the beginning of the aorta. The coronary arteries carry oxygen-rich blood to all parts of the heart.The right and left sides of your heart are divided by an internal wall of tissue called the septum. The area of the septum that divides the two upper chambers (atria) of the heart is called the atrial or interatrial septum. The area of the septum that divides the two lower chambers (ventricles) of the heart is called the ventricular or interventricular septum. The heart has four valves. The valves include the aortic valve, the tricuspid valve, the pulmonary valve, and the mitral valve. The four cardiac valves respond passively to pressure and flow changes within the heart. They function as loose flaps (leaflets or cusps) that seal the valvular orifices against regurgitation of blood when closed but fold out of the way when the valve is open, to provide an obstruction-free orifice. During the closed phase, the three cusps of the semilunar valves (aortic and pulmonic) overlap along an area (the lunula) between the free edge and a line marked by a white ridge on the ventricular surface of the cusp (linea alba). The overlap is substantial; in the aortic valve, for example, the total cuspal area is about 40% greater than the valve orifice area. Each aortic cusp has a small nodule (nodules of Arantius or Magagnis nodules) in the center of the free edge, which facilitates closure. The free margins of the atrioventricular (AV) valves (mitral and tricuspid) are tethered to the ventricular wall by many delicate chordae tendingeae, attached to papillary muscles, which are contiguous with the underlying ventricular walls. Normal mitral valve function depends on the coordinated actions of cusps, chordae tendingeae, papillary muscles and associated left ventricular wall (collectively the mitral apparatus). Tricuspid valve function depends on analogous structures. The function of semilunar valves depends on the integrity and coordinated movements of the cusps and their attachments. Thus dilatation of the aortic root in hypertension or syphilis can keep the aortic valve cusps from coming together during closure, just as left ventricular dilatation or a ruptured chorda or papillary muscle can keep the mitral valve from complete closure, each resulting in regurgitant flow (Schoen 94: 518). The heart uses the four valves to ensure your blood flows only in one direction. Healthy valves open and close in coordination with the pumping action of the hearts atria and ventricles. Each valve has a set of flaps called leaflets or cusps. These seal or open the valves. This allows pumped blood to pass through the chambers and into your blood vessels without backing up or flowing backward.Blood without oxygen from the two vena cava fill the hearts right atrium. The atrium contracts (atrial systole). The tricuspid valve located between the right atrium and ventricle opens for a short time and then shuts. This allows blood to enter into the right ventricle without flowing back into the right atrium.When the hearts right ventricle fills with blood, it contracts (ventricular systole). The pulmonary valve located between the right ventricle and pulmonary artery opens and closes quickly. This allows blood to enter into the pulmonary artery without flowing back into the right ventricle. This is important because the right ventricle begins to refill with more blood through the tricuspid valve. Blood travels through the pulmonary arteries to the lungs to pick up oxygen. Oxygen-rich blood returns from the lungs to the hearts left atrium through the pulmonary veins. As the hearts left atrium fills with blood, it contracts. This event also is called atrial systole. The mitral valve located between the left atrium and left ventricle opens and closes quickly. This allows blood to pass from the left atrium into the left ventricle without flowing back into the left atrium. As the left ventricle fills with blood, it contracts. This event also is called ventricular systole. The aortic valve located between the left ventricle and aorta opens and closes quickly. This allows blood to flow into the aorta. The aorta is the main artery that carries blood from the heart to the rest of the body. The aortic valve closes quickly to prevent blood from flowing back into the left ventricle, which is already filling up with new blood. A heartbeat actually is a complicated series of very precise and coordinated events that take place inside and around the heart. Each side of the heart uses an inlet valve to help move blood between the atrium and ventricle. The tricuspid valve does this between the right atrium and ventricle. The mitral valve does this between the left atrium and ventricle. The "lub" is the sound of the mitral and tricuspid valves closing. Each of your hearts ventricles has an outlet valve. The right ventricle uses the pulmonary valve to help move blood into the pulmonary arteries. The left ventricle uses the aortic valve to do the same for the aorta. The "DUB" is the sound of the aortic and pulmonary valves closing.Each heartbeat has two basic parts: diastole (relaxation) and atrial and ventricular systole. During diastole, the atria and ventricles relax and begin to fill with blood. At the end of diastole, atria contract (an event called atrial systole) and pump blood into the ventricles. The atria then begin to relax. Next, ventricles contract (an event called ventricular systole) and pump blood out of the heart. When asleep the heart beats slowly, maybe only 50 or 60 beats per minute. When running up a hill, it might be beating at 160, or even higher. In atrial fibrillation (AT), the ventricles may beat up to 100-175 times a minute, in contrast to the normal resting rate of 60-100 beats a minute. Each beat of the heart is set in motion by an electrical signal from within the heart muscle. The pulse, or heart rate, is the number of signals the SA node produces per minute. The hearts electrical system controls all the events that occur when the heart pumps blood. The electrical system also is called the cardiac conduction system. The electromagnetic signals coming from the heart are fifty times stronger and can be detected eight feet away than the brain, the next biggest signal generator. The hearts electrical system is made up of three main parts: The sinoatrial (SA) node located in the right atrium of the heart.The atrioventricular (AV) node located on the interatrial septum close to the tricuspid valve.The His-Purkinje system is located along the walls of the hearts ventricles.In a normal, healthy heart, each beat begins with a signal from the (sinoatrial node) SA node. This is why the SA node is sometimes called the hearts natural pacemaker. (Wilson and Childre 06: 85, 83, 84, 91). The signal is generated as the two-vena cava fill the hearts right atrium with blood from other parts of the body. The signal spreads across the cells of the hearts right and left atria. This signal causes the atria to contract. This action pushes blood through the open valves from the atria into both ventricles.The signal arrives at the (atrioventricular) AV node near the ventricles, where it slows for an instant to allow your hearts right and left ventricles to fill with blood. The signal is released and moves to the His-Purkinje bundle located in the walls of your hearts ventricles.From the His-Purkinje bundle, the signal fibers divide into left and right bundle branches through the Purkinje fibers that connect directly to the cells in the walls of the left and right ventricles. As the signal spreads across the cells of the ventricle walls, both ventricles contract, but not at exactly the same moment. The left ventricle contracts an instant before the right ventricle. This pushes blood through the pulmonary valve (for the right ventricle) to the lungs, and through the aortic valve (for the left ventricle) to the rest of the body.As the signal passes, the walls of the ventricles relax and await the next signal.This process continues over and over as the atria refill with blood and other electrical signals come from the SA node (Sanders 08). A human heart is made up of billions of cells, but researchers say fewer than 10,000 are responsible for controlling the heartbeat (Gallagher 12). Although nearly the entire volume of the myocardium is occupied by cardiac muscle cells, myocytes compose only approximately 25% of the total number of cells. The remainder are endothelial cells, associated with capillaries, and connective tissue cells. Inflammatory cells are generally rare, and collagen is sparse in the normal myocardium. In addition, specialized excitatory and conducting myocytes containing only a few contractile myofilaments are involved in the regulation and the rate and rhythm of the heart (Purkinje cells). These myofibers are plentiful in (1) the SA node, located at the junction of the right atrial appendage with the opening of the vena cava; (2) the AV node, located at the junction of the medial wall of the right atrium with the interventricular septum; and (3) the bundle of His, which courses down the interventricular septum toward the apex to divide into right and left branches that further arborize the respective ventricles. Lesions involving these specialized structures underlie many of the disturbances in cardiac rhythm (Schoen 94: 518). 2. Blood Vessels, Marrow, Lymph, Spleen and Kidneys Thecirculatory systemis anorgan systemthat permitsbloodandlymphcirculation to transport nutrients (such asamino acidsandelectrolytes), oxygen,carbon dioxide,hormones,bloodcells, etc. to and fromcellsin the body to nourish it and help to fight diseases, stabilizebody temperatureandpH, and to maintainhomeostasis. The circulatory system is the network of elastic tubes that carries blood throughout the body. It includes the heart, lungs, arteries, arterioles (small arteries) and capillaries (very tiny blood vessels). These blood vessels carry oxygen- and nutrient-rich blood to all parts of the body. The circulatory system also includes venules (small veins) and veins. These are the blood vessels that carry oxygen- and nutrient depleted blood back to the heart and lungs. If all these vessels were laid end-to-end, theyd extend for about 60,000 miles. Thats enough to encircle the earth more than twice (Sanders 08). Arteries and veins have distinctive structures. Arterial walls are generally thicker than their venous counterparts, to withstand the higher blood pressures in arteries. The thickness of the arterial walls gradually diminishes as the vessels become smaller, but at the same time the wall-to-lumen ratio becomes greater. Veins have a larger overall diameter, a larger lumen, and a narrower wall than corresponding arteries. The blood vessel walls are composed of three layers: inner endothelium known as the intima, middle smooth muscle known as the media and outer connective tissue known as the adventitia. There are also elastic elements between the Intima and Media, known as the Internal Elastic Lamina, and between the Media and the Adventitia, known as the External Elastic Lamina. The inner layer of each artery is covered by protective cells, which make up the endothelium. The cells of the endothelium, the lining of the arteries, make chemicals such as nitric oxide, which cause the artery to dilate and interfere with blood clotting, and endothelin, which promotes blood clotting and constriction of the arteries. In another balancing act, the endothelial cells make a second type of chemical (prostacycline) that dilates arteries and inhibits clotting (clumping of the blood platelets), while platelets themselves make and release a chemical (thromboxane) that promotes clotting and constriction of arteries. The pathogenesis of atherosclerosis as the result of hyperlipidemia is hypothesized to be caused by damage to the endothelium. The fastest blood flow is in the middle of the artery and the slowest is along the artery wall (Spence 06: 29, 30, 31). Circulatory System  Credit: Wikipedia '13 Arteries are divided into three types: (1) large or elastic arteries, including the aorta and its major branches, whose vascular walls are perfused with vasa vasorum vessels within vessels; (2) medium-sized or muscular arteries (such as the coronary or renal arteries), also referred to as the distributing arteries, local blood flow and blood pressure are regulated by changes in lumen size through smooth muscle cell contraction (vasoconstriction) or relaxation (vasodilatation) controlled in part by the autonomic nervous system and in part by local metabolic factors and cellular interactions, halving the diameter increases resistance 16 fold, and small changes in the lumen size of small blood vessels by vasoconstriction or plaque can have a profound flow-limiting effect; and (3) arterioles are small arteries (usually less than 2 mm in diameter) that course, for the most part, within the substance of tissues and organs; the smallest (generally 20 to 100 m in diameter, have primarily smooth muscle cell-containing media) regulate blood flow in capillary beds and bear the brunt of blood pressure elevations, that abnormal stress of which alters their structure. Thus atherosclerosis is a disease largely of elastic and muscular arteries, whereas hypertension is associated with functional and structural changes in the small muscular arteries and arterioles (Schoen '94: 468). The term capillary is restricted to those vessels that have approximately the diameter of a red blood cell (7 to 8 m). Slow flow, large surface area, approximately 700 m2, and walls only one cell thick render capillaries ideally suited to the rapid exchange of diffusible substances between blood and extravascular tissue. Blood returning to the heart from capillary beds flows initially into the postcapillary venules and then sequentially through collecting venules and small, medium and large veins. Because the pressure in the venules is lower than that in the capillary bed, as well as lower than interstitial tissue pressure, fluid can enter the circulation from the tissue surrounding the venules. Veins are thin-walled vessels with relatively large lumina. Veins have scant connective tissue and the media is not well developed, and are thus predisposed to abnormal irregular dilation, compression and easy penetration by tumors and inflammatory processes. The valves found in many veins, particularly those in the extremities, serve to eliminate back flow(Schoen 94: 468, 469). The bone marrow is both a reservoir for stem cells and a unique microenvironment in which the orderly proliferation and differentiation and release of precursor cells takes place. In between the endothelial lined sinusoidal network of bone marrow lie clusters of hematopoietic cells and fat cells. A reasonable estimate of hemopoietic activity of the marrow may be obtained by examining the ratio of at cells to hematopoietic elements in bone marrow biopsies. In normal adults this ratio approaches 1:1 but with marrow hypoplasia (e.g. aplastic anemia) the proportion of fat cells is greatly increased and conversely, fat cells may virtually disappear in diseases characterized by increased hematopoiesis (e.g. leukemias). The relative proportion of cells in the bone marrow is almost always deranged in diseases of the blood and bone marrow. Normally, the marrow contains about 60% granulocytes and their precursors; 20% erythroid precursors; and 10% unidentified or disintegrating cells. Thus, the normal myeloid-to-erythroid ratio is 3:1. The dominant cell types in the myeloid compartment included myelocytes, metamyelocytes, and granulocytes. In the erythroid compartment the dominant forms are polychromatophilic and orthocromic normoblasts. The function of red cells is the transport of oxygen into tissues (Saunders 94: 585, 586). Lymphatics are collapsed, thin-walled, endothelium-lined channels devoid of blood cells, found in tissue sections. Although the major function of the lymphatics is as a protective drainage system returning interstitial tissue fluid to the blood, they also constitute an important pathway for disease dissemination through transport of bacteria and tumor cells to distant sites. Lymphocytes and monocytes not only circulate in the blood and lymph but also accumulate in discrete and organized masses, called the lymphoreticular system. Components of this system include lymph nodes thymus, spleen, tonsils, adenoids and Peyers patches. Less discrete collections of lymphoid cells occur in the bone marrow, lungs, and gastrointestinal tract and other tissues. Lymph nodes are the most widely distributed and easily accessible component of the lymphoid tissue. Lymph nodes are discrete structures surrounded by a capsule composed of connective tissue and a few elastic fibrils. The capsule is perforated at various points by afferent lymphatics that empty into the peripheral sinus subjacent to the capsule. Situated in the cortex or peripheral portion of the node are spherical aggregates of lymphoid tissue, the primary follicles, which represent B-cell areas. On antigenic stimulation, the primary follicles enlarge and develop pale-staining germinal centers composed of follicular center cells. Surrounding these germinal centers are mantles of small unchallenged B cells. The T cells occupy the parafollicular regions. Anterior View of the Lymphatic System  Credit: Wikipedia The medullar cords, occupying the central portion of the node, contain predominantly plasma cells and some lymphocytes. The size and morphology of lymph nodes are modified by immune responses. As secondary lines of defense, they are constantly responding to stimuli, even in the absence of clinical disease. Trivial injuries and infections effect subtle changes in lymph node histology. More significant bacterial infections inevitably produce enlargement of nodes and sometimes leave residual scarring. For this reason, lymph nodes in adults are almost never normal and they usually bear the scars of previous events, rendering the inguinal nodes particularly inappropriate for evaluative biopsies (Saunders 94: 629, 630). The spleen is to the circulatory system what the lymph nodes are to the lymphatic system. Among its functions are filtration from the bloodstream of all foreign matter, including obsolescent and damaged blood cells, and participation in the immune response to al blood-borne antigens. Designed ingeniously for these functions, the spleen is a major repository of mononuclear phagocytic cells in the red pulp and lymphoid cells in the white pulp. Normally in the adult it weighs about 150 gm and measures some 12 cm in length, 7 cm in width, and 3 cm in thickness. It is enclosed within a thin, glistening connective tissue capsule that appears slate gray and through which the dusky red, friable parenchyma of the splenic substance can be seen. The red pulp of the spleen is traversed by numerous thin-walled vascular sinusoids, separated by the splenic cords, or cords of Billroth. The endotherlial lining of the sinusoid provides passage of blood cells between the sinusoids and cords. The splenic cords are spnogelike and consist of a and consist of a labyrinth of macrophages loosely connected through long dendritic processes to create both a physical and a functional filter through which the blood can slowly seep. During the course of the day the total volume of blood passes through the filtration beds of the splenic cords. 1/120 of all red cells are destroyed daily by phagocytosis. Engulfment by splenic macrophages accounts for approximately half this removal of obsolescent red cells from the circulation. The phagocytes are also active in removal of ther particulate matter from the blood, such as bacteria, cell debris, and abnormal macromolecules produced by inborn errors of metabolism. In humans the normal spleen harbors only about 30 to 40 ml of erythrocytes, but with splenomegaly this reservoir is greatly increased. The normal spleen also stores approximately 30 to 40% of the total platelet mass in the body. With splenomegaly this platelet storage may markedly increase, sometimes up to 80 to 90% of the total platelet mass. Similarly the enlarged spleen may trap a sufficient number of white cells to induce leukopenia (Saunders 94: 667-669). Human kidneys serve to convert more than 1700 liters of blood per day into about 1 liter of a highly specialized concentrated fluid called urine. In so doing, the kidney excretes the waste products of metabolism, precisely regulates the body's concentration of water and salt, maintains the appropriate acid balance of plasma, and serves as an endocrine organ, secreting such hormones as erythropoietin, renin and prostaglandins. Each human adult kidney weights about 150 gm. Although both kidneys make up only 0.5% of the total body weight they receive about 25% of the cardiac output. Of this, the cortex is by far the more richly vascularized, receiving 90% of the total renal circulation. As the ureter enters the kidney at the hilus, it dilates into a funnel-shaped cavity, the pelvis, from which derive two to three main branches, the major calyces; the latter subdivide again into about three to four minor calyces. There are about 12 minor calyces in the human kidney. On cross-section the kidney is made up of a cortex and a medulla, the former 1.2 to 1.5 cm in thickness. The medulla consists of renal pyramids, the apices of which are called papillae, each related to a calyx. Cortical tissue extends into spaces between adjacent pyramids as the renal columns of Bertin. From the standpoint of diseases, the kidney can be divided into four components: blood vessels, glomeruli, tubules and interstitium. The main renal artery divides into anterior and posterior sections at the hilus. From these, interlobar arteries emerge, course between lobes, give rise to the arcuate arteries, which arch between cortex and medulla, in turn giving rise to the interlobular arteries. From the interlobular arteries, afferent arterioles enter the glomerular tuft, where they progressively subdivide into 20 to 40 capillary loops arranged in several units or lobules. Capillary loops merge together to exit from the glomerulus as efferent arterioles. Efferent arterioles from superficial nephrons form a rich vascular network that encircles cortical tubules (peritubular vascular network), while deeper juxtamedullary glomeruli give rise to the vasa recta, which descend as straight vessels to supply the out and inner medulla. These descending arterial vasa recta then make several loops in the inner medulla and ascend the venous vasa recta. Occlusion of any branch results in an infarction of the specific area it supplies. Glomerular disease that interferes with blood flow through the glomerular capillaries has profound effects on the tubules, within both the cortex and the medulla, because all tubular capillary beds are derived from the efferent arteries. The renal medulla is especially vulnerable to ischemia. The major characteristics of glomerular filtration are an extraordinary high permeability to water and small solutes, accounted for by the highly fenestrated endothelium and impermeability to molecules the size of albumin (+3.6-nm radius; 70,000 kd) call the glomerular barrier function (GBM). The proximal tubular cells reabsorb two-thirds of filtered sodium and water as well as glucose, potassium, phosphate, amino acids and proteins. The proximal tubule is particularly vulnerable to ischemic damage (Saunders '94: 927-931, 978). There is a cascade of events referred to as the neurohormonal response because its a long series of around 1,400 reactions involving nervous system signals to many glands all over the body. The autonomic nervous system (ANS) is the part of your nervous system thats automatic. This part of the nervous system requires no thoughts or calculations kicks in immediately to regular autonomic functions such as the heartbeat and when faced threats to survival. The ANS has two branches. The sympathetic (active) and the parasympathetic (relaxed). The sympathetic branch of the autonomic nervous system is frequently called you fight or flight system. With either response an entire cascade of events occurs the nerves in the brain quickly send signals along the nerves in the body that constrict blood vessels, immediately raising blood pressure. Heart rate jumps and you can run faster. Arteries in your skin constrict, making it less likely that youll bleed to death. Blood is directed away from organs that really arent necessary, like your kidneys and digestive tract. Pupils dilate and the hair on the back of the neck stand up and become environmentally sensitive, in fractions of a second. The parasympathetic branch dominates when nothing is perceived threatening in the environment. Blood is preferentially being delivered to your stomach and intestines to help absorb and digest food. Heart rate is probably a little slower than usual. Blood pressure is also lower (Wilson and Childre 06: 67- 69, 71, 65-66). The heart and cardiovascular system are particularly affected by the functioning of the adrenal glands located atop the kidneys. Adrenaline is an important hormone and neurotransmitter released during the fight or flight response regarding an injury or emergency situation and is sometimes used as an alternative to a defribulator to reverse cardiac arrest resulting from anapholactic shock. While adrenaline is produced in the central core of the adrenal glands, found atop the kidneys, cortisol is produced in one of the three outer layers. When the adrenal cortex is destroyed by accident, surgery, or disease, death occurs within days unless the patient receives aldosterone and cortisol (Graveline 04: 53, 51-52). Aldosterone protects the body from excessive loss of sodium and water and is known in scientific circles as a mineral corticoid. Cortisol is known as a glucocorticoid because it helps control blood sugar levels and glucose metabolism, but it also has powerful mineral corticoid and immune system functions and is fundamentally involved in the biologic response to the stress in our lives. Cortisol is known by some as the mother of all stress hormones and is released in large quantities during times of stress. Once it is released into the bloodstream, cortisols main action is to raise blood sugar or glucose by breaking down stored sugars from places like the liver and muscles. Both directly and indirectly (by interacting with other hormones) cortisol raises blood pressure by causing constriction of arteries and interacting with the kidneys to save salt and water. Cortisol supports survival by raising blood sugar and blood pressure. This potent hormone is also triggered by any negative emotion, such as anxiety, anger, or hostility as well as depression. The adrenal gland also produces a hormone called DHEA (dehydroepiandrosterone). DHEA seems to counteract some of the effects of cortisol and is related to positive emotions such as happiness, love, care, gratitude, and appreciation. DHEA can be converted to one of the sex hormones, estrogen or testosterone and DHEA supplements can cause side effects related to the sex hormones, such as facial hair in women or prostate enlargement or stimulation of prostate cancer in men. DHEA gradually declines with age so that by around age seventy-five its only at about 25 percent of the level it was fifty years earlier. The juxtaglomerular (JG) apparatus snuggles closely against the glomerulus where the afferent arteriole enters it. The JG apparatus is a small endocrine organ, the JG cells being the principal sources of renin production in the kidney. Malignant hypertension is usually associated with high levels of renin, angiotensin and aldosterone perpetuated by hyper-reninemia (Saunders '94: 927-931, 978). 3. Blood Blood is a specialized body fluid. It has four main components: plasma, red blood cells, white blood cells, and platelets. Blood appears red because of the large number of red blood cells, which get their color from the hemoglobin. Blood has many different functions, including transporting oxygen and nutrients to the lungs and tissues, forming blood clots to prevent excess blood loss, carrying cells and antibodies that fight infection, bringing waste products to the kidneys and liver, which filter and clean the blood and regulating body temperature. The blood that runs through the veins, arteries, and capillaries is known as whole blood, a mixture of about 55 percent plasma and 45 percent blood cells. About 7 to 8 percent of total body weight is blood. An average-sized man has about 12 pints of blood in his body, and an average-sized woman has about 9 pints. The bone marrow, lymph nodes and spleen are all involved in hematopoiesis the production of red and white blood cells. Traditionally, these organs and tissues have been divided into myeloid tissue, which includes the bone marrow and the cells derived from it (e.g. erythrocytes, platelets, granulocytes, and monocytes), and lymphoid tissue, consisting of thymus, lymph nodes and spleen. In the human embryo, clusters of stem cells, called blood islands, appear in the yolk sac in the third week of fetal development. At about the third month of embryogenesis some of these cells migrate to the liver, which then becomes the chief site of blood formation until shortly before birth. Beginning in the fourth month of development, hematopoiesis commences in the bone marrow. At birth, all the marrow throughout the skeleton is active and is virtually the sole source of blood cells. In the full-term infant, hepatic hematopoiesis has dwindled to a trickle, but may persist in widely scattered small foci, which become inactive soon after birth. Up the age of puberty, all the marrow throughout the skeleton is red and hematopoietically active. Usually by 18 years of age only the vertebrae, ribs, sternum, skull, pelvis and proximal epiphyseal regions of the humerus and femur retain red marrow, the remaining marrow becoming yellow, fatty, and inactive. Thus, in adults, only about one-half of the marrow space is active in hematopoiesis. With an increased demand for blood cells in the adult, the fatty marrow may become transformed to red, active marrow increasing red cell production (erythropoiesis) seven-to-eight fold. If marrow precursor cells are destroyed by metastatic cancer or irradiation, producing anemia, extramedullary hematopoiesis may reappear, first within the liver and then in the spleen and lymph (Saunders 94: 583,584). All the formed elements of blood T cells, B cells (plasma cells), platelets, erythrocytes, leukocytes, macrophages and eosinophils have a common origin in a pluripotent hematopoietic stem cell. Gametes formed by the union of sperm and egg are known as omnipotent stem cells. The pluripotent hematopoietic stem cell is the common precursor that gives rise to lymphoid stem cells and and trilineage myeloid stem cells. The lymphoid stem cell, is believed to be the origin of precursors of T cells (pro-T cells), B cells (pro-B cells) and possibly natural killer (NK) cells. From the multipotent myeloid stem cell arise at least three types of committed stem cells capable of differentiating along the erythroid/megakaryocytic, eosinophilic, and granulocyte-macrophage pathways. From various committed stem cells, intermediate stages are derived, such as, proerythroblasts, myeloblasts, megakaryoblasts, monoblasts and eosinophiloblasts. These in turn give rise to mature progeny. Since mature blood elements have a finite life span, their numbers must be constantly replenished (Saunders 94: 584). Acomplete blood count (CBC)test gives your doctor important information about the types and numbers of cells in your blood, especially the red blood cells and their percentage (hematocrit) or protein content (hemoglobin), white blood cells, and platelets. The results of a CBC may diagnose conditions like anemia, infection, and other related disorders such as cancers of the blood. A complete blood count (CBC) is dome by automated cell counters that measure the hemoglobin, red blood cell count, red blood cell volume distribution, platelet count, and white blood cell count. The percentage of whole blood volume that is made up of red blood cells is called the hematocrit and is a common measure of red blood cell levels. The mean cell volume (MCV) (based on volume distribution), mean cell hemoglobin (MCH) (hemoglobin divided by RBC count), mean cell hemoglobin concentration (MCHC) (hemoglobin divided by hematocrit) and the red cell distribution width (RDW). The red cell indices and RDW are used together with a direct inspection of the Wright-stained blood smear to evaluate red blood cell morphology (Hillman 98: 334-336). The iron level with Total Iron Binding Capacity (Fe and TIBC) test detect certain kinds of anemia, such as iron deficiency after blood loss. Serum Haptoglobin Test detect intravascular destruction of RBCs associated with hemolytic anemia. Hemoglobin electrophoresis enable one to detect abnormal forms of Hgb (hemaglobinopathies). Direct and indirect Coombs tests detect the presence of antibodies to RBC found in tissue and fetal rejection. A reticulocyte count (Retic count) is a test for determing bone marrow function in which immature RBC as a percentage of total RBC production. Theplatelet countand plasma clotting tests (prothombin time, partial thromboplastin time, and thrombin time) may be used to evaluate bleeding and clotting disorders. To count the percentage of total white blood cell volume occupied by specific white blood cells a CBC with Differential is ordered. The white blood cell (WBC) differential is a measure of the total number of white blood cells and the percentages of the five types of WBC descriptive of infection, stress and bone marrow failure (Griffin '84: 3-16).. Complete Blood Count (CBC), Coagulation Tests and White Blood Cell (WBC) Differential TestNormal RangeCommentsComplete Blood Count (CBC)Red Blood Cell (RBC) countM 4.7-6.2 million/cu mm F 4.2-5.4 million/cu mmLow anemia, hemorrhage High chronic anoxiaHemoglobin (Hgb)M14-18 g/dl F12-16Same as aboveHematocrit (Hct)M42-52% F37-47%Same as aboveMean corpuscular volume (MCV)80-95 cu/u High - RBC macrocytic Low RBC microcoticMean corpuscular hemoglobin concentration (MCHC)32-36 g/dl (32-36%)Low Hypochromic cellIron (Fe)60-190 g/dlLow-iron deficiency anemiaTotal iron binding capacity (TIBC)250-420 g/dlSame as aboveSerum haptoglobin100-150 mgLow-Hemolysis liver disease High-Inflammatory diseaseHemoglobin electrophoresisHgb A1 95-98% Hgb A2 2-3% Hgb F 0.8-2% Hgb S 0% Hgb C 0%Variations indicate hemoglobinopathies, High Hgb F thalassemia found in Central asians. Hgb S-sickle cell anemia and Hgb C mild hemolytic anemia found in American blacks Direct Coombs' and Indirect CoombsNegativeTo detect antibodies against RBC in transplant rejectionReticulocyte counts0.5%-2% of total RBCLow-inaquate RBC production High-Polycythemia veraWhite Blood Cell (WBC) count5000-10,000/cu mmHigh-infection Low-Bone marrow failurePlatelet count150,000-400,000/cu mmLow-Bone marrow failure, hypersplenism, accelerated consumption High-Hemorrhage, polycythemia vera, malignanciesCoagulation TestsProthrombin test (PT)11-12.5 seconds (85-100%)High-Deficiency of factors V and VIIProthrombin time test (PTT)30-40 secondsHigh-Deficiency of factors II, V, VIII, IX, XI, XIIPlatelet count150,000-400,000/cu mmLow-Bone marrow failure, hypersplenism, accelerated consumption High-Hemorrhage, polycythemia vera, malignanciesBleeding time1-9 minutesHigh Thrombocytopenia, marrow infiltration, inadequate platelet functionEublobin lysis time90 minutes-6 hoursLow-FibrinolysisFibrin degradation products (FDP) test < 10g/mlHigh DIC, fibrinolysisWhite Blood Cell (WBC) DifferentialWhite Blood Cell (WBC) count5000-10,000/cu mmHigh-infection Low-Bone marrow failureNeutrophils50-70High-Inflammation, Invasive tumorsEosinophils2-4High-Allergic states, Drug reactions, Parasitic Infections, Some skin disease and neoplasmsBasophils0.5High-Asthma, some Carcinogens, Inflammatory bowel disease, Chronic inflammationMacrophages5-7High-Chronic infections, Liver disease, NeutropeniaLymphocytes20-35High-some CarcinomasPlasma Cells?Multiple myelomaSource: Griffin '86: Table 1.1 pg. 5-6; Table 2-3 pg. 32 The liquid component of blood is called plasma, a mixture of water, sugar, fat, protein, and salts. B cells sometimes morph into plasma cells. The main job of the plasma is to transport blood cells throughout your body along with nutrients, waste products, antibodies, clotting proteins, chemical messengers such as hormones, and proteins that help maintain the body's fluid balance. Once thought to be just dust particles in blood, platelets were first recognized as a special class of blood cells (actually cell fragments) by an Italian researcher in 1882.Unlike red and white blood cells, platelets are not actually cells but rather small fragments of cells. Platelets help the blood clotting process (or coagulation) by gathering at the site of an injury, sticking to the lining of the injured blood vessel, and forming a platform on which blood coagulation can occur. This results in the formation of a fibrin clot, which covers the wound and prevents blood from leaking out. Fibrin also forms the initial scaffolding upon which new tissue forms, thus promoting healing. A higher than normal number of platelets can cause unnecessary clotting, which can lead to strokes and heart attacks; however, thanks to advances made inantiplatelet therapies, there are treatments available to help prevent these potentially fatal events. Conversely, lower than normal counts can lead to extensive bleeding. Known for their bright red color, red cells, also called erythrocytes or RBCs, are the most abundant cell in the blood, accounting for about 40-45 percent of its volume. The shape of a red blood cell is a biconcave disk with a flattened center in other words, both faces of the disc have shallow bowl-like indentations (a red blood cell looks like a donut). Red cells contain a special protein called hemoglobin, which helps carry oxygen from the lungs to the rest of the body and then returns carbon dioxide from the body to the lungs so it can be exhaled. Blood appears red because of the large number of red blood cells, which get their color from the hemoglobin. The percentage of whole blood volume that is made up of red blood cells is called the hematocrit and is a common measure of red blood cell levels. Production of red blood cells is controlled by erythropoietin, a hormone produced primarily by the kidneys. Red blood cells start as immature cells in the bone marrow and after approximately seven days of maturation are released into the bloodstream. Unlike many other cells, red blood cells have no nucleus and can easily change shape, helping them fit through the various blood vessels in your body. However, while the lack of a nucleus makes a red blood cell more flexible, it also limits the life of the cell as it travels through the smallest blood vessels, damaging the cells membranes and depleting its energy supplies. The red blood cell survives on average only 120 days. White blood cells, also called leukocytes, protect the body from infection. They are much fewer in number than red blood cells, accounting for about 1 percent of your blood. There are five main types: neutrophils, lymphocytes, macrophages, eosinophils and basophils. The most common type of white blood cell is the neutrophil, which is the immediate response cell and accounts for 55 to 70 percent of the total white blood cell count. Their job is to consume unwelcome cells. Each neutrophil lives less than a day, so your bone marrow must constantly make new neutrophils to maintain protection against infection. Transfusion of neutrophils is generally not effective since they do not remain in the body for very long. The other major type of white blood cell is a lymphocyte. There are two main populations of these cells: T cells and B cells. T lymphocytes, or T cells, secrete potent substances to attract and regulate other immune system cells, that do the actual work, and directly attack various infected cells and tumors. B lymphocytes, or B cells, are immune cells that actually produce antibodies, which are proteins that specifically target bacteria, viruses or other foreign materials. B cells have long memories for their enemies and may remain in the body for years, ready at any time to turn into antibody factories whenever an antigen they recognize appears. This is how a vaccination works: a tiny bit of a (usually) killed virus, or antigen, such as polio, measles, or flu, is injected into your blood-stream, provoking B cells to produce antibodies. Then, if you ever encounter the fully functional form of the virus, your body can quickly marshal its defenses and produce millions of the required antibodies without delay. Macrophages engulf and destroy large cells, such as bacteria or yeast, as well as the debris from natural cell formation in a growing body. Eosinophils make up 4 percent or less of active white blood cells. They attack larger cells, in part by secreting toxins that trigger inflammation. Basophils release granules of germ-killing toxins and histamine, a substance that triggers inflammation when they encounter damaged tissue (Berger 04: 23, 24). The immune system knows which are good cells and which are bad cells because the surface of every sell in your body sports special proteins called human leukocyte antigens (HLAs). Your blood contains more than 1 trillion antibodies. Antibodies are made up of chains of molecules that form a Y shape. The sections that make up the tips of the Ys arms vary greatly from one antibody to another; this is called the variable region. It develops a unique shape based on the antigen it was created to react to, so it can lock onto that antigen just like a key fitting into a lock. Sometimes this locking neutralizes the antigen on its own, rendering it harmless; sometimes it ruptures the cells of the foreign body; and sometimes it forces antigens to clump together, creating sitting-duck target for other immune cells to attack. There are five classes of antibodies, each with a slightly different function and operating method. Scientists call them immunoglobulins, or Igs for short. Of the five, IgE is the one we could call the allergy antibody, since IgE antibodies are the main culprits contributing to allergies. IgE binds the allergen molecule either to basophils, or to cells called mast cells found in the mucous linings of tissues throughout the body, such as the throat, nose, lungs, skin or stomach lining. This binding triggers the mast cells or basophils to release inflammatory chemicals, such as histamine, prostaglandins, and leukotrienes. The inflammatory process begins, with swelling, creation of mucus, reddening, heat and vessel constriction an allergic reaction (Berger 04: 27, 28, 30). Austrian-American physician Karl Landsteiner (1868-1943) announced in 1901 that human blood can be classified into only a few general classes or types, which are known today as A. B, AB, and O. The chemical nature of the antigens responsible for the blood types that make up the ABO groups was first discovered in 1953. If a person with type A blood receives type A blood from a donor, there is no risk because the recipients body recognizes and accepts the type A blood. If the same person is given type B blood, however, his or her immune system does not recognize the type B blood cells, ad its anti-B antibodies begin to attack the transfused blood. The physical process of testing for ABO blood types is actually quite simple and requires only two reagents ant-A serum and anti-B serum. The sample is tested with each reagent one at a time. According to the Red Cross blood bank, the population of the United States is approximately 39 percent type A, 46 percent type O, 11 percent type B, and 4 percent type AB (Robbins 01: 73). Narrowing the field of suspects of from 100 percent to 40 percent however does not help much. A second system of blood typing with which many people are familiar is the Rh system, named for the blood factors (Rh+ and Rh-) that were first observed in rhesus monkeys. The availability of two systems of blood typing increases the possibility of identifying a blood sample. Over the past half-century, immunochemists have discovered a number of other antigen-antibody systems in the blood Newton '07: 33, 36 39). Properties of ABO Blood Typing Blood GroupAntigensTest ResultCan Give Blood ToCan Receive Blood From Frequency in PopulationAAAnti-BA and ABA and O40-42%BBAnti-AB and ABB and O10-12%ABA and BBoth anti-A and anti-BABA, B, AB and O3-5%OHNeither anti-A and anti-BA, B, AB and OO43-45%Source: Newton '07: 37 Narrowing the field of suspects of from 100 percent to 40 percent however does not help much. A second system of blood typing with which many people are familiar is the Rh system, named for the blood factors (Rh+ and Rh-) that were first observed in rhesus monkeys. The availability of two systems of blood typing increases the possibility of identifying a blood sample. Over the past half-century, immunochemists have discovered a number of other antigen-antibody systems in the blood. The International Society of Blood Transfusion (ISBT) currently recognizes 26 such blood-grouping systems In addition to the ABO and Rh systems, such groupings include the MNS, Lutheran, Kell, Lewis, Duffy, Kidd, Diego, Cartwright, Xg, and Scianna systems. Of the 26 ISBT blood-typing systems available today, only the ABO and Rh systems are commonly used in forensic serology. In order to specify more precisely the characteristics of a blood sample, a serologist is likely to analyze other components found in blood, primarily polymorphic proteins or isoenzymes. In order to specify more precisely the characteristics of blood sample, a serologist is likely to analyze proteins found in blood, primarily polymorphic proteins or isoenzymes such as: Adenosine deaminase (ADA), Adenylate kinase (AK), Erhtyrocyte acid phosphatase (EAP), Esterase-D (EsD), Glucose-6-phosphate dehydrogenase (G-6-PD), Glyoxylase I (GLOI), Glutamic pyruvate transminase (GPT), Haptoglobin (Hp), Peptidase A (PeP A), Phosphoglucomutase (PGM), 6-Phosphogluconate dehydrogenase (6-PGD) and Transferin (Tf). These tests are generally adequate to establish paternity with around 1 percent margin of error. Another useful adjunct to classic ABO blood testing is the human leukocyte antigen (HLA) test. These antigens exist on white blood cells, in contrast to almost all other polymorphic proteins and isoenzymes that occur in red blood cells. HLA types are classified into four classes A-D, each of these includes a number of subclasses 23 known types of HLA-A, 47 types of HLA-B, eight types of HLA-C and 4 types of HLA-D. In paternity testing the chance of a man having the same type of HLA as the child in question is very low, about one in 92. ABO testing alone can exclude the possibility that a man is the father of a child about 20 percent of the time. HLA testing can exclude the same possibility about 90 percent of the time. In combination, the two tests can exclude the possibility of parenthood by about 97 percent of all cases (Newton '07: 33, 36, 40, 41, 46, 47, 39, 40). Type II hypersensitivity, also known as tissue specific, cytotoxic, or cytolytic hypersensitivity, is characterized by antibodies that attack antigens on the surface of specific cells or tissues. Often the reaction is immediate (15 to 30 minutes after exposure to the antigen). Hyperacute graft rejection is a type II hypersensitivity that affects transplanted tissues. It occurs when the transplanted donor tissue has an antigen to which the recipient has preformed antibodies. For example, when tissue from a blood type A or B donor is transplanted. Into a blood type O recipient, the recipient has anti-A and Anti-B antibodies. These antibodies will immediately attack the foreign transplanted tissue. Onset begins immediately after revascularization occurs in the transplant procedure. At this time, the blood supply from the patient is established in the newly transplanted organ. The patients antibodies attack the foreign protein antigens and for an antigen-antibody complex. Effector cell infiltration and complement-mediated lysis of donor tissues, inflammation, vascular thrombosis and hemorrhage occur. The reaction happens so quickly that within 48 hours after transplantation the graft tissue is ravage and no longer functioning. To prevent hyperacute graft rejection, tissue and blood typing of donors and recipients of transplanted tissue is extensive. Lists of potential recipients are matched to donors through organ donation laboratories both regionally and nationally. Only rarely has hyperacute graft rejection occurred because of an error in tissue or blood typing (Peterson '05: 254). II. Cardiovascular Conditions Ischemic Heart Disease Ischemic heart disease (IHD) is the leading cause of death in the United States and many industrialized nations. Sudden cardiac death (SCD) strikes about 300,000 to 400,000 annually. Coronary atherosclerosis with greater than 75% stenosis, involving more than one of the three major vessels is present in 80 to 90% of victims; only 10 to 20% of cases are of nonatherosclerotic origin. Usually there are high-grade stenosis (greater than 90%). Acute coronary changes such as, thrombosis, plaque fissuring, intraplaque hemorrhage, are commonly found in 75 to 80% of fatal heart attacks. A healed myocardial infarct is present in about 40%, but in those who have been rescued by prompt therapy from sudden cardiac arrest new myocardial infarction is found in 25% or less. The ultimate mechanism of death is almost always a lethal arrhythmia (Sanders 08). Cardiovascular diseases, including stroke, are the No. 1 killer in the United States for both men and women.Coronary heart disease, is America's No. 1 killer. Stroke is No. 3 and a leading cause of serious disability.Of the estimated 50 million, 166 out of 1,000, with unhealthy levels of lipoprotein in their blood, 7 million Americans feel angina (23 in 1,000), 1.5 million will suffer an acute myocardial infarction (heart attack) for which 550,000 will be hospitalized (1.8 out of 1,000) and of the 2.4 million people who died in 2004, 666,000 died from heart disease (2.2 out of 1,000) and 150,000 from stroke.People suffering chronic angina pectoris have about a 20% chance of suffering a fatal heart attack over ten years (Sanders 08) depending on how many and how complete the occlusion of the arteries is, the five year survival ranges from 50 to 98% (Heger '04: 113). In the United States during 1972 more than one million people died from major cardiovascular disease, a majority from heart attacks and strokes. Between 1940 and 1960 there was a marked increase in deaths from cardiovascular diseases among American males over 45 years of age (Elvin-Lewis 77). Since then heart attacks and strokes in North America have declined by 60 percent (after adjusting for age). Myocardial infarction may occur at any age, but the frequency rises progressively with old age. Five percent of myocardial infarctions occur in people under age 40 years, and 45% occur under age 65. Blacks and whites are affected equally often. Throughout life men are at significantly greater risk of myocardial infarction than women. However, the use of oral contraceptives, increases the risk of myocardial infarction, especially in smokers older than age 35. Newer formulas have reduced estrogen content with reduced risk at all ages. Moreover, epidemiologic evidence strongly suggests that estrogen replacement therapy protects menopausal women against myocardial infarction (Schoen 94: 529). The risk of heart attack is four times greater to a man in his fifties than to one in his thirties, and greatest among men in the 50 to 60 year age group. For the most part, this improvement has been due to a reduction in the traditional risk factors identified in the Framingham Heart Study, in which the population of Framingham, Massachussetts, just west of Boston, has been followed for more than fifty years, with regular research examinations. In that study it became apparent that independent predictors of risk included age, sex, congenital defects, lipidemia, high blood pressure, thickening of the heart muscle (left ventricular hypertrophy), glucose intolerance (diabetes and prediabetes) and sedentary lifestyle (Spence 06: 75). The cardinal risk factors for coronary disease in the United States are hypercholesterolemia, hypertension, and inactivity (Elvin-Lewis 77: 179). Angina pectoris is characterized by paroxysmal attacks of substernal or precordial chest discomfort (variously described as constricting, squeezing, choking, or knife-like) caused by transient (15 second to 15 minutes) myocardial ischemia that falls short of inducing the cellular necrosis that defines myocardial infarction, heart attack, which causes chronic angina until the necrotic myocardial tissue is scarred over and healed after about 5 days to 7 weeks (Schoen 94: 527). Angina is chest pain or discomfort that occurs when an area of your heart muscle doesn't get enough oxygen-rich blood. It's thought that nearly 7 million people in the United States suffer from angina. About 400,000 patients go to their doctors with new cases of angina every year. Angina may feel like pressure or squeezing in your chest. The pain also may occur in your shoulders, arms, neck, jaw, or back. It can feel like indigestion. Angina itself isn't a disease. Rather, it's a symptom of an underlying heart problem. Angina is usually a symptom of coronary artery disease (CAD), the most common type of heart disease. CAD occurs when a fatty material called plaque builds up on the inner walls of the coronary arteries. These arteries carry oxygen-rich blood to your heart. When plaque builds up in the arteries, the condition is called atherosclerosis.There are three overlapping patterns of angina pectoris (1) stable or typical angina, related to cardiovascular exercise (2) Prinzmetals or variant angina, coronary artery spasm at rest that responds to nitroglycerin and calcium channel blockers and (3) unstable or crescendo angina that falls short of inducing infarction, and is sometimes referred to as pre-infarction angina or acute coronary insufficiency (Schoen 94). Chronic angina lasts until the tissue has satisfactorily healed and scarred over, from 5 days to 7 weeks from the last heart attack. However, the tissue will not heal unless a vegan, non-fat, no animal product, low carb, sugar and salt free diet ministers to daily cardiovascular exercise, and several courses of antibiotics are used over several months to sterilize the necrotic tissue to enable it to heal. A mostly vegan diet will probably be needed for the rest of the patients angina free life (Sanders 08). Nitrates are the most commonly used medicines to treat angina and in conjunction with statin drugs seems to be the most successful prescription drug available for the treatment of congestive heart failure. They relax and widen blood vessels. This allows more blood to flow to the heart while reducing its workload. Nitroglycerin is the most commonly used nitrate for angina. Nitroglycerin that dissolves under your tongue or between your cheeks and gum is used to relieve an angina episode. Nitroglycerin in the form of pills and skin patches act too slowly to relieve pain during an angina attack (Sanders 08). Nitrates are safe and affective for the treatment of stable angina pectoris. Short acting nitrates are used for the relief of the acute attacks, whereas long-acting nitrates are used for antianginal prophylaxis. With continuous application of the drug at a constant rate, tolerance can develop within 24 hours so a nitrate-free interval is the strategy for preventing tolerance With oral isosorbide dinitrate, dosing at 7am, noon and 5 pm appears to avoid tolerance problems With a patch-free interval of 10 to 12 hours, patches retain their effectiveness (Heger et al '04: 114). The acute coronary syndromes of unstable angina, acute myocardial infarction and sudden death share a common pathophysiological basis, with coronary atherosclerotic plaque rupture as the pathologic hallmark and associated intraluminal platelet-fibrin thrombus. Typical angina commonly results from myocardial oxygen deficiency caused by stenosed (blocked) coronary arteries. In unstable angina, a relatively small fissure or disruption of an atherosclerotic plaque may lead to a sudden change in plaque morphology, with platelet aggregation or mural thrombus and frequently vasoconstriction leading to transient reduction in coronary blood flow. Sudden coronary death frequently involves a rapidly progressing coronary lesion, in which plaque disruption and often partial thrombus (and possibly embolization) lead to regional myocardial ischemia that induce a fatal ventricular arrhythmia (Schoen 94: 528). A heart attack (myocardial infarction) occurs when blood flow to a section of heart muscle becomes blocked. If the flow of blood isnt restored quickly, the section of heart muscle becomes damaged from lack of oxygen and begins to die.Heart attack is a leading killer of both men and women in the United States. But fortunately, today there are excellent treatments for heart attack that can save lives and prevent disabilities. Treatment is most effective when started within 1 hour of the beginning of symptoms. Heart attacks occur most often, about 90% of the time, as a result of a condition called coronary artery disease (CAD). In CAD, a fatty material called plaque builds up over many years on the inside walls of the coronary arteries (the arteries that supply blood and oxygen to your heart). Eventually, an area of plaque can rupture, causing a blood clot to form on the surface of the plaque. If the clot becomes large enough, it can mostly or completely block the flow of oxygen-rich blood to the part of the heart muscle fed by the artery.During a heart attack, if the blockage in the coronary artery isnt treated quickly, the heart muscle will begin to die and be replaced by scar tissue. This heart damage may not be obvious, or it may cause severe or long-lasting problems. Diabetes is a risk factor for heart attack.Some 21 million Americans have diabetes, meaning their bodies can't properly regulate blood sugar, or glucose. Diabetics already are at increased risk of heart disease. Type 2 diabetes, the most common form, is linked to obesity, which in turn harms the heart. Plus, high blood sugar over time damages blood vessels (Sanders 08: 23). In other words, fat and sugar, may induce ischemia in inactive people with compromised cardiovascular health and should be avoided. Blood supplying the heart muscle comes entirely form two coronary (heart) arteries, both lying along the outside surface of the heart. If one of these arteries or any part of one suddenly becomes blocked the portion of the heart being supplied by the artery dies. The death of a portion of the heart muscle is called a heart attack, myocardial infarction. The amount of the heart affected by the sudden occlusion will depend on the severity of this attack and will determine whether the individual dies or survives. If the heart continues to function, the dead portion is eventually walled off as new vascular tissue supplies the needed blood to adjacent areas (Elvin-Lewis 77: 177). When coronary angiography was performed within 4 hours of the onset of apparent myocardial infarction, a thrombosed coronary artery was found in almost 90% of cases. The incidence of acute occlusion, however, fell to about 60% when angiography was delayed until 12 to 24 hours after onset. Thus with the passage of time, at least some occlusions appear to clear spontaneously because of lysis of the thrombus or relaxation of spasm or a combination of the two. The progression of ischemic necrosis in the myocardium begins in the subendocardial zone. With more extended ischemia, a wavefront of cell death moves through the myocardium to involve progressively more of the transmural thickness of the ischemic zone. Necrosis is usually complete in 3 to 6 hours in experimental models. Provided exposure to environmental and dietary cardiotoxins, namely animal products, is eliminated, and toxic insult ceases, the necrotic muscle elicits acute inflammation and pain, typically most prominent at 2 to 3 days, thereafter macrophages remove the necrotic myocytes, in 5 to 10 days, and the damaged zone is progressively replaced by the ingrowth of highly vascularized granulation tissue, at 2 to 4 weeks, which progressively becomes less vascularized and more fibrous. In most instances, scarring is well advanced by the end of the sixth week, but the efficiency of repair depend on the size of the original lesion (Schoen 94: 528, 530). Heart With Muscle Damage and a Blocked Artery  Credit: American Heart Association Only severe ischemia, with blood flow of 10% or less of normal, lasting at least 20 to 40 minutes or longer leads to irreversible damage (necrosis) of some cardiac myocytes. After the onset of an acute ischemic event, one of several pathways may be followed. One is brief and marked by sudden cardiac death (SCD) within 1 to 2 hours in 20% of patients (probably an overestimate because most patients are silent about their heart attacks), accounting for about half of ischemic heart disease deaths. If the patient with acute myocardial infarction reaches the hospital, 10-20% of cases are uncomplicated and 80 to 90% are complicated. Common complications include cardiac arrhythmias (75-95% of complications), left ventricular congestive failure and mild-to-severe pulmonary edema (60%), cardiogenic shock, pump failure from a large infarct, usually greater than 40% of left ventricle, with nearly 70% mortality rate accounting for two-thirds of in-hospital deaths (10 to 15%), rupture of free wall, septum or papillary muscle (1-5%) and thromboembolism (15 to 40%). The overall total mortality within the first year is about 35%, including those victims who die before reaching the hospital. The early mortality rate during hospitalization is approximately 10 to 15% and in the year following infarction is another 7 to 10%. Thereafter there is a 3 to 4% mortality among survivors with each passing year (Schoen 94: 528, 537 539). The clinical diagnosis of acute myocardial infarction is mainly based on three sets of data: (1) symptoms, (2) electrocardiographic (ECG) changes and (3) elevation of specific serum enzymes, particularly creatine phosphokinase (CPK) and lactate dehydrogenase (LDH), although other diagnostic modalities, such as echocardiography (for visualization of abnormalities of regional wall motion), radioisotopic studies (such as radionuclide angiography (for chamber configuration), perfusion scintigraphy (for regional perfusion) and magnetic resonance imaging (for structural characterization, are available. The CPK serum level rises above baseline within 4 to 8 hours and may peak very early or not for several days, falling to baseline in about 4 days. The LDH level does not begin to rise until about 24 hours, peaks in 3 to 6 days, and may not return to normal until the end of the second week. There are two types of myocardial infarction the transmural infarct and the subendocardial (nontransmural) infarct. The more common type is the transmural infarct, in which the ischemic necrosis involves the full or nearly full thickness of the ventricular wall in the distribution of a single coronary artery. This pattern of infarction is usually associated with coronary atherosclerosis, plaque rupture, and superimposed thrombosis. In contrast, subendocardial (nontransmural) infarct constitutes an area of ischemic necrosis limited to the inner one-third or at most one-half of the ventricular wall, often extending laterally beyond the perfusion territory of a single coronary artery (Schoen 94: 537). In chronic ischemic heart disease the pericardial surface of the heart may have adhesions as a result of healing associated with past myocardial infarcts. Invariably there is moderate to severe stenosing atherosclerosis of the coronary arteries and sometimes total occlusions resulting from organized thrombi. Discrete, gray-white scares of healed previous infarcts are usually present. The mural endocardium is generally normal except for some superficial, patchy, fibrous thickenings. The clinical diagnosis of chronic ischemic heart disease is generally made largely by the insidious onset of congestive heart failure (CHF) in patients who have past episodes of myocardial infarction or angina attacks, and excludes millions of people who have suffered constant angina pectoris for more than six months (the typical definition of chronic disease). Before necrotic heart tissue has fully scarred, 7 weeks from last infarction, the chronic ischemic heart disease patient has an auto-immune predisposition to infectious endocarditis, nearly always of bacterial origin, usually Streptococcus pyogenes (rheumatic heart disease), S. faecalis, S. sanguis, that respond best to penicillin, although any antibiotic such as erythromycin given to people with an allergy to penicillin, will do, Peptostreptococcus, Bactroides fragiles that respond best to metronidazole (Flagyl ER) or Staphylococcus aureus whose resistant strains can only be treated with doxycline), viruses and fungi can also infect the heart. One-quarter of adults over age 45 take cholesterol-lowering statin drugs. 17 percent of patients taking the pills reported side effects, including muscle pain, nausea, and problems with their liver or nervous system. About two-thirds of people with side effects quit taking statins. All in all, half of all the people who been prescribed the drugs quit them at last temporarily. Twenty percent quit for more than a year. The vast majority of people don't have side effects. Many of the people in this study who quit the drug were able to get back on statins. The FDA haswarnedthat taking statins slightly increases the risk of diabetes, cancer, dementia and nerve damage, even in people at a healthy weight and with no other risk factors. No research has been done to see if the diabetes, cancer, dementia and nerve damage go away when patients stop taking statins. Long-term statin use may cause nerve damage, that damage often reverses when statins are discontinued, but the process can take months. Not continuing the drug has a lot more to do with people just not wanting to take drugs for a lifetime (Shute '13). A 1994 study called the Scandinavian Simvastatin Survival Study (also called 4S) found that lowering cholesterol can prevent heart attacks and reduce death in men and women who already have heart disease and high cholesterol. For over 5 years, more than 4,400 patients with heart disease and total cholesterol levels of 213 mg/dL to 310 mg/dL were given either a cholesterol-lowering drug or a placebo (a dummy pill that looks exactly like the medication). The drug they were given is known as a statin, and it reduced total cholesterol levels by 25 percent and LDL-cholesterol levels by 35 percent. The study found that in those receiving statin, deaths from heart disease were reduced by 42 percent, the chance of having a nonfatal heart attack was reduced by 37 percent, and the need for bypass surgery or angioplasty was reduced by 37 percent. A very important finding is that deaths from causes other than cardiovascular disease were not increased, and so the 42 percent reduction in heart disease deaths resulted in a 30 percent drop in overall deaths from all causes (Sanders 08: 28). In 1996 the results of the Cholesterol and Recurrent Events (CARE) Study also showed the benefits of cholesterol lowering in heart disease patients. This study reported that even in patients with seemingly normal cholesterol levels (average of 209 mg/dL), cholesterol lowering with a statin drug lowered the risk of having another heart attack or dying by 24 percent.A study published in 1998, the Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) study, examined the effects of cholesterol lowering in people with CHD (those who had already experienced a heart attack or had been hospitalized for angina) and who had relatively average cholesterol levels. The LIPID study used a statin drug to lower cholesterol levels in the treatment group. All study participants were counseled about following a cholesterol-lowering diet. The LIPID results showed that a drop of 18 percent in total cholesterol and 25 percent in LDL-cholesterol produced a 24 percent decrease in deaths from CHD among the treatment group compared with the control group (Sanders 08: 28, 29). Eating the standard American diet thats based on meat and dairy products, with plenty of white flour and white sugar, one-third of the women and one-half of the men in the US population die of heart disease. Meanwhile, vegetarians and vegans (vegetarians who consume no dairy products or eggs) not only have far less heart disease, but also have lower rates of cancer, hypertension, diabetes, gallstones, kidney disease and obesity. Not only is mortality from coronary artery disease lower in vegetarians than non-vegetarians, but vegetarian diets have been successful in arresting coronary artery disease. The daily intake of cholesterol by non-vegetarians is 300-500 mg/daily, lacto-ovo-vegetarians 150-300 mg/ daily and vegans zero, their cholesterol levels were 210, 161 and 133 respectively, safe levels of cholesterol are less than 150. The ideal ratio of total cholesterol to HDL (high-density lipoproteins) is 3.0 to 1 or lower, the average American males ratio is 5.1 to 1 and the average vegetarians ratio, on the other hand, is 2.9 to 1. When it comes to heart disease the evidence is against animal products. Vegans live on average six to ten years longer than the rest of the population and in fact seem to be healthier on every measurement we have of assessing health outcomes. A low-fat plant based diet would lower the heart attack rate about 85 percent, and cancer rate 60 percent (Robbins 01: 14 , 15, 21, 22, 47). Modified nutritional habits of high-risk American men, substituting diets moderate in calories, total fat, and carbohydrate, low in saturated fat, cholesterol, and simple sugars reduced heart disease mortality by about one-half and the sudden death rate was only one-fourth as great, and total mortality was lower by 40%. In a study of coronary heart disease in seven countries only the concentration of cholesterol in the blood proved to be the outstanding risk factor within and between national groups. As these data indicate, Japanese men have the lowest incidence of coronary heart disease of any industrialized nation, they smoke heavily and they have high blood pressure, but they eat a low cholesterol diet. The death rate from heart disease is 300% higher in cigarette smokers than in non-smokers in the United States. Curiously, the effects of cigarette smoking are equivocal: the practice is not related statistically to heart disease among, for example, Japanese men who smoke heavily. Reasons for an increased risk include lowered ability of the lungs to exchange oxygen and carbon dioxide, toxicity form nicotine (which makes the heart beat faster and causes small arteries to narrow thereby increasing blood pressure and the work load on the heart). Obesity (10-20%) above ideal weight adds to the work load of the heart and is to be avoided. Lack of regular daily exercise is a factor in coronary disease. Men engaging in heavy physical work seem to have a significantly lower death rate from coronary disease than more sedentary job holders (Elvin-Lewis 77: 182, 183). A 30 percent reduction in heart attacks has been found in people who follow a Mediterranean diet, as good as statin drugs (Shute '13). Not only is mortality from coronary artery disease lower in vegetarians than non-vegetarians, but vegetarian diets have been successful in reversing coronary artery disease by osmosis of lipids in the bloodstream. The daily intake of cholesterol by non-vegetarians is 300-500 mg/daily, lacto-ovo-vegetarians 150-300 mg/ daily and vegans zero, their cholesterol levels were 210, 161 and 133 respectively, safe levels of cholesterol are less than 150. The ideal ratio of total cholesterol to HDL (high-density lipoproteins) is 3.0 to 1 or lower, the average American males ratio is 5.1 to 1 and the average vegetarians ratio, on the other hand, is 2.9 to 1. When it comes to heart disease the evidence is against animal products. Vegans live on average six to ten years longer than the rest of the population and in fact seem to be healthier on every measurement we have of assessing health outcomes. A low-fat plant based diet would lower the heart attack rate about 85 percent, and cancer rate 60 percent (Robbins 01: 14 , 15, 21, 22, 47). Besides a vegan diet, an athletic level of cardiovascular exercise and sporadic prophylaxis with NSAIDs, antibiotics and antifungal drug to cure rheumatic complaints and achieve higher levels of athletic performance hopefully transcending concerns about health to develop beautiful large strong muscles, even on rainy days or when crippled by an idiopathic disorder. Statin cholesterol lowering drugs are an essential medicine for reducing the risk of death from heart attack or ischemic stroke but recovery is not given as a reason for discontinuing statin use. Statin drugs reduce the risk of death in patients with hyperlipidemia by around 50 percent and the stroke risk by 30 percent but the reasons given for quitting statins does not include a cure. Nitrates and Nitrites can be effective at restoring normal blood flow within 5 minutes and lead to a complete recovery from angina pectoris or congestive heart failure in some patients, it should be tried in an office visit to see if a prescription is wanted. The treatment of congestive heart failure would be much improved with the use of the supreme herb for the heart - Hawthorne leaves, berries and flowers as an herbal tea infusion, tincture or syrup are good for the heart and kidneys. Hawthorne works in part by dilating the arteries and veins, enabling blood to flow more freely and releasing cardiovascular constrictions and blockages. It strengthens the heart muscle while helping to normalize and regulate blood pressure. It also helps maintain healthy cholesterol levels. Hawthorne is outstanding both to prevent heart problems and to treat high or low blood pressure, heart disease, edema, angina and heart arrhythmia. Hawthorn doesnt store in the body and isnt accumulative in action, its important to take on a regular basis if using as a heart tonic (Gladstar '12). Drugs used to treat coronary artery disease Supreme herb for the heartHawthorne is outstanding both to prevent heart problems and to treat high or low blood pressure, heart disease, edema, angina and heart arrhythmia.Lipid-lowering drugsHMG-CoA reductase inhibitors (statins): Used to prevent cholesterol buildup in the coronary arteries. Can also prevent the inflammatory response that could cause atheromatous plaques to rupture in the heart and precipitate a heart attack. Side effects include muscle and liver injury.Niacin (nicotinic acid), cholestyramine, gemfibrozil, clofirate: Used to treat high cholesterol and high triglycerides.VasodilatorNitroglycerine: used to treat chest pain (called angina) from coronary artery disease. Can lower blood pressure. Should not be used by patients using sildenafil (Viagra).Antiplatelet MedicationsAcetylsalicylic acid (aspirin): Used to help prevent and treat heart attacks. Clopidogrel (Plavix): Used with acetylsalicylic acid (aspirin) after placement of a stent to prevent the stent and coronary artery from occluding.Rare DiseasesRituxan (rituximab) or cyclosphamide IV and prednisone for Wegener's granulomatosis, microscopic polyangiitis and Polyarteritis nodosa (PAN)Gamma globulin IV administered with aspirin for Kawasawki DiseseSource: Cohen '05 Dissolution of a clot in an unwanted location, thrombolysis, was originally used for the treatment of deep vein thrombosis and pulmonary embolism but is now also used for treating acute peripheral arterial thrombosis and embolism and for thrombosed prosthetic heart valves, catheters and shunts. Thrombolytic agents used currently act directly or indirectly as plasminogen activators. Thrombolytic therapy with various fibrinolytic agents such as streptokinase or tissue-type plasminogen activator (tPA) is used in about 15% of myocardial infarcts, in an attempt to dissolve the thrombus that initiated the infarct, to re-establish blood flow to the area at risk for infarction, and possibly to rescue the ischemic heart muscle. Thrombolysis re-establishes the patency of the occluded coronary artery in about 70% of cases, and significantly improves survival rates. Reperfusion of the myocardium with blood, sufficiently early, within 15 to 20 minutes, after onset of ischemia may prevent all necrosis. Reperfusion after a longer interval can salvage at least some myocytes that would have died with more prolonged or permanent ischemia. However, reperfusion injury can cause cell death of myocytes that were still viable before reperfusion. Persistance of total occlusion with failure of clot lysis occurs in approximately 30% of patients undergoing thromblytic therapy. The major complications of thrombolytic therapy that lessen enthusiasm for its use in patients with occlusive vascular disorders include hemorrhage due to the systemic fibrinolytic state (15% of patients) and thrombotic reocclusion (15 to 35% of patients). Reocclusion is related to the continued presence of the factors, responsible for the original thrombus initiation (Schoen 94: 535, 537, 512). Because platelet aggregation has been strongly implicated in the pathogenesis of unstable angina pectoris and myocardia infarction, Aspirin, a platelet inhibitor, shows a 51% lower incidence of myocardial infarction and death in the aspirin group (324 mg/day) than the placebo group, although it is generally conceded that lower doses (1mg/kg) work as well and are less inhibitory to the arterial endothelium's production of prostacyclin than higher doses. Aspirin causes irreversible acetylation of platelet cyclooxygenase, thereby preventing the formation of thromboxane A2 an extremely potent vasoconstrictor and platelet activator. The thienopyridine drugs ticlopidine and clopidogrel (Plavix) are also effective antiplatelet drugs used to prevent stent cosure, generally, clopidogrel is preferred, because it is safer, more potent, and faster acting and can be taken once a day. Plavix is used with acetylsalicylic acid (aspirin) after placement of a stent to prevent the stent and coronary artery from occluding. Glycoprotein (GB) IIb/IIIa Receptor Antagonists prevent fibrinogen binding and platelet aggregation and is used by paitents at high risk and those undergoing percutaneous coronary intervention. Three GP IIb/IIIa receptor antagonists are currently available abciximab (long lasting 12 hours affect on platelets) an, eptifibatide, and tirofiban that have short half live of 2 to 3 hours. Severe thrombocytopenia (less than 20,000/mL) is seen in 0.5% of patients. Unfractionated heparin (UFH) reduces the risk of sudden cardiac death, myocardial infarction and recurrent ischemic events when combined with ASA in the setting of unstable angina pectoris. Unless there is a contraindication, full-dose heparin anticoagulation appears to be a logical therapy in the earl coronary care unit setting followed by chronic low-dose aspirin in patients with intermediate or high risk unstable angina pectoris. Most of the benefit is short term and most trials have limited heparin use to 2 to 5 days. Severe thrombocytopenia (less than 100,000/mL) occurs in 1 to 2% UFH auto-immune induced thrombocytopenia with thrombosis occurs in less than 0.2% of cases. Low-molecular-weight heparin (LMWH) is safer and alleviates the need for partial thromboplastin time testing (Heger et al '04: 124-126). Clinical trials testing three new drugs appear to offer some promise to heart patients. Two of the drugs, cangrelor and inclacumab, might improve outcomes for patients undergoing cardiac interventions such as angioplasty or stenting, while a third drug, Inspra, seems to lower heart patients odds for death and heart failure following a heart attack. All three trials were funded by the respective drugs makers, and all three were presented Sunday at the annual meeting of the American College of Cardiology (ACC) in San Francisco. In the first trial, researchers compared an as-yet approved blood thinner called cangrelor against the current standard medication, Plavix (clopidogrel), for patients who have recently had a stent implanted in an artery to help improve blood flow. According to the ACC, more than 600,000 coronary artery stent procedures are conducted in the United States each year, but doctors have long sought safer alternatives to Plavix to help prevent clots. Plavix comes with one big drawback for patients rushed to the hospital with suspected heart attack: It is taken in pill form, and its anti-clotting effects (with accompanying bleeding risk) may not wear off for up to a week. Cangrelor may help get around that issue. Even though it is delivered intravenously and begins acting quickly, its anti-clotting effects also fade quickly within an hour should any bleeding complications occur. So, doctors might feel free to give heart patients cangrelor upon admittance to the hospital and then send them immediately for angioplasty a minimally invasive procedure to reopen clogged vessels or stenting, if needed. In the trial, which was funded by cangrelors maker, New Jersey-based The Medicines Company, researchers compared short-term outcomes for 11,000 patients who underwent stent placement at one of 153 centers around the world. Some of the patients got cangrelor, while others got Plavix. The research team reported that cangrelor reduced by 22 percent the odds of a patient dying, having a heart attack or having a clot develop in the stented vessel within two days of the procedure, compared to patients who took Plavix. Safety profiles were similar: Severe bleeding at 48 hours after the stenting procedure occurred in 0.16 percent of those on cangrelor and 0.11 percent of those given Plavix. More than 1 million Americans each year undergo angioplasty. But angioplasty can also trigger damage to heart tissues, and it was thought that the new drug might help minimize that risk. cangrelors price has not yet been set, but it likely will carry a much higher price tag than Plavix. A second study focused on the drug eplerenone, marketed by Pfizer as Inspra. The drug is currently FDA-approved to help lower high blood pressure and to ward off heart failure after heart attack. In the new Pfizer-funded trial, slightly more than 1,000 patients who had had a heart attack caused by complete blockage of an artery took either Inspra or a placebo in addition to standard treatments. Patients were followed for an average of a bit more than 10 months. Those taking Inspra were 38 percent less likely than those on a placebo to have outcomes such as death by cardiovascular causes, rehospitalization due to heart failure, irregular heart rhythms or other indicators of heart failure. A third and smaller trial, published simultaneously online in theJournal of the American College of Cardiology, looked at another still-unapproved drug, the anti-inflammatory agent inclacumab, for use in patients undergoing angioplasty. More than 1 million Americans each year undergo angioplasty. But angioplasty can also trigger damage to heart tissues, and it was thought that the new drug might help minimize that risk. In the study, which involved 322 patients with a common form of heart attack, participants got either various doses of inclacumab or a placebo about an hour before their angioplasty. The research team assessed changes in levels of troponin I a protein found in the blood that indicates heart damage as a means of telling whether the drug was effective or not. The researchers reported that 24 hours after the procedure, patients who had gotten the highest dose of inclacumab saw their troponin I levels drop by more than 24 percent compared to those on a placebo indicating less heart tissue damage. Levels of another marker of heart tissue damage, called CK-MB, fell by more than 17 percent over 24 hours compared to placebo, the team added. There was also no bad signal [from the data] in terms of increased rates of bleeding or infection with the use of inclacumab (Mundell '13). Decade-old heart attack scars healed after being injected with stem cells from a patients' own bone marrow. So far, eight patients have received the experimental treatment in an ongoing clinical trial. All eight had suffered heart attacks an average of 5 1/2 years prior; one of the patients had his heart attack 11 years earlier. All had dangerously enlarged hearts, with areas of scar tissue from their heart attacks. The researchers harvested bone marrow progenitor cells from four patients and adult stem cells from another four patients. Using a catheter, they then injected the cells into the walls of the patients' hearts. Within three months, the scarred areas of the patients' hearts began to work again. About six months after treatment, and for a year later -- the length of the study so far -- all eight hearts regained a more normal size. They shrank 15% to 20%, three times more than current treatments can achieve. Whether just plain old bone marrow or [adult stem] cells, injected into the scar, and three months later, the area that was completely dead started to contract again. Stem cells are being explored in the treatment of people with recent heart attack damage -- but the "landmark area" is the use of stem cells to treat end-stage heart failure. Stem cells actually reverse the enlargement and their propensity to get worse (DeNoon 11). Since 1963 Congress and the American Heart Association has required the president to proclaim February "American Heart Month."The AHA recommends that patients with acute heart disease should take the ambulance, otherwise they are likely to be turned away (Sanders 08:1).Social Security implemented Compassionate Allowances in October 2008 to provide benefits quickly, within a month, to applicants whose medical conditions are so serious that their conditions obviously meet disability standards of medicine and finance. There currently are 88 specific diseases and conditions that qualify as a Compassionate Allowance.On November 9, 2010, the sixth Compassionate Allowances Outreach hearing was hosted in Baltimore, MD at the University of Maryland Baltimore County. The subject of the hearing was cardiovascular disease and multiple organ transplants. Commissioner Astrue joined Susan B. Shurin, Acting Director of the National Heart, Lung, and Blood Institute, National Institutes of Health, and other Social Security officials in listening to testimony from some of the leading experts on cardiovascular disease and multiple organ transplants. It was estimated that in 2010 150,000 people with cardiovascular disability would benefit from the fast-track disability processes. Cardiovascular disease is the leading cause of death for both men and women in America. More than 95,000 people are currently waiting for an organ transplant and nearly 4,000 are added to the waiting list each month (Lassiter 10). The reason for the high bar on receiving disability payments for cardiovascular conditions is probably because suffering from chronic angina pectoris is an indication to get a physical labor job and the transition from sedentary bureaucrat to physical labor is better bankrolled by unemployment insurance. In fact, survival rates of males who retire and receive social security benefits is many years shorter than females, who do not seem to need work to exercise. Social Security has an obligation to pay disability but compatible lifestyle is also a concern. Although receiving disability is a good way to finance a vegan diet and exercise program, many men, particularly suddenly retired blue collar workers, and sedentary workers who retired because they didn't independently maintain minimal standards of physical fitness, die quickly of fast food and inactivity. Heart patients are disabled sedentary workers who benefit greatly from physical labor and should make the career change. Full-time work, as a physical laborer, with an adequate vegan diet, tends to be the most effective cure for heart disease, but daily cardiorespiratory exercise, particularly for the retired and disabled, or anyone with a heart condition, cannot be dependent upon the availability of sufficiently vigorous physical labor for pay in the market. A one hour daily intense exercise program or four hour walk is the minimum exercise needed for any cardiovascular rehabilitation, or general health for people receiving disability or retirement pensions or attempting to engage in sedentary work. Although long hours behind the computer screen are no long compatible with life in people with heart conditions, as evidenced by the angina which informs the scholar it is time to stop writing, for optimal performance, simplicity and mental clarity that can be described as the virtue of patience, preoccupation with the mind, mental health and academics must be balanced with diligent concern for physical health and activity one hour of writing for one hour of jogging, chapter for 100 push-ups and crunches. Writing on a radioactive computer screen is much more demanding on the heart than reading a book. Arteriosclerosis The most common form of heart disease is coronary artery disease. The heart is nourished through the coronary arteries, which arise from the proximal (first part of the) aorta. The coronary arteries consist of a left coronary artery (which branches into the left anterior descending and the left circumflex coronary arteries) and a right coronary artery. Blockages in these arteries (or in their branches) may lead to a lack of blood flow and oxygenation of heart tissue (called ischemia). This occurs when there is inflammation of the artery wall and scar tissue forms. When the blockage is severe and lasts long enough (usually following plaque rupture), the person may have a heart attack (also called a myocardial infarction) when the heart muscle tissue dies as the result of not getting enough oxygen (Cohen 10: 1-7). Coronary artery disease (CAD) which may manifest itself as chest pain (angina), heart attack, arrhythmias, or sudden cardiac arrest. When blood supply to the brain and limbs is impaired, atherosclerosis can cause mini-strokes, strokes and peripheral artery disease. Two-thirds of Americas have some plaque buildup by age 35. Each year approximately 800,000 Americans have their first heart attack and 500,0000 Americans will have a recurring attack according to the American Heart Association. There is a link between atherosclerosis and sudden cardiac arrest. Atherosclerosis is the buildup of calcium and fatty deposits in the arterial walls. CAD with a prior heart attack is a leading risk factor for sudden cardiac arrest. Sudden cardiac arrest kill nearly 300,000 Americans each year (Cohen 10: 45). According to the U.S. government, one in every 300 Americans will be killed by a blocked artery in 2007.Every 34 seconds an American dies as the result of a blocked cardiac artery.As an American, there's a 90 percent chance that poor circulation will trigger a serious health problem at some point in your life.More than 6.8 million Americans undergo heart bypass, balloon angioplasty and other circulation-related procedures each year.700,000 Americans will suffer a sudden blockage of blood flow to the brain in 2007- 83 every hour of the day.Each year, about 1.1 million people in the United States have heart attacks, and almost half of them die. Mortality differs significantly by race or ethnic group as measured by age adjusted death rates.In 1998 these death rates per 100,000 people from heart disease in the United States were 211.8 for black non-Hispanics, compared to 145.3 for white non-Hispanics, 101.5 for Hispanics, 106 for American Indians and 78 for Asians (Sanders 08). Arteriosclerosis means hardening of the arteries and includes three morphologic variants: (1) atherosclerosis, characterized by intimal thickening and lipid deposition; (2) Monchebergs medial calcific sclerosis, characterized by calcification of the media of muscular arteries; and (3) arteriolosclerosis, marked by proliferative or hyaline thickening of the walls of small arteries and arterioles. Atherosclerosis is a process in which the wall of an artery fills with fat, fibrous tissue and, in later stages, grains of calcium. If the plaque gets large enough, it limits the flow of blood. When that happens and tissue downstream from the blockage dies, the result is a heart attack or stroke (Brown 13). Atherosclerosis is by far the most common and important form of arteriosclerosis causing 90% of all heart disease. Atherosclerosis overwhelmingly accounts for more death and serious morbidity in the Western world than any other disorder. Nearly 50 percent of deaths in the United States can be attributed to atherosclerosis related disease such as myocardial infarction (heart attack), cerebrovascular accident (stroke), or aortic aneurysm. The death rate related to atherosclerosis in the United States is among the highest in the world, lower than for Finland and Scotland, but above that of other well-developed affluent countries, such as Canada, France and the other Scandinavian countries. The rates are comparably low in Asia, Africa and South and Central America. For example death rates from ischemic heart disease in Japan are one-sixth of those in the United States. Japanese who migrate to the United States and adopt the lifestyles and dietary customs of their new home acquire the predisposition to atherosclerotic diseases of the American population (Schoen 94: 473, 474). Arteriosclerosis and its offspring atherosclerosis are the primary contributors to death and disability in this country. This condition of progressive arterial damage leading to varying degrees of narrowing and even complete obstruction of major arteries. History tells us that some of the earliest knowledge about arteriosclerosis and its very advanced form, atherosclerosis, came from dissections of the human body done in Renaissance Italy. Credit generally is given to Leonardo da Vinci for the first of these dissections in the 15th century. Abnormalities in arterial walls were found early on and related to social standing, for the most severe abnormalities were found in the wealthy classes of merchants and professionals. In the 19th century Karl Rokitansky compiled a comprehensive handbook of tissue changes he had observed. He suggested that elements of the blood, including blood clots and serum, formed layers on the arterial linings. Over time, a hardened, calcified layer resulted that came to be called arteriosclerosis. In the late 19th century Rudolph Virchow, who introduced tissue microscopy to the field of pathology, elaborated further on the process of this arterial change. Mucoid degeneration was a term he used to describe the very earliest sign of arterial change. In this condition, a mucoid substance is deposited within the intima, the tissue lining the inside of the artery. Subsequently he noted the accumulation of fatty substances from the blood within this mucoid deposit. He called these raised, swollen areas atheromas. This word, from the Greek athere, for porridge, reflected the porridge-like appearance of the fatty mucoid substance to Virchows critical eye. The term atherosclerosis refers to the advanced for of the human disease where multiple plaques of this process are present. Arteriosclerosis refers to generalized hardening of the arterial walls by a collection of fibrous connective tissue and calcium salts. The two conditions frequently co-exist with atheromatous plaques developing in arteries already lined with sclerotic changes. Virchow suspected an infectious factor when he noted that leukocytes, the cells of infection, occasionally were present in the bases of atheroma plaques (Graveline 04: 57-59). Formulated in 1973 and modified in 1986 and 1993 the contemporary view of the pathogenesis of atherosclerosis is called the response to injury hypothesis. The injury postulated is a form of endothelial dysfunction without necessary denudation, which increases permeability to plasma constituents, including lipids, and permits blood monocytes and eventually platelets to adhere to endothelium. Monocytes adhere and subsequently enter the intima, transform into macrophages and accumulate lipid to become foam cells, contributing to the evolution of the lesion. Single or short lived injurious events can be followed by restoration of endothelial function and regression of the lesion. Repeated or chronic injury, however, results in the development of an atheromatous plaque. Endothelial injury has been induced in experimental animals by mechanical denudation, hemodynamic forces (AV fistula), immune complex deposition, irradiation, and chemicals to cause intimal smooth muscle proliferation and in the presence of high-lipid diets, typical atheromas. Endothelial cells (EC) have a number of properties and functions for the maintenance of the permeability barrier namely (1) the elaboration of anticoagulant and antithrombotic molecules such as prostacyclin, thrombomodulin, plasminogen activator and heparin-like molecules; (2) elaboration of prothrombotic molecules Von Willenbrand factor (Factor VIIIa), tissue factor, plasminogen activator inhibitor and (3) extracellular matrix production (collagen, proteoglycans). In some situations, EC dysfunction comprises a loss of surface heparin-like proteoglycan molecules that prevent thrombus formation and inhibit smooth muscle cells growth, thereby promoting thrombosis and intimal thickening, and depressed release of EC-derived relaxing factors, leading to abnormal vasoconstriction. These changes can result in acute occlusion of a vessel by spasm or a localized thrombotic event and may contribute to atherosclerosis (Schoen 94: 480, 470, 471). Atherosclerosis is a slow progressive disease caused by hyperlipidemia (Schoen 94: 473) after initial damage to the endothelium. Sclerosis, means scarring and ather, the ancient Greek word for gruel or porridge, because the material that makes up plaque the lesions of an affected artery looks like oatmeal. Plaque is grungy, yellowish and crumbly, with cholesterol crystals in it. It can induce clotting of the blood or can break off an embolize downstream, where it blocks branches and stops the flow of blood to whatever part of the brain, foot bowel, kidney or heart the branches supply. Most people imagine that an atherosclerotic plaque is a deposit of cholesterol and fat in the artery wall, like a collection of egg yolk and butter fat that has been left there from excess fat in the blood. It is actually more like scar tissue in the artery wall. Plaque is made up of inflammatory cells, fibrous tissue and smooth muscle cells that grow into the artery lining where it is injured, much like scar tissue (Spence 06: 28). Hyperlipidemia is a major risk factor in atherosclerosis. Atherosclerotic plaques are rich in cholesterol and cholesterol esters, which are derived largely from lipoproteins, such as LDL (low density lipoprotein) cholesterol, triglycerides, C-reactive protein and homocysteine, in the blood. The dietary intake of cholesterol and saturated fats, such as those present in egg yolk, animal fats, and butter, raises the plasma lipoprotein levels, conversely a diet without cholesterol or fat found in animal products or vegetable oils, lowers the plasma lipoprotein levels, enabling atheromas to be reabsorbed into the bloodstream, by osmotic process of lipoprotein levels, in the blood. Greenland Eskimos, who have a high dietary fat consumption, were thought to have low rates of ischemic heart disease, because of the high content of omega-3 fatty acids in their diets (present in fish and fish oils) (Schoen 94: 474, 475, 476). In a recent study of 137 mummies probable or definite atherosclerosis was evident in 34percent of the mummies. Only 4percent, however, had atherosclerosis in the coronary arteries, where it can cause heart attacks. The 51 ancient Peruvians, who in life presumably ate a lot of beans and complex carbohydrates such as sweet potatoes and manioc, had atherosclerosis in 25percent of their mummies. Three of the five Aleutian hunter-gatherers, who ate a paleo diet high in meat and devoid of sweets and grains, showed atherosclerosis. One woman who died in her late 40s had the kind of disease we see in people with bypass surgery (Brown 13). Atherosclerosis  Credit: American Heart Association Besides releasing hormones, damaged platelets also release substances that stimulate growth of the artery wall and cause the inner lining, the endothelium, to thicken. Damage to the endothelium, the lining of the artery, sets off a series of unhappy events. First, it attracts platelets and white blood cells to attach to the normally smooth endothelium. Next, it leads some white blood cells (monocytes) to migrate under the endothelium into the innermost layer of the artery itself (the intima), where they transform into macrophages that eat cholesterol and accumulate cholesterol forming a fatty streak. Finally smooth-muscle cells migrate from the middle muscular layer of the artery (the media), grow in the intima, and cause it to thicken further, forming a plaque. Although it would seem logical to assume that when plaque develops in the artery wall, it should stick out into the opening in the tube-like vessel and cause it to narrow, what actually happens is that the artery enlarges to accommodate the plaque so the flow rate along its wall remains constant. This growth is termed compensatory enlargement or vascular remodeling. At some point, an event occurs, such as a rupture of the plaque or a hemorrhage into the plaque. The scar formation in the plaque causes it to encroach on the arterys flow channel. The plaque become inflamed, and infected, and if it ruptures, the protective fibrous cap of the plaque cracks open and the granular contents of the plaque may embolize downstream or provoke the local formation of clot, blocking the artery completely. In other cases, a hemorrhage into a plaque, rather than an outward rupture, cause a sudden blockage of the artery. Virtually all heart attacks and about 70 to 80 percent of strokes, begin with a plaque rupture (Spence 06: 31, 32, 35). The basic lesion the atheroma, or fibrofatty plaque- consist of a raised focal plaque within the intima, having a core of lipid (mainly cholesterol and cholesterol esters) and a covering fibrous cap. Atheromas are sparsely distributed at first, but as the disease advances, they become more and more numerous, sometimes covering the entire circumference of severely affected arteries. As the plaques increase in size, they progressively encroach on the lumen of the artery as well as on the subjacent media. Consequently, the small arteries, plaques are occlusive, compromising blood flow to distal organs and causing ischemic injury, but in large arteries they are destructive, weakening the affected vessel wall, causing aneurysms or rupture or favoring thrombosis. Moreover, extensive atheromas are friable, often yielding emboli of their grumous contents into the distal circulation (atheroemboli), most commonly noted in the kidneys, and in cerebrovascular accidents (CVA, strokes) (Schoen 94: 473). Atheromatous plaques appear white to whitish yellow and impinge on the lumen of the artery. Plaque formation is often presaged by a fatty streak composed of lipid-filled foam cells. Plaques vary in size from 0.3 to 1.5 cm in diameter but sometimes coalesce to form larger masses. The superficial surface of these lesions tend to be firm and white (the fibrous cap). The centers of larger plaques may contain a yellow, grumous debris, called an atheroma, Greek for gruel. The distribution of atherosclerotic plaques in humans in the abdominal aorta is much more involved than the thoracic aorta, and aortic lesions tend to be much more prominent around the ostia of its major branches. The most heavily involved vessels are the coronary arteries (usually within the first 6 cm), the popliteal arteries, the descending thoracic aorta, the internal carotid arteries, and the vessels of the circle of Willis. Vessels of the upper extremities are usually spared, as are the mesenteric and renal arteries, except at their ostia. Atherosclerotic lesions usually involve the arterial wall only partially around its circumference and are patchy and variable along the vessel length and the severity of atherosclerosis in one artery does not predict the severity in another. In advanced atherosclerosis, progressive fibrosis may convert the fatty atheroma to a fibrous scar. Almost always, atheromas in advanced disease undergo patchy or massive calcification, causing brittleness, that can be detected by intravascular ultrasound or ultrafast computed tomographic scanning (Schoen 94: 477, 478). In general vascular abnormalities cause clinical disease by (1) progressive narrowing the lumina of vessels and producing ischemia of the tissue perfused by that vessel; (2) provoking intravascular thrombosis, causing acute obstruction or embolism (or both); or (3) weakening the walls of vessels, thereby leading to dilation and rupture. Congenital anomalies of blood vessels may predispose the myocardium to infarction or may cause sudden death. Among these diverse vascular anomalies, two have particular importance: developmental or berry aneurysms (involving the cerebral vessels) and arteriovenous fistulas or aneurysms. Abnormal communications between arteries and veins can arise as developmental defects, from rupture of an arterial aneurysm into the adjacent vein, from penetrating injuries that pierce the walls of artery and vein and produce an artificial communication, or from inflammatory necrosis of adjacent vessels. The connection between artery and vein may consist of a well-formed vessel, a vascular channel formed by the canalization of thrombus, or an aneurysmal sac, which can induce cardiac failure. Thrombosis is a complication of late-stage atherosclerosis that can lead to embolism as the fibrinous thrombosis becomes superimposed by plaque. Plaques may be equivalent to benign monoclonal neoplastic growths (such as leiomyomas) perhaps induced by exogenous chemical (e.g. cholesterol). Both herpes virus and cytomegalovirus have been detected in human atheromatous plaques that have existed long enough to be exposed. In larger vessels, such as the aorta, the important complications of these plaques are large mural thrombi that may dislodge and yield peripheral emboli, aneurysmal dilation due to destructive impingement of the atheromatous plaques on the media, or rupture of cholesterol emboli into the bloodstream. In smaller arteries, the narrowing of the lumen by atheromatous plaques, especially if accompanied by thrombosis or hemorrhage, can lead to occlusion, causing myocardial infarction or stroke (Schoen 94: 482-484, 467, 472, 473). A stroke occurs when a blood vessel that brings oxygen and nutrients to the brain bursts or is clogged by a blood clot or some other particle. Because of this rupture or blockage, part of the brain doesnt get the blood and oxygen it needs.Deprived of oxygen, nerve cells in the affected area of the brain cant work and die within minutes. And when nerve cells cant work, the part of the body they control cant work either. The devastating effects of stroke are often permanent.There are four main types of stroke. Two are caused by blood clots or other particles (ischemic strokes), and two by bleeding (hemorrhage). Cerebral thrombosisand cerebral embolismare caused by clots or particles that plug an artery. They account for about 7080 percent of all strokes. Ruptured blood vessels cause cerebraland subarachnoid hemorrhages. These (bleeding) strokes have a much higherfatality rate than strokes caused by clots.Stroke is a medical emergency. Every second counts!Stroke affects different people in different ways. It depends on the type of stroke, the area of the brain affected and the extent of the brain injury. Brain injury from a stroke can affect the senses, motor activity, speech and the ability to understand speech. It can also affect behavioral and thought patterns, memory and emotions. Paralysis or weakness on one side of the body is common (Sanders 08). Cerebral thrombosis results when a blood clot bocks a cerebral vessel that has been narrowed by atherosclerotic deposits. Cerebral hemorrhage is bleeding of a vessel into the brain. Progressive cerebrovascular sclerosis occurs when arteries supplying the brain are progressively narrowed, resulting in chronic cerebrovascular insufficiency and giving rise to dizziness, transient paralysis, forgetfulness and senility. Atherosclerosis is the underlying cause, either by weakening the artery walls with subsequent rupture and bleeding or by narrowing of the arteries predisposing to sudden occlusion by blood clots (Elvin-Lewis 77: 178). About 75 percent of strokes can be prevented in high-risk patients. In most cases the symptoms are transient, or the stoke is mild enough that a good recovery is likely. Treatment with the clotbuster drug tPa within three hours after the stroke increases by 40 percent the chance of someone who has suffered a stroke going home without a severe disability. tPA (tissue plasminogen activator) is a naturally occurring substance the body makes to dissolve clots. This can be manufactured and used as a clot-busting drug to open up blocked arteries in people who are experiencing a stroke or heart attack ,but to be effective it has to be used soon after the artery becomes blocked. In difficult cases, new approaches can make a big difference in controlling blood pressure, lowering cholesterol, and preventing arterial disease. The key to controlling difficult high blood pressure is a simple blood test to measure the activity of one kidney enzyme called renin, and an adrenal gland hormone called aldosterone. The levels of fat in the blood after a meal turn out to be more important than the level of cholesterol measured in a fasting cholesterol test. Most people who have muscle problems from cholesterol-lowering drugs in the family called statins can resolve them by reducing the dose, adding ezetimibe (a generic drug marketed as Zetia or Ezetrol)_ and taking CoQ10, a dietary supplement. The Most neglected treatable cause of artery disease is high levels of an amino acid called homocysteine, which can be treated with vitamins (Spence 06: viii). The measures recommended for stroke prevention are quitting smoking, controlling blood pressure adhering to a Mediterranean diet (plus exercise) and taking cholesterol-lowering drugs, opening up blocked arteries, taking drugs (Aspirin) that reduce blood clotting and treating homocysteine with vitamins. Drugs that lower the level of cholesterol in the blood probably reduce by about 30 percent in four year the risk of any stroke, and by about 50 percent the risk of strokes due to atherosclerosis plaque deposits, often called hardening of the arteries as opposed to strokes due to high bod pressure. Opening up blocked arteries via either surgery on the carotid (neck) artery or stenting (inserting a metal expanding sleeve into a narrowed artery to hold it open) reduces stroke risk substantially: in persons in whom the carotid artery is narrowed by 70 percent or more and who have had warning symptoms of stroke, surgically removing the inner layer of the artery with the plaque that is blocking the artery (endarterectomy) reduces stroke or death by two-thirds over two years. (For patients with a narrow carotid artery who have not yet had warning symptoms of a stroke, surgery is only for those at high risk of stroke, as evidence by the particles breaking off the plaque (microemboli) that can be detected by ultrasound of the brain arteries (transcranial Doppler) (Spence 06: ix, X). Transient blockage of the carotid artery or its major branches, the anterior and middle cerebral arteries, commonly causes weakness and numbness on the opposite side of the body (face, arm, and leg). This may be accompanied by thickening of speech from either side, or by aphasia, if it is the carotid artery on the dominant side. Occasionally the numbness or weakness may spare the face or leg; rarely if the anterior cerebral artery alone is affected the leg alone may be affected. Ischemia (blocked blood flow) in the brainstem due to a problem with the vertebral arteries or basilar artery may cause numbness or weakness down one side of the body, but commonly the symptoms have a variation such as numbness on both sides of the face, or around the mouth, or the face on one side and the arm and leg on the opposite side. When numbness or weakness affects only the leg, then the problem may be in the spinal cord or in the nerve roots in the lower back the sciatic nerve or one of its branches. Similarly, numbness in one hand alone is commonly from a problem with the median nerve (carpal tunnel syndrome) or form a disc in the neck that affects a nerve root that goes down the arm or the nerve that winds around the elbow, the ulnar nerve (funny bone). Weakness in both legs simultaneously, particularly if accompanied trouble with bladder control, often indicates a problem with the spinal cord. When something is compressing the spinal cord and causing symptoms, the compression must be relieved to avoid permanent paralysis (Spence 06: 22, 23). The arteries that run up through the bones in the back of the neck are the vertebral arteries. The vertebral arteries penetrate the base of the skull, and then join up to form the basilar artery which supplies the brainstem. Then the basilar artery branches to form the two posterior cerebral arteries, which supply the back part of the brain (the occipital lobes) and the interior mesial (underneath, toward the center) temporal lobes. The blood vessels supplying this part of the brain are called the vertebrobasilar system. Visual symptoms (flashing lights, zigzag lines, loss of vision in both eyes or in the visual field off to one side) point to involvement of the occipital lobes. Impaired visual processing, for example, being unable to recognize familiar faces, or becoming lot in familiar surroundings, indicate involvement of the nearby cortex that serves visual association. Permanent impairment of short-term memory suggests permanent damage in both temporal lobes; temporary impartment of short-term memory, which is called transient global amnesia, points to temporary loss of blood flow to the mesial temporal lobes. Double vision points to involvement of the top part of the brainstem (the midbrain), vertigo or facial numbness, to involvement in the middle party (the pons) and the thickening of speech (dysarthria) and trouble with swallowing to the lowest party (the medulla). Numbness or weakness on one side or both sides of the body may occur when lesions in any part of the brainstem affect the nerves that run from the spinal cord to the brain, or vice-versa. Clumsiness and staggering suggest involvement of the cerebellum. Sudden loss of blood flow to the cranial nerve nuclei and their connections to the brainstems may cause facial numbness and weakness, double vision, difficulty swallowing, thickness of speech, vertigo, tinnitus (ringing in the ear) and deafness (Spence 06: 24). The artery that supplies blood to the eye (ophthalmic artery) is a branch of the internal carotid artery (the main artery that carries blood to the front part of the brain) and a typical attack would involves sudden loss of vision in one eye, recovering over minutes. This is called amaurosis fugax, which translates as fleeting blindness. It is important to distinguish between loss of vision in one eye and loss of vision in one half of the visual field, because this is what determines where the problem is coming from. If the problem is only in one eye, it originated in the carotid artery on the same side; if the loss of vision is off to one side in both eyes, it may be from a problem in the vertebral arteries of the basilar artery, which together supply blood to the back part of the brain on the side of the brain opposite the visual loss. Getting the diagnosis wrong could lead to an unnecessary operation on a narrowed carotid artery that is not causing symptoms - surgery for asymptomatic carotid narrowing (Spence 06: 19, 20). Vascular inflammatory injury, often with necrosis of blood vessels (vasculitis) is encountered in diverse diseases and clinical settings. The terms arteritis, vasculitis and angiitis are used interchangeably. In many patients with vasculitis the serum reacts with cytoplasmic antigens in neutrophils by immunofluorescence and immunocheimical assays, indicating the presence of antineutrophil cytoplasmic autoantibodies (ANCA). Classification and characteristics of vasculitis are organized into large vessel, medium-size vessel and small vessel vasculitis. Large vessel vasculitis includes Giant cell (temporal) arteritis and Takayasus arteritis. Medium sized vessel vasculitis includes Polyarteritis nodosa (classic polyarteritis nodosa) and Kawasaki disease. Polarteritis nodosa, also known as classic polyarteritis nodosa, presents as a necrotozing inflammation of medium-sized or small arteries without glomerulonephritis or vasculitis in arterioles, capillaries or venules. Small vessel vasculitis includes Wegeners granulomatosis, Churg-Strauss syndrome, microscopic polyangiitis (microscopic polyarteritis), Henoch-Schonlein purpura, essential cryoglobulinemic vasculitis and cutaneous leukocytoclastic angiitis. Giant cell (temporal) arteritis is the most common form of vasculitis, it involves granulomatous arteritis of the aorta and its major branches, with a predilection for the extracranial branches of the carotid artery, that often involves the temporal artery and usually occurs in patients older than 50. It is often associated with polymyalgia rheumatic, a flu-like syndrome with joint stiffness often with claudification of the jaw and visual symptoms including blindness. A genetic predisposition exists in those exhibiting increased HLA-DR4 antigen. Clinical improvement almost always achieved with corticosteroid treatment. Takayasus arteritis presents as a granulomatous inflammation of the aorta and its major branches and usually occurs in patients under 50, predominantly females 15 to 40 years old, most common in Asia. This granulomatous vasculitis of medium and larger arteries was described in 1908 by Takayasu as a clinical syndrome characterized principally by ocular disturbances and marked weakening of the pulses in the upper extremities (pulseless disease), related to fibrous thickening of the aortic arch with narrowing or virtual obliteration of the origins of the great vessels arising in the arch. The salient clinical features include weakening of the pulses of the upper extremities with markedly lower blood pressure in the upper extremities; ocular disturbances, including visual defects, retinal hemorrhages, and total blindness; hypertension; and various neurologic deficits, ranging from dizziness and focal weakness to complete hemiparesis (Schoen 94: 494). Polyarteritis nodosa (PAN) group is characterized by systemic involvement with the vasculitic process and includes the classic type of vasculitis also called macroscopic form of PAN. Classic PAN is manifested by necrotizing inflammation of small or medium-sized muscular arteries typically involving renal, coronary and visceral vessels and sparing the pulmonary circulation. PAN is a disease of young adults, although it may occur in children and older individuals. The most common manifestations are fever of unknown cause and weight loss; hypertension, usually developing rapidly; abdominal pain and melena (bloody stool) due to vascular lesions in the alimentary tract; diffuse muscular aches and pains and peripheral neuritis, which is predominantly motor. About 30 percent of PAN patients have hepatitis B antigen in their serum. Angiography shows vascular aneurysms or occlusions of main visceral arteries in 50 percent of cases. Untreated, the disease is fatal but therapy with corticosteroids and cyclophosphamide results in remissions or cures in 90 percent. Effective treatment of the hypertension is a prerequisite for a favorable prognosis. Kawasaki disease is an arteritis involving large, medium-sized, and small arteries and associated with mucocutaneous lymph node syndrome, the coronary arteries, aorta and veins may be involved, it usually occurs in children and infants under four years old. The acute illness is manifested by fever, conjunctival and oral erythema and erosion, edema of the hands and feet, erythema of the palms and soles, a skin rash often with desquamation, and enlargement of cervical lymph nodes. It is usually self-limited. Epidemic in Japan, the disease has been reported in Hawaii and increasingly in the United States. Approximately 20 percent of patients develop cardiovascular sequelae, with a range of severity from asymptomatic coronary artery extasia or aneurysm formation to giant coronary artery aneurysms (7 to 8 mm) with rupture or thrombosis, myocardial infarction or sudden death. It is the leading cause of acquired heart disease in children in the United States. Acute fatalities occur in 1 to 2 percent of patients. Intravenous gamma globulin administered with aspirin appears to reduce the prevalence of long-term coronary artery abnormalities (Schoen 94). Wegeners granulomatosis causes a granulomatous inflammation involving the respiratory tract and necrotizing vasculitis and often necrotizing glomeronephritis, affecting small to medium-sized vessels. The peak incidence is in the fifth decade. Typical clinical features include persistent pneumonitis with bilateral nodular and cavitary infiltrates (95%), chronic sinusitis (90%), mucosal ulcerations of the nasopharynx (75%) and evidence of renal disease (80%). Other features include skin rashes, muscle pains, articular involvement, mononeuritis or polyneuritis and fever. Untreated the course of the disease is malignant, 80% of patients die within 1 year. This grim prognosis is improved dramatically by the use of immunosuppressive cytotoxic drugs, such as cyclophosphamide, up to 90% of patients demonstrate significant improvement. Churg-Strauss syndrome presents as eosinophil rich granulomatous inflammation involving the respiratory tract and necrotizing vasculitis affecting small to medium-sized vessels and associated with asthmas and blood eosinophilia. Microscopic polyangiitis, also known as microscopic polyarteritis, appears as necrotizing vasculitis and pulmonary capillaritis, with few or no immune deposits affecting small vessels of the skin, mucous membranes, lungs, brain, heart, gastrointestinal tract, kidneys and muscle. The major clinical features are hemoptysis, hematuria, and proteinuria; bowel pain or bleeding; and muscle pain or weakness. Cutaneous vasculitis is manifested by palpable purpura. Most patients respond well simply to removal of the offending agent. Henoch-Schonlein purpura is vasculitis with IgA- dominant immune deposits affecting small vessels. Typically involves skin, gut and glomeruli and associated with arthralgias or arthritis. Essential crypglobulinemic vasculitis is with cryoglobulin immune deposits affecting small vessels, associated with crypglobulins in serum, skin and glomerluli are often involved. Cutaneous leukocytoclastic angiitis is isolated cutaneous leukocytoclastic angiitis without systemic vasculitis or glomerulonephritis (Schoen 94: 489). Thromboangiitis obliterans (Buergers disease) is a distinctive disease characterized by segmental, thrombosing, acute and chronic inflammation of intermediate and small arteries and sometimes veins of the extremities. The condition has occurred almost exclusively in men who were heavy cigarette smokers. Buergers disease begins before the age of 35 years in most patients and before 20 years in some, in some cases it affects the arms as well as the legs. Small microabscesses within the thrombus create a pattern quite distinct from the bland thrombosis of atherosclerosis. The early manifestations are a superficial nodular phlebitis, cold sensitivity of the Raynaud type in the hands, and pain in the instep of the foot induced by exercise. Eventually patients suffer from vascular insufficiency that often leads to excruciating pain and ultimately gangrene of the extremities. Remissions and relapses correlate with cessation or resumption of smoking (Schoen 95: 498). Raynauds disease refers to paroxysmal pallor or cyanosis of the digits of the hands or feet, and infrequently the tips of the nose or ears (acral parts). It is caused by intense vasospasm of local small arteries or arterioles, principally of young, otherwise healthy women. The fingers turn from white to blue to red. Later in the course, intimal proliferation can appear in the artery walls. Raynauds disease reflects an exaggeration of normal central and local vasomotor responses to cold or emotion. In contrast, Raynauds phenomenon refers to arterial insuffiency of the extremities secondary to the arterial narrowing induced by various conditions, including systemic lupus erythematosus, systemic sclerosis (scleroderma), atherosclerosis, or Buergers disease. Indeed Raynauds phenomenon may be the first manifestation of any of these conditions (Schoen 94: 499). Peripheral artery disease refers to changes in the aorta and its branches, the arteries. Aortic aneurysms can form along any part of this main blood vessel, or one of its branches. Sometimes the force of blood under high pressure will rip the lining of the aorta, this is called aortic dissection, or a dissecting aneurysm if it occurs in one of the enlarged areas. A number of changes can occur in the arteries, the veins and the optic nerve that connect to the eye, and the retina, where vision is detected on the back surface of the eyeball. Treatment for severe diabetic eye complications is more successful when blood pressure is normal (Wilson & Childre 06: 9, 40). Varicose veins and phlebothrombosis/thrombophlebitis together account for at least 90% of clinical venous disease. Varicose veins are abnormally dilated, tortuous veins produced by prolonged, increased intraluminal pressure. The superficial veins of the leg are the preponderant site of involvement, however, portal hypertension, usually due to cirrhosis of the liver, leads to varices in the esophageal and hemorrhoidal veins. It is estimated that 10 to 20% of the general population eventually develop varicose veins in the lower legs. The condition is much more common over age 50, in obese persons, and in women, a reflection of the elevated venous pressure in the lower legs caused by pregnancy. Occupations that require long periods of standing and long automobile or airplane rides frequently lead to marked venous stasis and pedal edema, even in normal individuals. Varicose dilation of veins renders the valves incompetent and leads to venous stasis, congestion edema, and thrombosis. Despite thrombosis of superficial varicose veins, embolism is very rare. Distention of the veins is often painful, but most patients have no symptoms until marked venous stasis and edema develop. Some of the most disabling sequelae are the development of persistent edema in the extremity and trophic changes in the skin that lead to stasis dermatitis and ulcerations. Because of the impaired circulation the tissues of the affected part are extremely vulnerable to injury. Wounds and infections heal slowly or tend to become chronic varicose ulcers. Because venous thrombosis inevitably leads to inflammatory changes within the vein wall, thrombophlebitis and phlebothrombosis are two designations for a single entity. Cardiac failure, neoplasia, pregnancy, obesity, the postoperative state, and prolonged bed rest or immobilization predispose to venous thrombosis. The deep leg veins account for more than 90% of cases of thrombophlebitis (Schoen 94: 504, 505, 506). An aneurysm is an abnormal bulge or ballooning in the wall of an artery. Arteries are blood vessels that carry oxygen-rich blood from the heart to other parts of the body. An aneurysm that grows and becomes large enough can burst, causing dangerous, often fatal, bleeding inside the body. Most aneurysms occur in the aorta. The aorta is the main artery that carries blood from the heart to the rest of the body. The aorta comes out from the left ventricle of the heart and travels through the chest and abdomen. An aneurysm that occurs in the aorta in the chest is called a thoracic aortic aneurysm. An aneurysm that occurs in the aorta in the abdomen is called an abdominal aortic aneurysm. Aneurysms also can occur in arteries in the brain, heart, intestine, neck, spleen, back of the knees and thighs, and in other parts of the body. If an aneurysm in the brain bursts, it causes a stroke.About 15,000 Americans die each year from ruptured aortic aneurysms. Ruptured aortic aneurysm is the 10th leading cause of death in men over age 50 in the United States. Many cases of ruptured aneurysm can be prevented with early diagnosis and medical treatment. Because aneurysms can develop and become large before causing any symptoms, it is important to look for them in people who are at the highest risk. Experts recommend that men who are 65 to 75 years old should be checked for abdominal aortic aneurysms.When found in time, aneurysms can usually be treated successfully with medicines or surgery. If an aortic aneurysm is found, the doctor may prescribe medicine to reduce the heart rate and blood pressure. This can reduce the risk of rupture.Large aortic aneurysms, if found in time, can often be repaired with surgery to replace the diseased portion of the aorta (Sanders 08). An aneurysm is a localized abnormal dilatation of any vessel. Aneurysms may occur in any artery or vein of the body, most commonly the aorta. A true aneurysms is bounded by generally complete but often attenuated arterial wall components, with quantitatively or qualitatively altered structure. The blood within a true aneurysm remains within the confines of the circulatory system. Atherosclerotic, syphilitic and congenital aneurysms are of this type. False aneurysms, also called pseudoaneurysms or pulsating hematoma, is an extravascular hematoma that communicates with the intravascular space. The vascular wall has been breached, and the wall of the aneurysmal sac consists of only outer arterial layers or periarterial tissue. A leak at the junction (anastomosis) of a vascular graft with a natural artery produces this type of lesion. Arterial dissections, usually of the aorta, arise when blood enters the wall of the artery, dissecting between its layers and creating a cavity within the vessel wall itself. The two most important causes of true aortic aneurysms are atherosclerosis and cystic medial degeneration. Syphilis also causes aortic aneurysms. Aneurysms are often classified by macroscopic shape and size. A berry aneurysm is a small spherical dilatation, rarely exceeding 1 to 1.5 cm in diameter, that is most frequently found in the brain. Saccular aneurysms are essentially spherical, involving only a portion of the vessel wall, and vary in size from 5 to 20 cm in diameter, often partially or completely filled with thrombus. A fusiform aneurysm is a gradual, progressive dilation of the complete circumference of the vessel up to 20 cm in length. Infection of a major artery that significantly weakens its walls is called a mycotic aneurysm. Mycotic aneurysms may originate either (1) from the lodgement of a septic embolus at some point within a vessel usually as a complication of infective endocarditis, (2) as an extension of an adjacent suppurative process or (3) by circulating organisms directly infecting the arterial wall. Syphilitic aneurysms are almost always confined to the thoracic aorta and usually involve the arch. Thoracic aortic enlargements give rise to signs and symptoms referable to (1) encroachment on mediastinal structures, (2) respiratory difficulties due to encroachment on the lungs and airways., (3) difficulty in swallowing due to compressure of the esophagus, (4) persistent cough due to irritation of or pressure on the recurrent laryngeal nerves, (5) pain caused by erosion of bone, (6) cardiac disease as the aortic aneurysm leads to dilation of the aortic valve or narrowing of the coronary ostia, and (7) rupture of the aneurysm (Schoen 94: , 499, 501). Atherosclerotic aneurysms usually occur in the abdominal aorta, most frequently between the renal arteries and the iliac bifurcation, or in the common iliac arteries, but the arch and descending parts of the thoracic aorta can be involved. Large aneurysms shorten longevity primarily owing to rupture, a danger directly related to the size of the aneurysm. The risk of rupture for a small abdominal aortic aneurysm (less than 4 cm) is about 2%, aneurysms larger than 5 cm are the most dangerous, with a risk 5 to 10% per year. Timely surgery is key, operative mortality for untreated aneurysms is approximately 5% whereas emergency surgery after rupture carries a mortality rate of more than 50%. Aortic dissection are based largely on aortic angiography, but the noninvasive techniques, two-dimensional cardiac ultrasound (especially transesophageal echocardiography), computed tomography (CT, and magnetic resonance imaging (MRI) are increasingly useful. At one time, aortic dissection was almost invariably fatal, but the prognosis has markedly improved. The development of surgical procedures involving the aortic wall and the early institution of intensive antihypertensive therapy permit salvage of 65 to 75 percent of patients (Schoen 94: 500, 504). 3. Endocarditis Bacterial endocarditis results from actual colonization of the endocardium by infectious agents through the interstitial capillary bed beneath the endothelium and the blood within the endo-cardial lumen. Chronic angina pectoris that doesnt fully go away after a day or two, week, month or year, usually happens when dead heart muscle from a myocardial infarction (heart attack) becomes infected with pyogenic organisms most obviously Streptococcus pyogenes, in about 50% of cases of endocarditis, which causes strep throat and rheumatic fever in children and rheumatic heart disease in adults with necrotic heart attack damaged cardiac muscle that doesn't go away like most infections, attacks the valves, creates huge septic vegetations over the myocardium and burdens the vegetarian patient with a 25 percent chance of dying over 10 years, if untreated by antibiotics. Untreated or drug resistant infection is the main reason that the body doesn't heal and acute injury progresses to chronic disease in six months, generally. Some streptococcal illnesses of the heart may last up to 6 weeks without antibiotics and can be severe. Organisms most commonly recovered from such infections are Streptococcus sanguis, S. faecalis, and in heroin addicts, also Candida parapsilosis. It has been reported that 90% of atherosclerotic plaques contain Chlamydia pneumoniae. Infective endocarditis is one of the most serious of all infections, it is characterized by colonization or invasion of the heart valves or the mural endocardium by a microbiologic agent, leading to the formation of bulky, friable vegetations laden with organisms. Not only the valves, but also the aorta (infective endoaortitis), aneurysmal sacs, or other blood vessels can also become infected. Virtually every form of microbiologic agent, including fungi, rickettsieae (Q fever) and chlamydiae, has at one time or another been responsible for these infections, but most cases are bacterial, hence the usual term, bacterial endocarditis. More than half of cases are attributable to various streptococci most prominently Streptococcus pyogenes, a group A strep the viridans, not the group A responsible for rheumatic fever   hemolytic streptococcus. They are the dominant cause of subacute disease, and as organisms of relatively low virulence, they generally gain a foothold only in heart having some underlying disease or predisposition. Although relatively rare in members of the affluent population who are treated with antibiotics rheumatic fever is an often overlooked important cause of atrial fibrillation, systemic embolism, pulmonary edema, pulmonary hypertension and dyspnea with pregnancy or minimal exertion that is easily treated with broad spectrum antibiotics (Heger et al '04: 197, 198). Staphylococcus aureus accounts for about 20 to 30% of cases, it can infect normal valves and pericardium with Staph lesions, and is a leading cause of acute endocarditis, and can lead to death within days to weeks of more than 50% of heart failure patients, if a lesion occludes an artery, and they are not promptly treated with doxycycline. Septic thrombophlebitis, often associated with bacteremia, can be an infection of the cerebral, pelvic, superficial or portal venous systems. When fibrin deposition and thrombus formation results from perivascular inflammation bacterial invasion of the clot can occur (Elvin-Lewis 77: 194). Failure of clinical recognition of infective endocarditis in 43 per cent of the forty-seven patients is a major factor in the relatively high mortality of this disease (Robinson et al '70). In about 5 to 20% of all cases of endocarditis no organism can be isolated from the blood because of prior antibiotic therapy, because of difficulties in isolation of the offending agent, or because organisms become deeply embedded within the enlarging vegetation and are not released into the blood. Bacteremias emanate frequently from the gut, oral cavity and trivial injuries, seeding the blood with cardiotoxic species such as Streptococcus viridans, S. faecalis, S. sanguis, Peptostreptococcus or Bactroides fragiles. With antibiotic treatment the vegetations sometimes undergo progressive sterilization, organization and can eventually become recalcified, leaving scars. With repeated blood samples, positive cultures can be obtained in 80 to 95% of cases. With early diagnosis and appropriate antibiotic treatment, the overall 5-year survival is in the range of 50 to 90%, being best for streptococcus induced subacute disease and worst for staphylococcal or fungal acute endocarditis (Schoen 94: 550-554). Staph infections are often resistant to all antibiotic treatment except doxycycline which is nearly always effective, but causes the permanent yellowing of developing teeth of children younger than 8. The lesions caused by staph are generally 1 to 2 cm in diameter and tend to grow in a cluster of similar lesions that can become colonized by Strep. Doxycycline, the once a day antibiotic, is not only cheap, it is effective against Staph and Strep, that responds better to penicillin. Rheumatic Heart Disease on Autopsy  Rheumatic fever (RF) caused by Streptococcus pyogenes (Lancefiled type A) is characterized by painful swollen joints, fever, myocarditis, rash on the trunk and inner aspects of the thighs and upper arms (erythema marginatum) and rheumatic nodules over the elbows, knees, hands, and ankles. Salicylates (aspirin) and glycosteroids have been found to suppress the acute febrile and exudative manifestation of rheumatic fever but cannot prevent cardiac damage, for which penicillin is needed (ElvinLewis 77: 303). Chronic rheumatic heart disease (RHD) is characterized principally by deforming fibrotic valvular disease (particularly mitral stenosis), which produces permanent dysfunction and severe, sometimes fatal, cardiac failure decades later. The incidence of rheumatic fever and RHD has steadily declined in the United States and other developed countries. In 1940, the mortality rate from RHD in the United States was 20.6 per 100,000 population, in 1982, it was 2.2. This decline in morbidity and mortality has been related to improved diet, better control of streptococcal infections by penicillin and an apparent overall reduction nin the virulence of the causative organisms. Globally, there an estimated 15 to 20 million new cases a year, and there are occasional resurgences in localized areas of the United States. During the 1980s there were major outbreaks in Salt Lake City, Pittsburgh and other large U.S. cities, reemergence of virulent strains of group A streptococcus are the cause (Schoen 94: 549). Between 1990 and 2000 prescriptions for antibiotics declined by 40%. RH is no longer just of concern to the uninsured. Patients with chronic rheumatic heart disease may need to buy their own antibiotics online. Sporadic antibiotic prophylaxis to treat bacterial infections is fundamental to the recovery from any serious disease. With the consumption of probiotics there are not any side-effects (Huffnagle '05). RF is a postinfectious, immunological disease that results either from (1) heightened immunologic reactivity to streptococcal antigens that evoke antibodies cross reactive with human tissue antigens or (2) some form of autoimmune reaction incited by a streptococcal infection. Initial attacks of RF follow some weeks after streptococcal infection (1 to 5 weeks). Around 3% of people get RF and RHD following streptococcal pharyngitis. During acute RF, widely disseminated, focal, inflammatory lesions are found in various sites. Most distinctive within the heart, they are called Aschoff bodies, and is a pancarditis as it can be found in any of the three layers of the heart pericardium, myocardium or endocardium, that serve as the foci of fibrinoid necrosis in the form of small (1 to 2 mm) friable vegetations (verrucae). These acute valvular changes cause little dysfunction but subendocardial lesions, may induce irregular thickenings called MacCallums plaques, usually in the left atrium. In chronic RHD, the mitral valve is virtually always deformed, but involvement of another valve, such as the aortic, may be clinically important. The RF is overwhelming the most frequent cause of mitral stenosis. The mitral valve alone is involved in 65 to 70% of cases, mitral and aortic in about 25%. The likelihood of acute arthritis increases with age at the time of the attack, appearing in about 90% of adults and less commonly in children. Lesions of the skin in the form of subcutaneous nodules or erythema marginatum are present in 10 to 60% of cases. Acute RF appears most often in children between the ages of 5 and 15 years. Both younger and older individuals, however, may be affected, and about 20% of first attacks occur in middle or later life. Typically, one joint after another becomes painful and swollen for a period of days and then subsides spontaneously, leaving no residual disability. Acute carditis develops in about 50 to 75% of children but only about 35% of adults, and comes with a 1% chance of sudden death, but untreated with antibiotics causes a 25% chance of dying from a heart attack over ten years and does not tend to heal of its own accord (Schoen 94: 550). Angina and rheumatism tend to clear up during or shortly after completing a course of antibiotics allowing an increase in physical acivity and a chance for the injured myocardial muscle to heal. But in progressive disease the tissue is likely to become reinfected and the diarrheal and dental cavity side-effects of chronic antibiotic consumption (antibiotics require probiotic supplementation) and the proliferation of antibiotic resistant cultures are serious issues that must be dealt with. Antibiotics may be necessary to treat bacterial endocarditis, usually caused by -hemolytic strains of pneumococcal bacteria, and the chronic heart patient will want to purchase them online. The bacteria can be found in most plaques and colonize  vegetations on atherosclerotic arteries and necrotic heart muscle that even with treatment is prone to re-infection. Penicillin is generally the most effective treatment for Streptococcus spp. but some people have a life threatening allergy to penicillin, and any antibiotic will work. Most of the bacterial species that infect the heart and kidneys are easily treated with a five day course of any twice a day broad-spectrum antibiotic. This is good because most physicians these days are very poor at treating antiobiotic resistance and have fallen out of love with the best medicine of the 20th entirely, despite the ease with which probiotics taken within two hours of antibiotics consumption and for two weeks after completing the course. Between 1990 and 2000 prescription of antibiotics declined 40% and uninsured people might not be only the patients with chronic rheumatic heart disease because they have not tried any antibiotics, or treated antibiotic resistant bacteria, virus and fungi, since they became infected. Doxycycline, the once a day antibiotic, that permanently yellows the teeth of children under 8, and metronidazole (Flagyl ER) are essential to solving the problem of antibiotic resistance. When pyogenic organisms such as Staphylococcus aureus and Bactroides fragiles are involved, acute bacterial endocarditis may result that does not respond to most antibiotic drugs. Bactroides fragilis, from as far away as the large intestine, can be involved, and there is definitely a connection between diet and the heart. Staphylococcus aureus, often transmitted by the meticulously washed hands of health care workers, tends to resistant to all antibiotics except doxycycline, and the lesions are painful and dangerous with 50% of acute endocarditis from Staph infection resulting in death, according to some health care professionals who don't necessarily know to prescribe doxycycline or use effective and strong chlorine bleach preparations for institutional cleaning and HibiClens for the hands, nonetheless Staph is particularly painful and causes large lesions that are readily colonized by Strep. The fecal coliform Bactroides fragiles and Peptostreptococcus, which may infect the heart, and Clostridium difficile which causes serious infectious diarrhea resist any antibiotic but metronidazole (Flagyl ER). To avoid idiopathic malabsortive disorders of the gut and kidneys it is probably more effective to treat E. coli, the most common cause of bladder and kidney infections, with metronidazole rather than Bactrim, which monopolizes the monograph for E. coli despite a long list of adverse drug reaction and nearly certain vitamin B12 deficiency, post-infectious auto-immune diarrhea and kidney disease due to malabsorption and antibiotic resistance of Clostridium difficile and the common streptococcus treated by all other antibiotics. Viruses and fungi are rare in the heart and many bacterial diseases are kind to the heart although they devastate other parts of the anatomy. Because Sporanox (itraconazole) is stongly contraindicated for the treatment of congestive heart failure due to interactions with Digitalis and hypertension drugs and fungal infections are not likely to compete with bacterial endocarditis, in the absence of profound immunosuppression with antibiotics. Candida albicans is the most common fungal pathogen to arise from antibiotic resistance, $1 athlete's foot cream (clotrimazole) applied topically to the affected area should be effective although an oral anti-Candidal remedy might be purchased over-the-counter to cure antibiotic associated diarrhea. Echovirus is an entero and respiratory infection that also attacks the heart cured only to Human Immune Globulin IV (Elvin-Lewis 77: 178, 28). Bacterial infections may spread into and through the lymphatics to create acute inflammatory involvements in these channels. The most common etiologic agents are the group A beta-hemolytic streptococci, although any virulent pathogen may be responsible for an acute lymphangitis. The affected lymphatics are dilated and filled with exudate, chiefly of neutrophils and histiocytes, that usually extends through the wall into the perilymphatic tissues and may in severe cases produce cellulitis or focal abscesses. The most common cause of lymphatic blockage are (1) spread of malignant tumors with obstruction of either the lymphatic channels or the nodes of drainage, (2) radical surgical procedures with removal of regional groups of lymph nodes, (3) postirradiation fibrosis, (4) filariasis, and (5) postinflammatory thrombosis and scarring of lumhatic channels. Persistence of the edema leads to an increase of subcutaneous interstitial fibrous tissue, with consequent enlargement of the affected part, brawny induration, peau dorange appearance of the skin and skin ulcers. Chylous ascites, chylothorax and chylopericardium are caused by rupture of obstructed, dilated lymphatics into the peritoneum, pleural cavity and pericardium. Almost invariably, this is due to obstruction of lymphatics by an infiltrating tumor mass (Schoen 94: 506). Myocarditis is best defined as an inflammatory involvement of the heart muscle characterized by a leukocytic infiltrate and resultant nonischemic necrosis or degeneration of myocytes. Of all patients with the recent onset of unexplained CHF, chest pain, or life-threatening arrhythmias, who have endomyocardial biopsy approximately 4 to 10% are demonstrated to have myocarditis. The causes of myocarditis include many microbiologic agents but most cases of well-documented myocarditis are viral in origin. The most frequently implicated agents are Coxsackievirus A and B, ECHO (treated with Human Immune Globulin IV), poliovirus (treated with metronidazole) and certain strains of influenza A and B viruses (treated with Tamiflu). In most instances, the cardiac involvement follows several days to a few weeks after a primary viral infection elsewhere. Less commonly, myocarditis is cause by a nonviral microbiologic agent or its toxins. A direct cardiac infection is caused by the protozoa Trypanosoma cruzi producing Chagas disease, which is uncommon in the northern hemisphere but affects up to one-half of the population in endemic areas of South America, and myocardial involvement is found in approximately 80% of infected individuals. About 10% of patients die during an acute attack, others may enter a chronic immune-mediated phase and develop progressive signs of cardiac insufficiency 10 to 20 years later. Metronidazole (Flagyl ER) seems to be called for. Trichinosis is the most common helminthic disease associated with cardiac involvement for which the antiprotozoal properties of metronidazole (Flagyl ER) are indicated. Injury to the myocardium by the potent exotoxin of the bacterium Corynebacterium diphtheria is characterized by patchy myocyte necrosis with only a sparse lymphocytic infiltrate. Lyme disease is a systemic illness caused by the bacterial spirochete Borrelia burgdorferi transmitted by the deer tick that has dermatologic, neurologic and rheumatologic manifestations that is effectively treated with any antibiotic. Myocarditis occurs in approximately two-thirds of patients with Lyme disease. Myocarditis occurs in many patients with acquired immunodeficiency syndrome (AIDS). Myocarditis can also be related to allergic reactions (hypersensitivity) to a particular drug, including some antibiotics, diuretics, and antihypertensive agents. Cardiac sarcoidosis and rejection of a transplanted heart may also be considered forms of myocarditis. Giant cell myocarditis is characterized by a widespread inflammatory cellular infiltrate containing multinucleate giant cells of macrophage origin. If the patient survives the acute phase of myocarditis, the inflammatory lesions heal with or without scarring (Schoen 94: 563, 564). Three major factors contribute to the widespread success of organ and bone marrow transplantation; (1) better selection of candidates, (2) improved maintenance immunosuppression (including the use of cyclosporine A, along with steroids and azathioprine) and (3) early histopathologic diagnosis of acute allograft rejection by sequential endomyocardial biopsy. When myocardial injury is not extensive, the rejection episode is usually successfully reversed by increased immunosuppressive therapy. Advanced rejection may be irreversible and fatal often as the result of infection and development of malignancies, particularly lymphomas (generaly related to fungus or the Epstein-Bar virus in the presence of profound chonic therapeutic immunosuppression of fungi). Graft-versus-host disease (GVHD) malignancy is a critical element for cure through allogeneic HCT. Reduced-intensity regimens have also made it possible to extend HCT to older patients (up to 75 years) and younger patients with health problems that make them ineligible for high-intensity regimens. Significant post-transplant problems can result from toxic effects related to the preparatory treatments, GVHD, infections, and relapse of the underlying disease. Continued research is leading to further improvements and better survival results (Schoen 94: 580). Oral corticosteroids can be very useful for the treatment of myocarditis, particularly that of viral origina for which there is no better treatment short of Human Immune Globulin IV. Nonsystemic arteritis is most frequently caused by the direct invasion of infectious agents, usually bacteria or fungi particularly aspergillosis and mucormycosis. Vascular lesions frequently accompany bacterial pneumonia, or occur adjacent to caseous tuberculous reactions, in the neighborhood of abscesses, or in the superficial cerebral vessels in cases of meningitis. Much less commonly they arise from the hematogenous spread of bacteria, in cases of septicemia or embolization from infective endocarditis. Vascular infections may weaken the arterial wall and result in the formation of a mycotic aneurysm. In systemic lupus erythematosus, mitral and tricuspid valvulitis is occasionally encountered and lead to the development of small, sterile vegetations from 1 to 4 mm in diameter, sterile, granular pink vegetations that may be single or multiple. Lesions are frequently located on the undersurfaces of the atrioventricular valves, but they may be scattered. Nonbacterial thrombotic endocarditis (NBTE) is a form of vegetative endocarditis most often encountered in debilitated patients, such as those with cancer or sepsis (Schoen 94: 554, 555) and is probably of fungal origin. Candida species, which are part of the normal flora of the skin, mouth and GI tract are the ost frequent cause of human fungal infections . Severe disseminated candidiasis is associated with neutropenia secondary to chronic granulomatous disease, leukemia, anticancer therapy or immunosuppression after transplantation. Cadida can be directly introduced into the blood by intravenous lines, catheters, peritoneal dialysis, cardiac surgery or intravenous drug abuse. Althoug the course of candida sepsis is less rampant than that of bacterial sepsis, disseminated Candida eventually causes shock and disseminated intravascular coagulation. Cadida has numerous molecules on its surface that mediate its adherence to host tissues and secretes aspartyl proteinase, which may be involved in tissue degradation and adenosine, which blocks neutrophil oxygen radical production. Candida infections of the oral cavity (thrush) and vagina produce superficial, white patches or large, almost fluffly membranes that are easily detached, although this may be painful, leaving a reddened, irritated underlying surface. Spread of oral candidiasis, as by the nasogastric tube, may lead to similar lesions in the esophagus. Candida also causes cutaneous eczematoid lesions in moist areas of the skin. Severe invasive candidiasis associated with antibiotic consumption and immunosuppression, or with phagocyte depletion involves the kidney in 90% of cases, causing multiple microabscesses in both the cortex and the medulla. The fungus occupies the center of the lesion, with a surrounding area of necrosis and polymorphonuclear infiltrate. Candida right-sided endocarditis resulting from direct inoculation of the fungi into the bloodstream, most often in drug addicts, gives rise to large, friable vegetations that frequently break off into emboli. In the lungs lesions are extensive and polymorphouds and often are hemorrhagic and infarct-like owing to fungal invasion of vascular walls. Meningitis, multiple subcutaneous abscesses, arthritis and osteomyelitis are some of the other presentations of disseminated candidiasis. The fungus may evoke little or no inflammatory reaction, cause the usual suppurative response, or occasionally produce granulomas (Samuelson & Von Lichtenberg '94: 354, 355). Antifungal drugs are available over-the-counter and online without prescription. Besides the timely use of athlete's foot cream (clotrimazole), rather than antifungal foor powder spray (Toftate) that causes diffuse pain and agina, which can be purchased for $1 and has time and time again proved its effectiveness against all sorts of fungal infections that can be reached with a topical application there are several oral antifungal drugs such as Lamisil and Grifulvin V available for the treatment of athlete's foot and toenail and fingernail onchymycosis but Sporanox (itraconazole) claims to be effective against all major known fungal pathogens, Candida, Aspergillis, Histoplasmosis, Cryptococcus, Mycormycosis and others and is prescribed -, 200 mg 3 times daily for 3 days, then 200 mg twice daily until no longer immune-compromised. The monograph has been edited so that it now reads; For primary prophylaxis of aspergillosis in immunocompromised individuals at high risk of invasive disease such as neutropenic patients with acute myelogenous leukemia (AML) or myelodysplastic syndrome (MDS) or hematopoietic stem cell transplant (HSCT) recipients with graft-versus-host disease (GVHD). IDSA considers posaconazole the drug of choice; alternatives are itraconazole or micafungin. The prophylaxis of invasive Aspergillus and Candida infections in patients, 13 years of age and older, who are at high risk due to being severely immunocompromised, such as hematopoietic stem cell transplant (HSCT) recipients with graft-versus-host disease (GVHD) or those with hematologic malignancies with prolonged neutropenia from chemotherapy and also fororopharyngeal candidiasis. Sporanox is hepatoxic and liver enzymes must be monitored on a monthly basis and is highly contraindicated in heart failure. IV amphotericin B is the preferred alternative to oral Sporonox (itraconazole). The effectiveness of oral antifungals is 60-80%. There is still a chance of re-infection after finishing the course of the medication. The re-infection rate is 15% but can be as high as 25% in diabetics. Serious adverse reactions are less than 0.5%. There are some interactions between these medication and other drugs such as cyclosporine, cimetidine, rifampin, terfenadine, and caffeine (Debrowolski 04: 14-16). Sporanox is strongly contraindicated in cases of congestive heart failure due to adverse reaction with antihypertensive and Digitalis drugs. Primary tumors of the heart are rare but metastatic tumors to the heart occur in about 5% of patients dying from cancer. The most common primary tumors, in descending order of frequency are myxomas, fibromas, lipomas, papillary fibroelastomas, rhabdomyomas, angiosarcomas and other sarcomas. The five most common all are benign and account collectively for 80 to 90% of primary tumors of the heart. Myxomas are the most common primary tumor of the heart in adults. About 90% are located in the atria. Surgical removal is usually curative, although rarely the neoplasm recurs months to years later. Lipomas are most often located in the left ventricle, right atrium or atrial septum and are not necessarily neoplastic. In the atrial septum, the depositions are called lipomatous hypertrophy. Papillary fibroelastomas cluster as hair-like projections up to 1 cm in diameter, covering up to several centimeters of the endocardial surface. Rhabdomyomas are the most frequent primary tumor of the heart in infants and children. Cardiac angiosarcomas and other sarcomas are not distinctive from their counterparts in other locations. Occasionally cardiac complications represent the dominant feature of the presentation of a noncardiac malignant tumor. Chemotherapy and radiation also manifest their own district cardiovascular side effects and toxicities (Schoen 94; 569-571). In patients with carcinoid tumors, cardiac involvement, is one of the sequelae of the carcinoid syndrome. The syndrome is characterized by distinctive episodic flushing of the skin and cramps, nausea, vomiting and diarrhea in almost all patients; bronchoconstrictive episodes resembling asthma in about one-third of patients, and cardiac lesions in about one-half. The carcinoid syndrome is encountered in about 1% of patients who have carcinoid tumors (argentaffinomas) whatever the primary site and in 10% of those with gastrointestinal carcinoid tumors with hepatic metastes (Schoen 94: 555). Cancer is an idiopathic disorder. Drug info removed the explanation that antineoplastic cancer drugs are antibacterial, antiviral and antifungal to better gauge the ability to reduce tumor size. Bone pain, known either as rheumatoid arthritis, or myeloma, is an extremely common serious complication of endocarditis, because it is crippling and this comprimises cardiorespiratory exercise, and retreating or untreated infections can metastasize through the bloodstream or break through the bone to marrow causing leukemia or through soft tissue to the lymphatic system, causing lymphomas. Bone pain is the primary physical symptom of leukemia and very common in lymphoma. Oral Thalidomide, used in conjunction with dexamethsaome, a corticosteroid, are the first FDA approved chemotherapeutic drugs usually taken by people diagnosed with multiple myeloma and plasma cell dyscracias. Initial necrosis is usually caused by exposure to toxic chemicals, such as benzene, or physical trauma to the bone. Untreated with basic antibiotics and antifungals, the necrotic tissue becomes septic and doesn't heal and the diseases progresses and becomes worse, and the mycotic infection of the necrotic tissue breaks through the bone and induces mutations distorting the peripheral complete blood count and white blood cell differential, although there is no more exposure to the toxic substance. The patient may be quite confused about their disease due to an affinity for the well-documented, intoxicating, effects of fungi such as brewer's yeast and psychedelic mushrooms. The pathogenesis of neoplastic white cell disease hypothetically relies heavily upon the failure to treat the large fungal cells causing neoplastic mutation in human cells. Athletes foot crme (clotrimazole) is often ffective at keeping the patient able to jog, used twice daily for three weeks, is likely to completely eliminate the fungal infection causing the arthritis anywhere the topical preparation can penetrate. Another antifungal foot powder spray (toftate), powder being prescribed for elders, however caused a diffuse pain to occur, and elders are definitely recommended to use clotrimazole (athlete's foot cream) as their basic antifungal, reminded of the fact they are not cured until they can run without any undue pain. Athlete's foot cream (clotrimazole) can be purchased for $1 and the only side-effect comes from the fact it passes the blood-brain barrier and can cause musculofacial tics if repeatedly applied to the face, and upper body in which case it should be applied to the feet. Metronidazole (Flagyl ER) may be needed to treat antibiotic resistant bacterial infections of the GI, bones and joints such as gouty group B Streptobacillus agalactiae, kidney infecting E. coli and Peptostrestococcus, doxycycline for Staph lesions causing subluxations of the vertebrae but rheumatic heart disease responds best to penicillin. Antibiotics, antifungals and antineoplastics must all be taken with probiotics within two hours of consumption and for two weeks after completing the course to avoid diarrhea, 30% of fecal matter should composed of bacterial cells, or dental cavities, as side-effect. 4. Valvulitis Disorders characterized by valvular involvement and dysfunction include calcific aortic valve stenosis, calcification of the mitral annulus, mitral valve prolapse, rheumatic heart disease, three forms of vegetative endocarditis (including infective endocarditis, nonbacterial thrombotic endocarditis and endocarditis of systemic lupus erythematosus and carcinoid heart disease. Endocarditis usually involves the heart valves. Major predisposing factors are congenital heart defects, rheumatic valvular disease, bicuspid or calcific aortic valves, mitral valve prolapse, and hypertrophic cardiomyopathy. Prosthetic valves are a particular risk. Occasionally, mural thrombi, ventricular-septal defects, and patent ductus arteriosus sites become infected. The actual nidus for infection is usually a sterile fibrin-platelet vegetation formed when damaged endothelial cells release tissue factor. Infective endocarditis occurs most often on the left side (eg, mitral or aortic valve). About 10 to 20% of cases are right-sided (tricuspid or pulmonic valve). IV drug abusers have a much higher incidence of right-sided endocarditis (about 30 to 70%). Pulmonary, Tricuspid, Aortic and Mitral Valves  Credit: Cleveland Clinic Functional disturbances of the valaves are stenosis and insufficiency. Stenosis is the failure of a valve to open completely, thereby impeding forward flow. Insufficiency or regurgitation in contrast, results from failure of a valve to close completely, thereby allowing reversed flow. Abnormalities of flow often produce abnormal heart sounds (murmurs). Valvular dysfunction can vary in degree from slight and physiologically unimportant to severe and rapidly fatal. Sudden destruction of an aortic valve cusp by infection may cause rapidly fatal cardiac failure owing to massive regurgitation. Mitral stenosis is however remarkably well tolerated. Valvular insufficiency may result from either intrinsic disease of the valve cusps or damage to the supporting structures (e.g. the aorta, mitral annulus, chordae tendineae, papillary muscles, ventricular free wall) without primary changes in the cusps. Valvular stenosis almost always is due to a primary cuspal abnormality and is virtually always a chronic process. (Schoen 94: 543). Audible events generated by the heart are classified as sounds if they are abrupt and murmurs if they consist of prolonged vibrations. Sounds result from an abrupt interruption of the momentum of local blood flow, whereas murmurs occur when there is disturbved or turbulent high-velocity flow. If the distal mitral valve sleeve has been converted to a funnel and fails to open, resulting in an opening snap that is transmitted back toward the source of the moving column of blood. The opening snap is heard at the base (close to the left atrium), whereas the murmurs caused by disturbed inflow are heard only at the apex (Heger et al '04: 181). Aortic valve incompetence can result from a number of pathologic processes that affect the valve leaflets and/or the aortic root. Congenital bicuspid valve deformity, with or without superimposed endocarditis, is the leading cause of aortic regurgitation in individuals younger than 30, whereas aortic root dilation from hypertension often causes valves to fail to coapt in older individuals. Rheumatic fever, Marfan disease, rheumatoid arthritis, aortitis, trauma and aortic dissection are additional etiologies. The primary pathophysiological finding is backflow into the left ventricle, which leads to arterial diastolic collapse, lowering of the arterial diastolic pressure, and a decrescendo early diastolic murmur. Two secondary outcomes are an increase in the systolic stroke volume and turbulent mitral valve inflow. Increased stroke volume and outflow velocity are accompanied by a misystolic murmur emulating that aortic stenosis. Turubulent mitral inflow causes middiastolic and presystolic murmurs (Austin Flint murmur) that emulates mitral stenosis in patients with severe aortic regurgitation. Prominent sounds can be heard as well. The second sound may be tambour (like a kettle drum) if the aorta is dilated. The first sound may be perceived as "split" because of the loud ejection sound. The findings in aortic regurgitation can be quite different if the condition is acute rather than chronic. Aortic regurgitation is usually well tolerated for many yars because of compensatory mechanisms that can counterbalance the impact of the leaky ventricle (Heger '04: 182-184). Aortic stenosis is the most frequent valve abnormality; it can be congenital or acquired. The definition of congenital aortic stenosis excludes congenital bicuspid and the rare uni-cuspid valves that do not cause functional stenosis at birth but have enhanced susceptibility to superimposed damage that later can cause stenosis. Acquired aortic stenosis is usually the consequence of calcification induced by the wear and tear of aging. With the decline in the incidence of rheumatic fever, rheumatic aortic stenosis now accounts for less than 10% of cases of acquired aortic stenosis. Therefore the overwhelming majority of cases represent age-related degenerative calcification and come to clinical attention primarily in the sixth to seventh decades of life with pre-existing bicuspid valves but not until the eighth and ninth decades with previously normal valves (Schoen 94: 544). In approximately 1 to 2% of the population, the aortic valve is congenitally bicuspid. Bicuspid aortic valves are generally neither stenotic nor symptomatic at birth or throughout early life, but they are predisposed to progressive calcification. The raphe that composes the incomplete commissure is frequently a major site of calcific deposits. With or without calcification, bicuspid aortic valves may also become incompetent or be complicated by infective endocarditis. As the stenosis worsens, angina or syncope, and risk of sudden death, may appear. The myocardial oxygen supply/demand balance is difficult to maintain when the ventricle must create more than 200 mg Hg pressure to deliver 100 mm Hg to the aorta, coronary perfusion is compromised when the ratio of capillaries to the myocardial mass is reduced by entriuclar hypertrophy and passage of capillary blood through the myofibers is obstructed by the prolonged systolic compressions (Heger et al '04: 189). The onset of symptoms such as angina, syncope of congestive heart failure, in aortic stenosis carries a poor prognosis if not treated by surgery (death in more than 50% within 3 years). There is no effective medical therapy for for aortic stenosis. Congestive failure can be treated with digoxin. Patients with aortic stenosis are often drastically improved by surgical aortic valve repair or replacement. Doppler echocardiography, which measures the flow velocities a well as structure, can be used repetitively to examine the progression of disease with time (Schoen 94: 545). Aortic valve replacement is required when the left ventricle is not tolerating the volume overload or that the systolic function of the left ventricle is declining. When endocarditis destroys the valve's ability to close competently, urgent surgery is required. The surgeon may be able to debride the infected tissue, including perivalvar absesses and affect a bacteriologic cure more effectively than with antibiotics alone. The choice of prosthetic valve should take into account the patient's age, life expectancy and ability to maintain and tolerate life-long anticoagulation. Tissue valves, fashioned from porcine aortic valves or bovine pericardium, permit freedom from anticoagulation, have a functional longevity of approximately 10 years and should be used for women who may consider future pregnancies. Although modern mechanical valves are unlikely to undergo component failure and should last indefinitely in the absence of infection, thrombosis or fibrous growth they require frequent assessment of prothrombin time and maintainence of therapeutic anticoagulation. Homograft cryopreserved (freeze-dried) aortic valves from human cadavers do not enjoy superior durability over xenograft (animal) tissue valves. The Ross precedure in which the patient donates his or her own pulmonic valve to the aortic position and has the explanted pulmonic valve replaced with a homograft, requires considerably more surgical complexity but in the hands of experience surgeons shows promise of durability as well as growth of the living tissue valve. Valvuloplasty, or valve repair without replacement, is only applicable to a small percentage of cases (Heger '04: 187, 188). In elderly people, especially women, degenerative calcific deposits can develop in the ring of the mitral valve. They can often be visualized as irregular, stony hard nodules (2 to 5 mm in thickness) that lie behind the leaflets. Rheumatic fever causes retraction of the leaflets and dilation of the mitral annulus. Rheumatic mitral regurgitation is three times more common in men than women. However in the United States rheumatic fever is overlooked as a cause of mitral valve prolapse, endocarditis, hypertension, ischemic disease and cardiomyopathy are more common. Mitral valve stenosis almost always results from rheumatic fever (Heger et al '04: 191, 192, 197). The process generally does not affect valvular function. Occasionally the calcium deposits may penetrate sufficiently deeply to impinge on the atrioventricular conduction system and produce arrhythmias (and occasionally sudden death). Because calcific nodules may provide a site for thrombi that can embolize, patients with mitral annular calcification have an increased risk of stroke. The calcific nodules can also be the nidus for infective endocarditis. Heavy calcific deposits are sometimes visualized on echocardiography or seen as a distinctive, rink-like opacity on chest radiographs. Mitral valve prolapse (myxomatous degeneration of the mitral valve) is a valvular abnormality, where one or both mitral leaflets are enlarged, redundant, or floppy and prolapse, or balloon back, into the left atrium during systole. The mitral valve often becomes incompetent, and the mitral regurgitation induces an accompanying late systolic or sometimes holosystolic murmur. This is an extremely common condition, thought to be present in about 5 to 10% of the population of the United States, most often young women, but is of serious import to only a small fraction of those affected. Mitral valve prolapse is a common feature of Marfan syndrome and occasionally occurs with other hereditary disorders of connective tissues. Most patients with mitral valve prolapse are asymptomatic, and the condition is discovered only on routine examination by the presence of a midsystolic click. Echocardiography reveals mitral valve prolapse. Although the great majority of patients with mitral valve prolapse have no untoward effects, approximately 3% develop one of four serious complications (1) infective endocarditis is manifold more frequent in these patients than in the general population, (2) mitral insufficiency, from either slow onset attributed to cuspal deformity, dilatation of the mitral annulus or chordal lengthening, or sudden death owing to chordal rupture, (3) stroke or other systemic infarct resulting from embolism of leaflet thrombi and (4) arrhythmias, both ventricular and atrial can develop, although sudden death is uncommon (Schoen 94: 547). Significant mitral stenosis is associated with pulmonary hypertension and inability of the right ventricle to overcome downstream resistance prevents an increase in fow that might magnify further left atrial pressure in reactive pulmonary hypertension (Heger et a '04: 201). Treatment of mitral valve prolapse with beta-adrenergic blocking agents often ameliorate symptoms and antibiotic prophylaxis should be used. Transient acute mitral regurgitation can sometimes be reversed within five minutes by sublingual nitrate administration. Digoxin and treatment of hypertension with artieral dilators or ACE inhibitors may be used chronically or to prepare patients for valve surgery. Lessening the symptoms of mitral stenosis can be achieved medically by preventing heart rate increases or treating existing sinus tachycardias or rapid response to atrial fibrillation with beta-adrenergic blocking agents. Beta blockers may be given in the presence of pulmonary edemia if the heart rate is elevate and can bring rapid relief by allowingthe elft atrium time to decompress. Arterial dilator drugs should be discouragd bcause they might cause refex tachycardia and increased fow rate through the stenotic valve. Unless there is a strong contraindication, anticoagulation with warfarin (Coumadin) is recommended in patients with mitral stenosis, especially if intermittent or chronic atrial fibrillation is present. (Heger et al '04: 202). Significant mitral stenosis should be relieved by mechanical means, either catheter-based ballon or direct surgical commissurotomy. Heavily calcified or immobile valves require replacement. A good-quality transthoracic echocardiogram combined with Doppler interrogation can provide data regarding the functional anatomy of the valve, the degree of stenosis and the presence of mural thrombus. Transesophageal echocardiography is a prerequisite for performance of either commissurotomy procedure because of the enhanced ability to screen the atrium for thrombus and the better images of the valve leaflets. Valve repair, rather than replacement, is often possible when mitral regurgitation warrants operative intervention becaue of progressive left atrial and ventiruclar enlargement. When the atrium achieves a diameter of more than 5 cm, (by echocardiographic measurement) the onset of atrial fibrillation is almost invariably predictable, if not already present. The leaflets are usually sufficiently redundant to tolerate resection of one-fourth of the leaflet area combined with reinforcement of the annulus (annuloplasty) to render the valve competent (Heger et al '04: 202, 203). Replacement of damaged cardiac valves with prostheses has become a common and often lifesaving mode of therapy. Tissue valves, fashioned from porcine aortic valves or bovine pericardium, permit freedom from anticoagulation, have a functional longevity of approximately 10 years and should be used for women who may consider future pregnancies. Although modern mechanical valves are unlikely to undergo component failure and should last indefinitely in the absence of infection, thrombosis or fibrous growth they require frequent assessment of prothrombin time and maintainence of therapeutic anticoagulation. Homograft cryopreserved (freeze-dried) aortic valves from human cadavers do not enjoy superior durability over xenograft (animal) tissue valves. Artificial valves fall primarily into two categories mechanical prostheses using different types of occluders, such as caged balls, tilting disks, or hinged flaps and tissue valves usualy bioprostheses consisting of chemically treated animal tissue, especially porcine aortic valve tissue, which has been preserved in a dilute glutaraldehyde solution and subsequently mounted on a prosthetic frame (called a stent). Mechanical valves are composed of nonphysiologic biomaterials that employ one to two rigid mobile poppet occlude(s), whereas tissue valves are flexible, trileaflet valves that function somewhat like natural valves. Approximately 60% of substitute valve recipients have a serious prosthesis-related problem within 10 years postoperatively ((Schoen 94: 556). The most frequent valve-related complications include (1) thromboembolism (local occlusion of the prosthesis by thrombus or distant thromboemboli), (2) partial dehiscence (separation) of the suture line anchoring the valve leading to a paravalvular leak, (3) infective endocarditis, (4) durability problems caused by structural deterioration, and (5) intrinsic (design-related) obstruction to forward flow. Thromboembolic complications constitute the major problem with mechanical valves. This necessitates long-term anticoagulation. Hemorrhagic side-effects, such as stroke or gastrointestinal bleeding, may arise. Infective endocarditis is an infrequent but serious potential complication developing in about 6% of patients within 5 years of valve replacement. Bioprosthetic valves may develop vegetations that directly involve the prosthetic valvular cusps and can embolize. The major contaminating organisms are staphylococcal skin contaminants (e.g. S. aureus, S. epidermidis) early (less than 1 month) postoperatively and streptococci later. Within 10 years postoperatively, at least 30% of tissue valves require replacement for calcification, often with tearing. Other complications, such as hemolysis induced by high blood shear, mechanical obstruction to flow and dysfunction due to ingrowth of fibrous tissue, may be serious (Schoen 94: 557). 5. Arrhythmia The U.S.Food and Drug Administrationis proposing new rules aimed at improving the reliability of emergency defibrillators following some 45,000 reports of device failures over the past seven years. The defibrillators, found in hundreds of airports, shopping malls and restaurants across the country, are designed to jump-start the heart after it has suddenly stopped. When the heart rhythm is too rapid and chaotic (as it is with ventricular fibrillation) and time is of the essence (as with unstable ventricular tachycardia) defibrillation is performed. Paddles are placed directly on the chest may be used as well as patches or pads to deliver electrical energy from the defibrillator to the chest. Electrical cardioversion and defibrillation are useful for breaking fast rhythms and terminate atrial fibrillation, atrial flutter, ventricular fibrillation, ventricular flutter and any rapid rhythm that does not respond to standard drugs and is not stable, such as when the patient is semiconscious or unconscious or has a low blood pressure (Cohen '10: 87, 89, 91). Sudden cardiac arrest is the condition in which a patient collapses suddenly due to a heart rhythm abnormality. A blockage in the left anterior descending artery is called the widowmaker. Sudden coronary death frequently involves a rapidly progressing coronary lesion, in which plaque disruption and often partial thrombus (and possibly embolization) lead to regional myocardial ischemia that induce a fatal ventricular arrhythmia (Schoen 94: 528). Sudden cardiac arrest victims have a 93 percent fatality rate. In the United States, sudden cardiac arrest takes a life every two minutes, nearly 1,000 individuals each day. The event is most often associated with rapid rhythms from the lower chamber, called ventricular tachycardia or ventricular fibrillation. The heart rhythm problems that cause sudden cardiac arrest most often affect people who have heart disease (an abnormal heart) caused by a heart attack, blockages of the coronary arteries, a weak heart muscle, thick heart muscles or other problems. Reversible causes of sudden cardiac arrest are neutralizing toxic drugs, correct electrolyte abnormalities, and remove blockage (stent) or bypass blockade (surgery). Someone in the household should be trained in cardiopulmonary resuscitation (CPR) (Cohen 10: 49, 45, 47). By counting the number of pulsations over a fifteen-second interval and multiplying that number by four, you can calculate the heart rate (in beats per minute). A normal heart rate is between 60 and 100 beats per minute. A slower than normal rhythm in which the heart rate is below 60 beats per minute indicates sinus bradycardia. If the rhythm exceeds 100 beats per minute, a sinus tachycardia would be present. Heart rates slower than 60 beats per minute can be normal if there are no symptoms such as fatigue, shortness of breath, light-headedness or dizziness. Rapid heart rates (greater than 100 beats per minute) may be normal or abnormal, depending on circumstances. Conditions that weaken the heart muscle may cause rapid heart rhythms, called tachycardias, with rates greater than 100 beats per minute and possibly much faster. The faster the heart rate, the great the chance that delivery of oxygen and other nutrients to the brain and other organs will be impaired. With very fast beats (over 200 a minute) the person will likely become light-headed and dizzy and even pass out. An irregular heart rate might indicate early beats, called premature contractions (coming from either the atria or the ventricles) or may be an indicator of a rhythm problem called atrial fibrillation, in which the atria beats at rates greater than 400 beats per minute. The heart may also beat too slowly (called bradycardia) with heart rates below 60 beat per minute. Reversible causes of bradycardia are nonessential medicines such as beta blockers, calcium channel blockers, digitalis, antiarrhythmic drugs such as sotalol and amiodarone, Lyme disease, hypothyroidism, electrolyte abnormality and drug toxicity. Sinus bradycardia is commonly caused by second-degree heart block, Mobitz type I (block typically occurs in the AV node), second-degree heart block, Mobitz type II (block typically occurs in the His bundle or below), third-degree heart block or complete heart block, Asystole (Cohen 10: 12, 61, 13, 22, 23, 14). Several forms of inherited arrhythmic diseases have common associated gene subtypes (1) Arrhythmogenic right ventricular dysplasia (fat deposits in right ventricular wall) exhibit gene subtypes PKP2, DSP, GSG2, (2) Hypertrophic cardiomyopathy (thickened heart muscle exhibiting gene subtypes MYH7, MYBPC3, (3) Long QT syndrome (has specific ECG patterns) exhibit gene subtypes KCNQ1 (long QT1); KCNH2 (long QT2); SCN5A (long QT3) and (4) Brugada syndrome (has specific ECG pattern) exhibits gene subtypes SCN5A (Cohen '10: 143). Blood flow through the heart chamber should be smooth and rhythmic. The electrical system (which is also called the conduction system) tells the heart (and its chambers) when and in what sequence it should contract and relax to pump blood to the rest of the body. The electrical impulses begin high up in the right atrium, in a structure called the sinus, or sinoatrial node (SA node). A node is defined as a beginning structure or a point for electrical signals to come together and then be redirected to another region in the heart. There are two nodes in the heart: the SA node and the atrial ventricular node (AV node). Impulses move from the SA node across the atrial structures to the AV node (located in the middle of the heart, between the atria and ventricles). A small delay in the electrical signal typically occurs in the AV node before the impulse travels to the His bundle it then moves down through the right and left bundles to specialized Purkinje fibers before activating the ventricles. The presence of disease in any of the specialized electrical conducting tissues may disrupt the flow of electricity through the heart, slowing or pausing the heart rate. Electrocardiogram (ECG) Reading  Credit: IVLine May 2010 A single electrocardiogram (ECG) recording of a heartbeat shows the electrical sequence of the heart. The electrical signal may be broken into different waves. The P wave represents atrial electrical activity; the QRS complex represents ventricular electrical activity; and the QT interval (from the beginning of the Q wave to the end of the T wave) represents the ventricles returning to a resting state. Sometimes a test is performed through the esophagus (called a transesophageal echocardiogram) where it is particularly useful in looking for the presence of blood clots in the left atrium. Blood clots may form in the left atrial appendage (a site that is not well visualized by standard echocardiogram) (Cohen 10: 60, 68). An electrocardiogram, or ECG, is an electrical recording from the limbs and the surface of the chest that shows the pattern of electrical activity in the heart. The ECG can detect rhythm disturbances such as atrial fibrillation, may detect the presence of an old myocardial infarction, and in some circumstances, particularly when repeated daily for several days, can detect a recent heart attack (myocardial infarction). The accuracy of this diagnosis by ECG is greatly aided by measuring enzymes or other markers from the heart released into the bloodstream when the heart muscle breaks down, such as CK (creatine phosphokinase) and troponin. An electrocardiogram requires sticking electrodes to the limbs and the chest, and then making a recording. It is completely safe and painless (except for the pulling of chest hair when the electrodes are removed) (Spence 06: 43). Atrial fibrillation is a very common heart rhythm problem. It is known as an irregular rhythm. The chance of developing atrial fibrillation increases with age. According to recent statistics from the American Heart Association, atrial fibrillation may be found in 3 to 5 percent of people over the age of 65. Atrial fibrillation begets atrial fibrillation (i.e. the longer you are in atrial fibrillation the longer you stay in atrial fibrillation). Early treatment may help to slow down the progression to persistent atrial fibrillation. Blood thinners (anticoagulants) are recommended in patients with congestive heart failure, hypertension, age greater than 75 years, diabetes, or history of stroke. First-line treatment is medication, including antiarrhythmic drugs. If antiarrhythmic drug therapy fails, catheter ablation should be considered. Inciting causes should also be treated; excess alcohol consumption, ischemia, hypertension, stimulant use, and thyroid disorders. Atrial flutter is more organized that atrial fibrillation. Atrial flutter should be treated like atrial fibrillation with respect to medications, including blood thinners (anticoagulants). Atrial flutter is much easier to cure with catheter ablation than atrial fibrillation. Catheter ablation can be considered a first-line therapy for symptomatic atrial flutter. Catheter ablation success rates for the typical forms of atrial flutter are higher than those achieved with atrial fibrillation. A long thin medical device called an ablation catheter is inserted by hand through a blood vessel and then is guided into the heart using x-ray or mapping equipment to find and treat abnormal rhythms. The success rate of catheter ablation is 90 percent or greater for superventricular tachycardia, such as atrial flutter, atrial tachycardia, AV node, AV node reentrant tachycardia, Wolff-Parkinson-White syndrome, 50 to 85 percent for atrial fibrillation, 50 to 75 percent for ventricular tachycardia from coronary artery disease and 90 percent or greater for focal ventricular tachycardia (Cohen 10: 35, 39, 87, 89). Loss of consciousness, passing out or fainting, is called syncope. Fainting is one of the most common reasons people are brought to the emergency room or admitted to the hospital. Common causes of syncope are neurocardiogenic syncope or vasovagal syncope, dehydration, heart rhythm problems, valve problems (aortic stenosis or mitral stenosis), seizure disorder or stroke. Syncope is one of the most common reasons a person visit the emergency room. Syncope from heart problems is often more serious (there is a higher chance of dying) than syncope from non-heart related problems if the heart problems are not successfully treated. Heart-related syncope is often readily treatable. A tilt table test can be used to assess syncope, especially if the history, physical exam, and ECG fail to elucidate any significant cardiac findings. An electrophysiology study (invasive heart rhythm test) is useful, especially when heart rhythm-related abnormalities are discovered in the history, physical exam, or ECG. External or implantable cardiac monitors are often helpful in finding a heart rhythm problem related to syncope. Extensive neurological evaluations may not be necessary and should not be routine for each syncope episode, but they may be performed on a case-by-case basis (Cohen 10: 55). Age and disease can lead to problems such as the heart pumping too fast or too slow - and it can even stop completely, in what is known as a cardiac arrest. The electrophysiology study (EP study) is a crucial procedure for identifying heart rhythm problems. During the EP study catheters are guided through blood vessels into the heart using an x-ray technique called fluoroscopy imaging. The catheters are placed through the veins, arteries, or both up into the chambers of the heart. The doctor is able to pace (stimulate) the heart at a faster rate than normal and take readings of the signals. Electrical signals are recorded directly from the heart. This test can reveal if a pacemaker or a defibrillator is needed. Ejection fraction (EF) measures the percentage of blood that is ejected from the heart. The EF can be calculated through various tests by determining the difference between the volume of blood in the left ventricle at the end of a full relaxation. If EF is less than 35 percent, an implantable cardioverter defibrillator, may be indicated. If the EF is greater than 50 percent, it is less likely an implantable defibrillator would be needed. An exception is hypertrophic cardiomyopathy, a condition in which the heart muscle is thickened and its contraction is very strong (hyperdynamic). The EF in this condition may be greater than 70 percent but there is a heightened risk for sudden death from ventricular arrhythmias, especially if the heart muscle is very thick or there is a family history of sudden death, ventricular tachycardia, or syncope (sudden loss of consciousness). The cardiac MRI is particularly useful at looking for an inherited condition called arrhythmogenic right ventricular dysplasia (in which fat deposits are seen within the wall of the right ventricle) who should be considered candidates for implantable cardioverter defibrillator (ICD) (Cohen 10: 71-72). T-wave alternans (TWA) is a test that can be performed in a doctors office. The patient is attached by electrodes to computerized equipment and undergo a stress test. An intravenous line is inserted and continuous ECG monitoring is performed. The computer analyzes the heart rhythm for a scientific phenomenon called microvolt T-wave alternans (TWA). TWA helps to determine the risk for ventricular tachycardia. It is not useful if the patient is in atrial fibrillation (Cohen 10: 78, 77). The solution for dysrhythmia is often an implanted battery-powered pacemaker which will jolt the heart to keep it in line. An implantable cardioverter defibrillator (ICD) is connected to at least one wire, which is typically inserted through a blood vessel into the heart. A doctor may prescribe an ICD if there might be a high risk for sudden cardiac death without one. An ICD helps to treat lethal arrhythmias such as ventricular tachycardia and ventricular fibrillation (Cohen 10: 16, 28). When the heart rate is too slow, a person may develop symptoms and may need to have a pacemaker surgically implanted to correct the problem. Disease inside or outside the specialized cardiac conduction tissue can also result in fast heart rhythm problems that might require treatment with medications, catheter ablation (a procedure that identifies the heart rhythm abnormality and destroys specific tissue to cure the rhythm problem) or an implantable device such as a defibrillator (Cohen 10). A pacemaker pulse generator is used to treat slow heart rhythms. One, two or three leads may be attached to the device depending on the number of heart chambers that are required to receive pacing therapy. ICDs were developed in the early 1980s and are very similar to pacemakers. ICDs help regulate both fast rhythms (tachycardias) and slow rhythms (bradycardias). Simply put, ICDs monitor the heart rate, and if it is greater than a predetermined (or programmed) value, the ICD may deliver therapy to treat the arrhythmia. Ventricular tachycardia or ventricular fibrillation may be treated by the delivery of a shock (defibrillation) or rapid pacing (also called antitachycardia pacing). This ability to deliver a shock to the heart to terminate tachycardias is one important difference between and ICD and a simple pacemaker. Implantable cardiac monitors are useful in identifying very rare or infrequent abnormal cardiac rhythms that may result in light-headedness, dizziness, or loss of consciousness. The term pacemaker dependent is used when a patient is completely dependent on the pacing function from the device and has little or no underlying heart rhythm. (Cohen 10: 106, 109, 117, 126). In 2012 a team of researchers at the Cedars-Sinai Heart Institute tried to restore the heart's own ability to dictate the beat by creating new pacemaker cells. They used a virus to infect heart muscle cells with a gene, called Tbx18, which is normally active when pacemaker cells are formed during normal development in an embryo. When heart cells were infected with the virus they became smaller, thin and tapered as they acquired the "distinctive features of pacemaker cells. When the virus was injected into a region of the hearts of seven guinea pigs, five later had heartbeats which originated from their new pacemaker. More animal testing would be needed before the technique would ever be considered in people (Gallagher '12). Common heart rhythm (antiarrhythmic) medication and their effects MedicineEffectsCommentsBeta-blockerPO Slows pulse (treats SVT, and atrial fibrillation or flutter) lowers blood pressure, helps treat heart failure and coronary artery disease.Avoid in patients with asthma; can cause impotence, depression, bradycardia and congestive heart failureCalcium channel blockerPO Slows pulse (treats SVT and atrial fibrillation or flutter); lowers blood pressureNot as good as a beta-blocker with coronary artery diseaseAdenosineIV for atrioventriuclar nodal reentrant supraventricular arrhythmia. Commonly causes brief ventricular escape rhythmsAmiodaroneIV Best drug treatment for ventricular tachycardia and atrial fibrillation or flutterMany potential side effects; can affect thyroid, liver, lungs; requires follow up every three months; ventricular tachycardia (proarrhythmia) is a rare complicationDiltiazemIV for urgent ventricular rate controlDofetilideCan treat atrial fibrillation or flutterCan bring on or worsen ventricular tachycardia (proarrhythmia)DronedaroneCan treat atrial fibrillation or flutterAmiodarone-like drug with fewer side effectsFlecainideCan treat SVT and atrial fibrillationCan bring on ventricular tachycardia (proarrhythmia)MexiletineEven less effective than sotalol for ventricular tachycardiaDoes not worsen ventricular tachycardia; can cause confusion, dizziness, numbness and tinglingProcainamideIV Sustained ventricular tachycardiaHypotension may occur with IV loadingPropafenone PO Can treat SVT and atrial fibrillationCan bring on ventricular tachycardia (proarrhythmia)SotalolPO Less effective than amiodarone for ventricular tachycardia and atrial fibrillation or flutterCan bring on or worsen ventricular tachycardia (proarrhythmia)VerapimilIV or PO for atrial fibrillation or flutter or atrioventricular nodal reentrant supraventricularHypotension resulting from vasodilation; consider pretreatment with calciumSource Table 25.1 Cohen 10: 95; Table 18.2 Heger, Nieman & Criley '04: 271 To perform chemical cardioversion the doctor may use medications known as antiarrhythmic drugs to help convert certain arrhythmias (such as atrial fibrillation and atrial flutter) into normal rhythms (Cohen 10: 87, 89, 91, 92, 94). Antiarrhythmia drugs have a number of adverse cardiac side-effects. Beta-blockers seem to be the most highly recommended for slowing the ventiruclar response rate in atrial fibrillation, converting reentrant supraventricular tachyarrhythmias, and suppressing ventiruclar arrhythmias, but chronic treatment with propranolol, metoprolol or timolol following myocardial infarction decreases 1 year mortality, but bradychardia and congestive heart failure, could result from decompensation. Drugs that slow the upstroke, such as quinidine, procainamide, diopyramide, lidocaine, mexiletine, tocainide, moricizine, propafenone and flecainide, have been found worsen outcomes when compared to no treatment in patients with ventricular arrhythmias at risk for sudden coronary death (Heger et al '04: 269-270). In general cardiac drugs are the second leading cause of fatal drug overdose and antiarrhythmia drugs are no exception (Bronstein '11). Hawthorne (Crataegus laevigata) is outstanding both to prevent heart problems and to treat high or low blood pressure, heart disease, edema, angina and heart arrhythmia. Hawthorne doesnt store in the body and isnt accumulative in action. Unlike prescription antiarrhythmia medicine Hawthorne does not have any adverse cardiac effects called decompensation in congestive heart failure, for instance when the treatment for tachycardia causes brachycardia, that is why Hawthorne is called the "supreme herb for the heart". Its important to take Hawthorne on a regular basis if using as a heart tonic (Glastar '12). 6. Congestive Heart Failure Congestive heart failure (CHF) is a constellation of problems rather than a specific disease. It means that the heart is not functioning properly, so that blood is not being pumped around the body efficiently. The end result is that tissues are not receiving adequate blood supply to meet their needs. People with heart failure frequently suffer from fatigue and tire easily when exerting themselves, because decreased pumping action form the heart does not deliver enough blood to the leg muscle during walking or other exercise. As blood pressure rises, it provides higher and higher resistance to the blood flowing out of the heart into the aorta. The higher the resistance in the pipes the harder the pump has to squeeze to get the blood out into the system to feed the organs and muscles. The lungs become congested with blood. This causes some of the water in the blood to squeeze through the very thin walls of the blood vessels into the air sacs of the lungs. That makes it harder to breathe, because oxygen cant pass through the air sacs into the blood vessels when the air sacs are flood with water. Eventually this backup causes edema, or swelling, in the rest of the body, especially the ankles. When the heart cant pump adequately, people get fatigued and develop shortness of breath when they try to exert themselves. Hypertension was the most common cause of congestive heart failure until the middle of the last century (Wilson & Childre 06: 33-35). CHF is a common clinical entity affecting nearly 5 million people in the United States, approximately 1 million will be hospitalized this year. Of CHF cases 75% have antecedent hypertension. Approximatley one-fourth of male and one-half of female myocardial infarction cases will develop CHF in 5 years. The 5-year mortality for CHF in general is about 50%. For severe class 4 CHF, there is 50% mortality in 1 year (Heger et al '04: 165). The New York Heart Association classification of congestive heart failure Class I: Patients with no limitation of activities; they suffer no symptoms from ordinary activitiesClass II: Patients with a slight limitation of activity; they are comfortable at rest and with mild exertionClass III: Patients with marked limitation of activity; they are comfortable only at restClass IV: Patients are symptomatic even at rest, and physical activity brings on discomfortSource: Table 33.2 Cohen 10: 132 Symptoms of heart failure are shortness of breath, leg swelling, decreased exercise tolerance, fatigue, light-headedness, dizziness, confusion, coughing or wheezing, weight gain and palpitation. Causes of heart failure are: (1) lack of blood flow to the heart (ischemia) (2) presence of a heart attack (myocardial infarction (3) weak heart muscle (cardiomyopathy) (4) thickened heart muscle (such as occurs in hypertrophic cardiomyopathy (5) leaky heart valves (valvular regurgitation) (6) tight heart valves (stenosis) (7) inherited conditions (8) drug toxicity (9) heart rhythm problems (arrhythmias) that weaken the heart muscle (tachycardia-induced cardiomyopathy) and (10) infection (such as virus) (Cohen 10: 131, 133). With age changes occur in the myocardium, chamber cavities, valves, coronary arteries, conduction system, pericardium and aorta. Brown atrophy is a term used to describe a small, brown heart with extensive lipofuscin deposits in the muscle cells. Basophilic degeneration describes the accumulation within cardiac myocytes of a gray bluish material, likely glucan, a probably byproduct of glycogen metabolism. With advances age, the amount of subepicardial fat increases, particularly over the anterior surface of the right ventricle. Elderly myocardium also has fewer myocytes, increased collagenized connective tissue and a variable deposition of amyloid. Moreover, associated with increasing age is a reduction in the size of the left ventricular cavity, particularly in the base-to-apex dimension, in part owing to a generally lower cardiac output. This chamber alteration, accompanied by a rightward shift and tortuosity of a dilated ascending aorta, causes the basal ventricular septum to bend leftward, bulging into the left ventricular outflow tract. The configuration, termed a sigmoid septum, can simulate the obstruction to blood leaving the left ventricle. Several changes of the valves are noted, including calcification of the mitral annulus, that is not usually of clinical significance, and aortic valve, frequently leading to aortic stenosis. In addition, the valves develop fibrous thickening, and the mitral leaflets tend to buckle back toward the left atrium during ventricular systole, simulating a prolapsing (myxomatous) mital valve. Moreover, small filiform processes (Lambls excrescences) are on the closure lines of aortic and mitral valves in nearly all subjects older than 60 years of age. Lambls excrescences are wear-and-tear lesions that arise from small thrombi on the valve contact margins. Although these morphologic changes are common in elderly patients at necropsy and may mimic disease, only in a minority are they associated with clinical cardiac dysfunction (Schoen 94: 519). Dysfunction of the heart or the overall cardiovascular system can only occur by one of the following mechanisms. (1) Disruption of the continuity of the circulatory system (e.g. gunshot wound through the thoracic aorta) that permits the blood to escape; in such cases the heart cannot fill, and the resistance against which it pumps is lost. (2) Disorders of cardiac conduction (e.g heart block) or arrhythmias owing to generation of impulses in an uncoordinated manner (e.g. ventricular fibrillation) which leads to contractions of the muscular walls that are not uniform and efficient. (3) A lesion preventing valve opening or one narrowing the lumen of a vessel (e.g. aortic valvular stenosis or coarctation), which obstructs blood flow and overworks the pump behind the obstruction. (4) Regurgitants flow (e.g., mitral or aortic valvular regurgitation) that causes some of the output form each contraction to efflux backward; this necessarily forces portions of the pump to expel the same blood several times and thereby induces substantial myocardial stress. (5) Failure of the pump itself. In the most frequent circumstances, damaged muscle itself contracts weakly or inadequately and the chambers cannot empty properly. In some conditions, however, the muscle cannot relax sufficiently, the left ventricular chamber cannot dilate during diastole, and the heart cannot properly fill (Schoen 94: 520). Any one of the causes mentioned above, when sufficiently severe or advanced, may ultimately impair cardiac function and render the heart unable to maintain an output sufficient for the metabolic requirements of the tissues and organs of the body producing congestive heart failure (CHF) (Schoen 94: 520). Cardiac output (CO) = stroke volume (SV) x heart rate (HR). Heart failure occurs when the heart weakens and cannot effectively pump blood to the rest of the body. Blood may back up from the left side of the heart into the lungs, causing congestion and shortness of breath, this is called left heart failure. Or blood may back up on the right side of the heart, resulting in leg swelling and swelling of other tissues and organs. This is called right heart failure. A person may have either right or left heart failure, or both (Cohen 10: 131). The effects of pure left-sided heart failure are largely due to pulmonary congestion and edema. Right-sided heart failure induces essentially a systemic venous congestive syndrome with hepatic and splenic enlargement peripheral edema, pleural and pericardial effusions and ascites. In contrast to left-sided failure, respiratory symptoms may be absent or quite insignificant in right-sided failure. In many cases of frank chronic cardiac decompensation, however, the patients presents with both right and left sided heart failure. To some extent the right and left sides of the heart act as two distinct anatomic and functional units. Under various pathologic stresses, one side or even one chamber may fail, so from the clinical standpoint, left-sided and right sided failure can occur separately. Nevertheless, because the vascular system is a closed circuit, failure of one side cannot exist for long without eventually producing excessive strain on the other, terminating in total heart failure (Schoen 94: 523, 522). Another classification of heart failure is related to an impaired ability of the heart to pump blood (systolic dysfunction) or to an increased stiffness of the ventricles, which impairs blood filling (diastolic dysfunction). In heart failure, the hearts contraction, relaxation, or both may be affected. Remodeling is a process in which the heart actually reshapes itself due to some injury or insult, such as long-standing fluid accumulation in the hart, which causes the heart muscle to stretch until it can no longer pump efficiently. In long standing or chronic heart failure, many of the hearts repair mechanisms, which were initially compensating and allowing the heart to pump effectively, turn maladaptive and actually make the situation worse. Cardiac hypertrophy is the compensatory response of the myocardium to increased work. Myocardial hyperfunction induces increased myocyte size (cellular hypertrophy) through addition of sarcomeres, the contractile elements that causes an increase in the overall mass and size of the heart. The diameter of cardiac myocytes can increase from the normal 15 m to 25 m or more in hypertrophy. Because adult myocytes cannot divide, augmentation of myocyte number (hyperplasia) cannot occur in the adult heart. The pattern of hypertrophy reflects the stimulus. Pressure-overloaded ventricles develop concentric hypertrophy, with an increased ratio of wall thickness to cavity radius. In contrast, volume-overloaded ventricles (e.g. mitral regurgitation) develop hypertrophy with dilatation (eccentric hypertrophy) with proportionate increase in ventricular radius and wall thickness. Left ventricular hypertrophy is an independent risk factor for cardiac mortality and morbidity, especially for sudden death and ischemic heart disease. Interestingly, an in contrast to pathologic hypertrophy, hypertrophy that is induced by exercise (physiologic hypertrophy) seems to have minimal or no deleterious effect (Schoen 94: 521). Pericardial lesions are almost always associated with disease in other portions of the heart, surrounding structures or secondary to a systemic disorder; isolated pericardial disease is unusual. Normally there is about 30 to 50 ml of thin, clear, straw-colored, translucent fluid in the pericardial space. Under a variety of circumstances, pericardial effusions may appear; because they accumulate slowly and are rarely larger than 500 ml, they are usually without clinical significance. Serous effusion in heart failure are common. The fluid is completely clear, or straw colored, and sterile. Caseous pericarditis creating caseation within the pericardial sac is, until presumed to be tubercuous in origin; infrequently mycotic infections evoke a similar pattern. Chronic or healed pericarditis, although frequently observed on autopsy is rarely of clinical importance, except in the form of adhesive mediastinopericarditis or constrictive pericarditis. Adhesive mediastinopericarditis occurs when the pericardial sac is obliterated, and adherence of the external aspect of the parietal layer to surrounding structures produces a great strain on cardiac function. With each systolic contraction the heart is pulling not only against the parietal pericardium, but also against the attacked surrounding structures, causing hypertrophy. Constrictive pericarditis encases the heart in a dense, fibrous, scar that limits diastolic expansion and seriously restrict cardiac output. Cardiac hypertrophy and dilatation cannot occur because of the dense enclosing scar, and the heart is consequently quiet with reduced output. The major therapy is surgical removal of the shell of constricting fibrous tissue (pericardiectomy). Hemopericardium is the accumulation of pure blood in the pericardial sac, distinct from hemorrhagic pericarditis, a condition in which there is an inflammatory exudate containing blood mixed with pus. Hemopericardiuim is almost invariably due to rupture of the heart wall secondary to myocardial infarction, traumatic perforation or rupture of the intrapericardial aorta. In such cases, blood rapidly fills the sac, under greatly increased pressure, producing cardiac tamponade. As little as 200 to 300 ml of pericardial fluid (blood) may be sufficient to cause death when it accumulates rapidly (Schoen 94: 566-568). The World Health Organization (WHO) defines cardiomyopathy, as heart muscle disease of unknown cause, generally referred to as primary or idiopathic cardiomyopathy and (2) specific heart muscle disease, defined as heart muscle disease of known cause of associated with disorders of other systems. Idiopathic dilated cardiomyopathy (DCM) is characterized by the gradual development of cardiac failure associated with four-chamber hypertrophy and dilatation of the heart, that often weighs two to three times normal, of unknown cause, although a familial occurrence has been found in 20% of cases. The primary abnormality is impairment of left ventricular myocardial contractility (systolic failure; in the end stage, patients may have ejection fractions of less than 25% (normal, approximately 50 to 65%). DCM may occur at any age but usually affects those 20 to 60. It is progressive and unremitting in most cases, fifty percent of patients die within 2 years and only 25% of patients survive longer than 5 years. Death is usually attributable to progressive cardiac failure or arrhythmia. Embolism from dislodgement of an intracardiac thrombus may occur. Cardiac transplantation is frequently recommended. Hypertrophic cardiomyopathy (HCM) is characterized by a heavy muscular hypercontracting heart, in striking contrast to the flabby hypocontracting heart of DCM. It is a diastolic rather than systolic disorder. The differential diagnosis must distinguish HCM from amyloidosis, HHD and age-related subaortic septal hypertrophy. The frequency of sudden death is 2 to 3% per year for adults and 4 to 6% per year for children. Restrictive cardiomyopathy (RCM) is a form of primary myocardial disease, with diastolic relaxation and impeded left ventricular chamber filling that must be distinguished from HCM and Endomyocardial fibrosis, a valvular disease primarily of children and young adults in Africa and other tropical areas. Loefflers endomyocarditis marked by endomyocardial fibrosis typically with large mural thrombi similar to those seen in the tropical disease. The release of toxic products of eosinophils, especially major basic protein, is postulated to initiate endocardial damage, with subsequent foci of endomyocardial necrosis accompanied by an eosinophilic infiltrate, followed by scarring of the necrotic area and layering of the endocardium by thrombus, and finally organization of the thrombus. Untreated or medically treated eosinophilic endomyocardial disease has a poor prognosis, so surgical endomyocardial stripping (decortication) is often recommended. Endocardial fibroelastosis is an uncommon heart disease of obscure etiology characterized by cartilage-like fibroelastic thickening, most common in the first two years of life, it is often accompanied by some form of congenital cardiac anomaly, most often aortic valve obstruction in about one-third of all cases. When focal it can be of no functional important, when diffuse, it may be responsible for rapid and progressive cardiac decompensation and death, particularly in children. Endomyocardial biopsy involves inserting a device (called a bioptome) into the right internal jugular vein, advancing it under fluoroscopic or echocardiographic guidance through the tricuspid valve toward the right side of the ventricular septum, and snipping a small piece of myocardium in its jaws. Each biopsy specimen is a 1 to 3 mm fragment of myocardium most frequently derived from the apical half of the right side of the ventricular septum (Schoen 94: 562). Peripartum cardiomyopathy is the designation given to a globally dilated heart when it is discovered within several months before or after delivery. In about half of these patients, proper function is restored, and dilatation of the heart disappears within months after delivery, in contrast to the classic course of dilated cardiomyopathy. Cardiac amyloidosis may appear along with systemic amyloidosis or may affect only the heart. The heart in cardiac amyloidosis varies from normal to firm, rubbery and noncompliant with thickened walls. In the cardiovascular senile form of amyloidosis the deposited proteins are known as senile amyloid (Asc) proteins. Clinically important amyloid deposits can occur in the hearts of patients with multiple myeloma. Iron overload can occur in hereditary hemochromatosis and hemosiderosis owing to multiple blood transfusions. Patients with iron storage disease present most commonly with a dilated pattern. Iron deposition is more prominent in ventricles than atria. Other than a rust-brown color the heart is indistinguishable from DCM. It is thought that iron causes dysfunction by interfering with metal-dependent enzyme systems. Cardiac manifestations are among the earliest and most consistent features of hyperthyroidism and hypothyroidism. In hyperthyroidism tachycardia, palpitations and cardiomegaly are common; supraventricular arrhythmias occasionally appear. In hypothyroidism cardiac output is decreased, with reduced stroke volume and heart rate (Schoen 94: 566). Alcohol or its metabolites, especially acetaldehyde, have a direct toxic effect on the myocardium, and alcoholic cardiovascular disease is not an idiopathic disorders. Chronic alcoholism may be associated with thiamin deficiency. The anthracycline chemotherapeutic agent doxorubicin (Adriamycin and daunorubicin are well recognized causes of toxic myocardial injury. The hazard is dose dependent (usually greater than 500 mb/m2) and attributed primarily to lipid peroxidation of myofiber membranes. Many other agents, such as lithium, phenothiazines, and cocaine have been implicated in myocardial injury and sudden coronary death. Common themes in cardiotoxicity of many chemicals and drugs are myofiber swelling and vacuolization, fatty change, individual cell lysis (myocytolysis) and sometimes patchy foci of necrosis. Electron microscopy usually reveals cytoplasmic vacuolization and lysis of myofibrils, typified by Adriamycin cardiotoxicity. With discontinuance of the toxic agent, these changes may resolve completely, leaving no apparent sequelae. Catecholamine effect is evident in drugs, such as cocaine, and appears as a foci of myocardial necrosis with contraction bands (Schoen 94: 566). In general cardiac drugs are the second leading cause of fatal drug overdose and antiarrhythmia and antihypertension drugs are no exception (Bronstein '11). Because 75% of cases of heart failure involve antecedent high blood pressure it is important to review hypertension medicines both for the treatment of malignant hypertension and as possible cause of cardiac failure. Drugs that block activation of angiotensin by blocking angiotensin-converting enzyme, ACE inhibitors such as captopril, enalapril, lisinopril or any drug with a proper name ending in pril), or by blocking angiotensin II at its receptor angiotensin receptor blockers (ARBs) (losartan irbesartan, candesartan, or other drug ending in sartan) will reduce urinary losses of potassium, magnesium and probably the other ions that are depleted by diuretics. Because potassium loss from the kidney is driven by exchange of potassium for sodium as regulated by aldosterone, salt intake is an important concern. The more salt eaten, the more potassium lost. Every sodium ion reabsorbed from the renal tubule leads to excretion of a potassium ion; high sodium intake aggravates potassium losses, and when potassium is depleted, potassium ions are exchanged for hydrogen ions, leading to acid urine with alkaline blood. Blocking the effect of high renin potassium and magnesium depletion by blocking the effect of angiotensin II with angiotensin receptor blockers (ARBs) prevent secondary hyperaldosteronism. This may be the best approach for people who have either congestive heart failure or secondary hyperaldosteronism from renal artery stenosis or other high-renin states. ACE inhibitors, also block formation of angiotensin II, but this effect wears off after a few weeks because there are other pathways for the formation of angiotensin II (Spence '05: 147, 148, 152). Beta-blockers seem to be the most highly recommended for slowing the ventiruclar response rate in atrial fibrillation, converting reentrant supraventricular tachyarrhythmias, and suppressing ventiruclar arrhythmias, but chronic treatment with propranolol, metoprolol or timolol following myocardial infarction decreases 1 year mortality, but bradychardia and congestive heart failure, could result from decompensation. Drugs that slow the upstroke, such as quinidine, procainamide, diopyramide, lidocaine, mexiletine, tocainide, moricizine, propafenone and flecainide, have been found worsen outcomes when compared to no treatment in patients with ventricular arrhythmias at risk for sudden coronary death (Heger et al '04: 269-270). Heart failure drugsAngiotensin-converting enzyme (ACE) inhibitors: Used to help improve the hearts function. May vasodilate the blood vessels and lower blood pressure, making it easier for the failing heart to pump blood. It may adversely affect the kidneys and cause a cough in some people. Note: ACE inhibitors or ARBs plus a beta blocker fulfill the AHAs Get with the Guidelines heart failure program for treating congestive heart failure.Angiotensin II receptor blockers (ARBs): Used to help improve the hearts function. May vasodilate the blood vessels and lower blood pressure, making it easier for the failing heart to pump blood. May adversely affect the kidneys.Beta blockers: Can improve heart function in patients with heart failure. Note that some medications act by blocking both alpha and beta receptors. One such drug, carvedilol, blocks the alpha-1 receptor as well as beta receptors. Digitalis: May make a weak heart pump stronger. May be useful if heart failure does not improve with ACE inhibitors or ARBs. Side effects include worsening heart rhythm problems and yellow vision. Dosage should be reduced in people with heart failure and kidney failure. Hawthorne: Supreme herb for the heart. Treats high or low blood pressure, heart disease, edema, angina and heart arrhythmia. Hawthorne doesnt store in the body and isnt accumulative in action. Unlike prescription antiarrhythmia medicine Hawthorne does not have any adverse cardiac effects.Source Table 25.2 Cohen 10: pg. 97-98 Digitalis purpurea, or foxglove had been used by illiterate farmers and housewives in England and on the Continent for centuries to treat congestive heart failure and arrhythmia. Digitalis slows the wildly beating ventricles to a normal level by blocking or delaying the conduction of the electric impulse through the atrioventricular node. By increasing the heart stoke, Digitalis increases the amount of blood being oxygenated by the lungs, as well as the blood in general circulation, by as much as 30% with each beat. Because of this improved action of the heart and circulation, the drug tends to improve renal secretion to relieve edema, and to aid the cardiac muscle to compensate for mechanical defects or structural lesions. More than 3 million heart patients in the United States routinely use the glycoside digoxin from D. lanata, and this is but one of six glycosides from Digitalis prescribed today. Digitalis whole leaf, digitoxin, digoxin, lanatoside C, acetyldigitoxin and deslanoside. Since the effective dose may be as high as 70% of the toxic dose, administration must be done carefully on an individual basis. Recently it has been recommended the use of whole leaf preparations over isolated glycosides. Cardiac glycosides bring only temporary relief and must be administered orally during the whole course of the disease. Adverse reactions are found in about 20% of hospitalized patients receiving Digitalis preparations (Elvin-Lewis 77: 184, 186). The FDA required warning for Digitalis and related cardiotonic drugs for human use in oral dosage forms, states "Digitalis alone or with other drugs has been used in the treatment of obesity. This use of digoxin or other digitalis glycosides is unwarranted. Moreover, since they may cause potentially fatal arrhythmias or other adverse effects, the use of these drugs in the treatment of obesity is dangerous"  HYPERLINK "http://edocket.access.gpo.gov/cfr_2011/aprqtr/21cfr201.317.htm" 21CFR201.317 to which could be appended, "Hawthorne is the supreme herb for the heart". Hawthorne (Crataegus laevigata) may be better for the treatment of congestive heart failure than both Digitalis and modern antihypertensive drugs used in the treatment of congestive heart failure, and is likely to cure more people than nitrates or nitrites. Patients leaving the emergency room would be much more likely to benefit with a recommendation for Hawthorne than for Aspirin, which does help to prevent platelet aggregation and thrombosis that occur in the only most advanced stages of atherosclerosis, and taken in excess the analgesic affect can leave the heart muscle feeling dead complicating the accurate diagnosis of infarction and estimate of myocardial damage, although not harmful, Aspirin is not worth the trip to the hospital. Hawthorne (Crataegus laevigata) is outstanding both to prevent heart problems and to treat high or low blood pressure, heart disease, edema, angina and heart arrhythmia. Hawthorne doesnt store in the body and isnt accumulative in action. Unlike prescription cardiovascular and antihypertensive medicine Hawthorne does not have any adverse cardiac effects that might cause decompensation in congestive heart failure, for instance when the treatment for tachycardia causes brachycardia, that is why Hawthorne is known as the "supreme herb for the heart". It is important to take Hawthorne on a regular basis if using as a heart tonic. One drinks four cups of strong herbal tea infusion or cups of water mixed with 2 droppers of tincture, 40 drops, a day, for as many months as the number of years the chronic disease has progressed untreated (Gladstar '12) or for one week to treat a simple infarction. Rheumatic heart disease (RHD) caused by Streptococcus pyogenes is often overlooked although it is the most common infectious cause of endocarditis, atherosclerosis, atrial fibrillation, systemic embolism, pulmonary edema, pulmonary hypertension, dyspnea with pregnancy or rheumatoid arthritis that causes minimal exertion and insufficient cardiovascular exercise (Heger et al '04: 197, 198). Antibiotic labels state, "To reduce the development of drug-resistant bacteria and maintain the effectiveness, antibacterial drugs, should be used only to treat or prevent infecions that are proven or strongly suspected to be caused by susceptible bacterias" at  HYPERLINK "http://www.law.cornell.edu/cfr/text/21/201.24" 21CFR201.24. All one needs to know about antibiotic resistance is that Strep is easily treated with penicillin; but almost any prescription antibiotic will work. Also effective are doxycycline that is uniquely effective for Staphylococcus aureus and S. dermidis including so called methicillin resistant stapholococcus aureus (MRSA), but causes permanent yellowing of the developing teeth of children younger than 8. Metronidazole is also uniquely effective for fecal coliform, including Bactroides fragilis that infects the heart, Escherichia coli that infects the kidney and urinary tract, antibiotic resistant Clostridium difficile, infections of the abdomen such as kidney or pancreatic infections or appendicitis, which otherwise costs $7,000-$25,000 for an emergency appendectomy. Except when taking metronidazole (Flagyl ER) which is uniquely safe and effective in the grastrointestinal tract, it is medically necessary to take probiotics within two hours of taking antibiotics, antifungals, NSAIDs or any chemotherapeutic agent and for two weeks after completing the course (Huffnagle '07). Topical antifungal foot cream is affordable and often helpful for crippling fungal infections. Sporanox (itraconazole) is a highly effective broad spectrum oral antifungal but it is strongly contraindicated for people with congestive heart failure because of adverse reactions with Digitalis and hypertensive drugs. A vegan diet is absolutely essential for the treatment of heart failure, and vitamin B12 supplementation is medically necessary for thin vegans, who do not have large fat reserves, and are not minimally vegetarian by consuming probiotic yoghurt and cheese aged longer than 2 months, daily, to prevent chronic post-infectious diarrhea, pernicious anemia and dental cavities, that are almost certain to occur after consuming several courses of antibiotics, not replenishing the beneficial bacteria, and thereby allowing the proliferation of such antibiotic resistant and pathogenic microbes as Stapholococcus aureus, Candida albicans and Clostriudium difficile (Sanders '12). Surgery for patients with end-stage congestive heart failure currently is limited to heart transplantation, frequently after a period of left ventricular assistance with a mechanical device. The number of heart transplants performed in the United States each year is limited to approximately 2,000 because of the shortage of donor organs. Patients older than age 60 have been shown to have similar early mortality ad length of hospitalization as younger gropus. Five year survival ranges from 71% in older patients to 82% in younger patients. Hypercholesteremia affects 60-80% of recipients and may contribute to coronary vasculopathy. Transplant atherosclerosis is responsible fro many later deaths. Statins reduce the level of cholesterol and appear to have the added advantage of decreasing the incidence of cardiac rejection (Heger et al '04: 264). Decade-old heart attack scars healed after being injected with stem cells from a patients' own bone marrow. So far, eight patients have received the experimental treatment in an ongoing clinical trial. All eight had suffered heart attacks an average of 5 1/2 years prior; one of the patients had his heart attack 11 years earlier. All had dangerously enlarged hearts, with areas of scar tissue from their heart attacks. The researchers harvested bone marrow progenitor cells from four patients and adult stem cells from another four patients. Using a catheter, they then injected the cells into the walls of the patients' hearts. Within three months, the scarred areas of the patients' hearts began to work again. About six months after treatment, and for a year later -- the length of the study so far -- all eight hearts regained a more normal size. They shrank 15% to 20%, three times more than current treatments can achieve. Whether just plain old bone marrow or [adult stem] cells, were injected into the scar, and three months later, the area that was completely dead started to contract again. Stem cells are being explored in the treatment of people with recent heart attack damage -- but the "landmark area" is the use of stem cells to treat end-stage heart failure. Stem cells actually reverse the enlargement and their propensity to get worse (DeNoon 11). Heart failure is by definition an inability to perform adequate cardiovascular exercise to maintain the tone of the heart muscle and integrity of the circulatory system and treatment of a serious heart condition, atherosclerosis, cancer or diabetes requires that sedentary activity by curtailed in deference to the success of the metabolism of a vegan diet, no fat, sugar or salt, by at least four hours of cardiovascular exercise or physical labor daily, to be cured. Cardio-toxin free exercise clothes are necessary for the heart to feel better and not worse, potentially to a life-threatening degree, during and after vigorous extended exercise. For most athletes it takes good equipment and a lot of athlete's foot crme and other necessary medicines to eliminate the rheumatic colonizations that impede the achievement of minimal levels of physical fitness and maintain it, without crippling injury or pain at all, to be free of angina pectoris, hyperlidipidemia and rheumatic disease and have the heart to engage and excel in sedentary academic pursuits, such as medical research. 7. Hypertension High blood pressure is reported to be the most common problem for which people go to doctors in the United States. Hypertension is one of the leading causes of heart attack and stroke. According to the National Institutes of Health, the number of adults with high blood pressure has risen dramatically over the last ten years from fifty million to sixty-five million. In 1990, approximately one in four adults in the United States had hypertension. In 2000, it was about one in three Americans, or sixty-five million people over the age of eighteen, with elevated blood pressure. High blood pressure is a major risk factor for the development of heart disease, including coronary artery disease (the number one killer of Americans) and congestive heart failure (the number one cause for hospital admission in people over the age of sixty-five). It is also a major risk factor for stroke and kidney damage. 30 to 50 percent of individuals with hypertension will be salt sensitive (Willson 06: 15, x, 1). High blood pressure is a major risk factor for the development of heart disease, including coronary artery disease (the number one killer of Americans) and congestive heart failure (the number one cause for hospital admission in people over the age of sixty-five). It is also a major risk factor for stroke and kidney damage. In large populations, the prevalence of hypertension rises with the levels of sodium intake. Most groups with very low sodium intake have no hypertension. When higher levels of salt are introduced, hypertension develops. Only about 5 to 10 percent of high blood pressure has a known cause. Despite the fact that less than half of people are salt sensitive, dietary salt restriction will lower blood pressure in most people. To be effective dietary restrictions extend to salt, fat and sugar. One problem with high blood pressure is that most people cant feel it. That means that a person could have elevated blood pressure for a long period of time and be completely unaware of it (Wilson & Childre06: x, 1, 22, 23, 28, 30). Hypotension is characterized by an abnormally low tension of muscle cells in peripheral blood vessels, which are marked by capillary permeability and fragility and is treated as congestive heart failure. The heart and kidneys however exhibit different methods of antibiotic resistance doxycycline or penicillin for the heart and metronidazole for the kidneys, fecal coliform and Escherichia coli to avoid the post-infectious malabsoption and adverse drug reactions of Bactrim. In the 1950s it was discovered that Reserpine and other Rauvolfia alkaloids, used in Ayurvedic medicine for the treatment of schizophremia, act on the sympathetic nervous system by depleting almost all the neurotransmitter substance, norepinephrine, from sympathetic nerve tissue. This neural blocking results in relaxation of the vessels and output of the heart, with subsequent reduction in blood pressure. Drug therapy can now control about 80% of all cases of hypertension (Elvin-Lewis '77). 12.5 mg hydrochlorothiazide (HCTZ) is the commonest and cheapest drug for treating high blood pressure, is enough (Spence '05). The ABC of adrenergenic blockers have however been abused in the treatment of congestive heart failure to the neglect of statins (Spence '05)(Heger '05)(Moore '98) and Hawthorne, the supreme herb for the heart, that amongst its many cartdiotonic properties, moderates both high and low blood pressure (Gladstar '12). Blood pressure is the force of the blood pushing out against the walls of the blood vessels. As blood is pumped out of the heart into the arteries that lead away from it, there is a certain pressure in the system created by this pumping actin of the heart. Blood pressure is measured in a few different ways, but the most common method is called sphygmomanometry that refers to inflating a blood pressure cuff on the arm (or leg, in some cases). Air is slowly let out of the cuff while the person taking your blood pressure listens with a stethoscope below the cuff to hear the pulse. When the person first hearts the pulse as the cuff deflates, the pressure is recorded as the systolic pressure. The bottom number is called the diastolic pressure. It reflects the pressure in the arteries when it normalizes. The circulatory system is a closed system. There are no valves anywhere in the pipes to let blood out. In addition to the pumping and filling of the heart, pressure is maintained in this closed system by the tension in the walls of the arteries. Arteries have a layer of muscle in their walls. This muscle layer can contract or relax and have a great impact on the pressure in the overall system. Arteries that supply blood to muscles and organs have the ability to dilate (enlarge) under conditions when more blood is required lowering blood pressure. Muscles help to squeeze the arteries and veins to raise pressure to normal. The blood pressure is therefore maintained by the constriction and relaxation of the arteries as well as the pumping of the heart (Wilson & Childre 06: 11-13). High blood pressure is a blood pressure reading of 140/90 mmHg or higher. Both numbers are important. Once high blood pressure develops, it usually lasts a lifetime. Blood pressure changes during the day. It is lowest as you sleep and rises when you get up. It also can rise when you are excited, nervous, or active.Still, for most of your waking hours, your blood pressure stays pretty much the same when you are sitting or standing still. That level should be lower than 120/80 mmHg. When the level stays high, 140/90 mmHg or higher, it implies high blood pressure. For example, 160/80 mmHg would be stage 2 high blood pressure. With high blood pressure, the heart works harder, your arteries take a beating, and your chances of a stroke, heart attack, and kidney problems are greater.Normal blood pressure is a reading of less than 120/80 mmHg (mmHg = millimeters of mercury, a unit for measuring pressure). Drops in blood pressure that dont threaten life are called hypotension. Some people do just fine with blood pressures of 85/50 and doctors treat some people with conditions such as congestive heart failure to reduce their pressures down to these levels. Other people feel terrible when their systolic pressure drops from 150 down to 130 (Wilson & Childre 06: 16). Hypotension is abnormally low blood pressure. Hypotension is blood pressure that is lower than 90/60 mmHg.In a healthy person, hypotension without signs or symptoms is usually not a problem and requires no treatment. Doctors will want to identify and treat any underlying condition that is causing the hypotension, if one can be found. Hypotension can be dangerous if a person falls because of dizziness or fainting. Shock, a severe form of hypotension, is a life-threatening condition that is often fatal if not treated immediately. Shock can be successfully treated if the cause can be found and the right treatment provided in time (Sanders 08: 24). Blood Pressure Sphygmomanometry Reading Normal (optimal): less than 120 systolic and less than 80 diastolic Prehypertension: 120-139 systolic or 80-89 diastolic, or both Stage 1 Hypertension: 140-159 systolic or 90-99 diastolic, or both Stage 2 Hypertension: greater than 160 systolic or greater than 100 diastolic, or both. High blood pressure is common and has been identified as one of the most important risk factors in both coronary heart disease and cerebrovascular accidents, it may also lead to congestive heart failure (hypertensive heart disease), aortic dissection, and renal failure. The detrimental effects of blood pressure increase continuously as the pressure increases. A sustained diastolic pressure greater than 90 mm Hg or a sustained systolic pressure in excess of 140 mm Hg are generally considered to constitute hypertension. By this criteria, screening programs reveal that 25 percent of the population is hypertensive. The prevalence increases with age, but in older groups the disease is likely to be mild, but in young adults tends to be more severe. Blacks are affected by hypertension about twice as often as whites and seem more vulnerable to its complications. About 90 to 95 percent of hypertension is idiopathic and apparently primary (essential hypertension). Of the remaining 5 to 10 percent most is secondary to renal disease or, less often, to narrowing of the renal artery, usually by an atheromatous plaque (renovascular hypertension). Infrequently, secondary hypertension is the result is the result of adrenal disorders, such as primary aldosteronism, Cushings syndrome, or pheochromocytoma. Both essential and secondary hypertension may be either benign or malignant, according to the clinical course. About 5 percent of hypertensive persons show a rapidly rising blood pressure, which, if untreated, leads to death within a year or two from accelerated or malignant hypertension Malignant hypertension usually develops in the fourth decade of life (Schoen 94: 484, 485). One problem with high blood pressure is that most people cant feel it. That means that a person could have elevated blood pressure for a long period of time and be completely unaware of it. The brain is very sensitive to high blood pressure, both acutely (moment to moment) and chronically (over the long term). 10% of strokes are hemorrhagic strokes, caused by a rupture of a blood vesse in the brain. Although much less common than ischemic strokes there is a 50% mortality rate and normal stroke treatment tissue plasminogen activator (tPA) which reduces disability by 30% would exacerbate the hemorrhage and increase the already extremely high risk of death. other type of stroke is caused by rupture of one of the blood vessels in the brain. The most common reason for this is high blood pressure. When pressure gets too high one of these vessels may burst, causing bleeding or hemorrhage in the brain. Hemorrhagic stroke is usually more serious and harder to recover form than embolic stroke. Aneurysm, or weakening in the wall of the arteries (in the brain) can be the source of hemorrhagic stroke. An aneurysm looks a little like a bulge on the inner tube of a tire. This segment of the artery wall is thinner and weaker, and can rupture. Dementia is a term used to describe decreased cognitive mental function. The term hypertensive encephalopathy describes a syndrome of severe hypertension accompanied by brain dysfunction and neurologic impairment. Complete resolution can be achieved if the blood pressure is quickly lowered, usually with intravenous medication in an intensive care environment (Wilson and Childre 06: 34, 36, 37). In the vast majority of cases, doctors have no idea what causes hypertension. They know the predictors that can contribute to it, such as stress, obesity, and diabetes. In medicine when doctors dont know the cause of something, its usually referred to as idiopathic, meaning were idiots when it comes to knowing the cause. When doctors dont know the cause of high blood pressure, a special term is used called essential hypertension (also called primary hypertension). Unfortunately, essential hypertension is the diagnosis in 90 to 95 percent of people who have high blood pressure. Some people have white coat hypertension which means that their pressure is only high when they are at the doctors office. Therefore doctors perform repeated tests. Real hypertension is very common and leads to many other illnesses and complications if not detected and treated in some way to bring the pressure back to the normal or optimal range. African-Americans have an increased incidence and prevalence of hypertension, and higher complication rates, including death, than whites and other ethnic groups. They also have a higher incidence of kidney damage as a result of high blood pressure, and more patients progress to the point of kidney failure and dialysis. Some researchers think African-Americans might be more susceptible to sodium overload. Obesity is a strong contributor to hypertension. Obesity contributes to other diseases as well. Type 2 diabetes is usually seen in middle age as a direct consequence of obesity. Type 2 diabetes contributes to coronary artery disease, eye disease, and many other conditions including premature death. Obesity is also a strong risk factor for the development of high cholesterol and heart disease. Sleep apnea, a disease of disordered breathing during sleep causing many other medical complications, is also predominantly a disease of the overweight (Wilson & Childre 06: 19-21). More than 50 percent of senior citizens in the United States develop high blood pressure although the incidence of high blood pressure among senior citizens in countries eating traditional low-fat plant based diets is virtually none. Ideal blood pressure 110/70 or less (without medication). Average blood pressure of vegetarians 112/69. Average blood pressure of non-vegetarians 121/77. High blood pressure is defined when the top number (systolic) is consistently over 140, or the bottom number (diastolic) is consistently over 90, while the person is at rest. Meat eaters have nearly triple the incidence of high blood pressure as vegans and very high blood pressure is thirteen times more common in meat eaters. 30-75 percent of patients with high blood pressure achieve substantial improvement by switching to a vegetarian diet and are able to discontinue high blood pressure medicine they were expected to have to take for the rest of their life (Robbins 01: 28, 29). Regular exercise, especially aerobic exercise (sustained exercise that raises the heart rate but doesnt put sudden strain on your system like heavy weight lifting), lowers blood pressure, strengthens the heart and cardiovascular system, helps your muscles to utilize the oxygen delivered by the blood more efficiently, improve energy levels and endurance, improve muscle strength, strengthen bones, increase flexibility and balance, reduce body fat, help to reduce tension, stress and depression, improve sleep, and increase self-esteem. Too much salt in the diet can be harmful. The chemical name for salt is sodium chloride. Nutrition labels on foods now list how much sodium is contained. Sodium is present in high amounts in certain types of foods. Ketchup and pickles are great examples of high-sodium foods. Many canned soups and most snack-food items (potato chips, corn chips, and the like are very high in salt also. Any type of meat that has preservatives to such as sausage, hot dots, or bacon, will contain high levels of sodium. Some people seem to be more sensitive to salt than others, meaning they will develop hypertension in response to excess sodium in their diet. There is no way to predict who might be salt sensitive. Evidence for a causative role of salt follows: In large populations, the prevalence of hypertension rises with the levels of sodium intake. Most groups with very low sodium intake have no hypertension. When higher levels of salt are introduced, hypertension develops. Certain animals seem predisposed to high blood pressure when fed high-sodium diets. Despite the fact that less than half of people are salt sensitive, dietary salt restriction will lower blood pressure in most people (Wilson & Childre 06: 22-23). There is an increased risk of having hypertension if you: are over the age of thirty-five, are overweight, eat foods that are high in salt or fat, or both, are not active, smoke, drink excess alcohol (more than two drinks per day), have family members with high blood pressure, are African-American, are pregnant, take oral contraceptives (birth control pills) or are under stress (Wilson and Childre 06: 24). Secondary hypertension is the name given to high blood pressure with a known etiology. Only about 5 to 10 percent of high blood pressure has a known cause. The kidneys are frequently the cause of hypertension for many reasons. This is because the kidneys help to regulate blood pressure. As blood is pumped out of the heart in to the main artery, the aorta, it travels throughout the body. The aorta gives off many arteries that feed all of the organs, muscles and other structures. When blood goes through the kidneys, it passes through the renal (kidney) arteries. The kidney are very complex filtering machines that filter out toxins that will then leave the body via the urine. Blood passes from the aorta through the renal artery and into the kidney, where it is pushed through a fine mesh of very small blood vessels that act like a sieve. After going through this filter, the blood travels through a loop of blood vessels that control salt and water balance. This allows water to be reabsorbed back into your circulation to keep everything in balance. Ultimately, toxins and whatever salt and water you dont need pass from the kidneys down pipes called ureters into the bladder, which you empty periodically when the urge hits you As kidney function deteriorates, doctors use the term renal insufficiency. When kidney function is extremely poor, and eventually absent, its called renal failure. The patient generally does not produce any urine At this point, the patient will die in the course of a couple of weeks if he or she does not undergo kidney dialysis, a complicated but routine procedure whereby the blood is withdrawn from a vein, sent through a series of external filters to remove toxins and water, and returned to circulation. People can live for years while undergoing dialysis, although their quality of life is usually significantly diminished. The other option for a patient with end-stage kidney disease is to undergo a kidney transplant operation (Wilson and Childre 06: 24, 28, 25, 37, 38). The magnitude of arterial pressure depends on two fundamental hemodynamic variables: cardiac output and total peripheral resistance. Vasoconstricting agents are angiotensin II, catecholamines, thromboxane, leukotienes, and endothelin. Vasodilators include kinins, prostaglandins and nitric oxide. Arterial hypertension can best be considered a disease dependent on factors that may alter the relationship between blood volume and total arteriolar resistance. The kidneys play an important role in blood pressure regulation by at least three mechanisms (1) renin-angiotensin system (2) sodium homeostasis and (3) renal vasodepressor substances. Environmental factors implicated in the causation of hypertension include stress, obesity, smoking, inactivity, and heavy consumption of salt. Hypertension is associated with two forms of small blood vessel disease: hyaline ateriolosclerosis and hyperplastic arteriolosclerosis (Schoen 94: 485, 486, 488). The body is very sensitive to changes in blood pressure. Special cells in the arteries, called baroreceptors, can sense if blood pressure begins to rise or drop. When the baroreceptors sense a rise or drop in blood pressure, they cause certain responses to occur throughout the body in an attempt to bring the blood pressure back to normal. For example, if you stand up quickly, the baroreceptors will sense a drop in your blood pressure. They quickly take action to make sure that blood continues to flow to the brain, kidneys, and other important organs. The baroreceptors cause the heart to beat faster and harder. They also cause the small arteries (arterioles) and veins (the vessels that carry blood back to the heart) to narrow (Wilson & Childre 06: 14). When the kidney senses low blood pressure it produces a hormone called renin. This hormone is spilled from the kidney into the circulation and acts on another chemical, which then acts on a another, and in the long run the message goes to the arteries in the body to squeeze down, thus raising the overall pressure in the system. This phenomenon of contracting arteries in the body is known as vasoconstriction. The arteries have muscles in their wall for exactly this reason. Another consequence of renin production by the kidneys is the triggering and the production and release of hormones and chemicals form the adrenal glands, which sit on top of the kidneys. These substances not only contribute to the constriction of the arteries, but also pass through the kidneys and cause them to reabsorb salt and water back into the circulatory system, thus helping to raise blood pressure by maintaining the fluid volume in your blood vessels. Many diseases, including hypertension, can create damage to the kidney. Tumors, infection, diabetes, autoimmune diseases (lupus, for example) or kidney stones can also cause kidney problems resulting in higher blood pressure. Buildup of cholesterol in the renal artery can create a partial blockage and thereby decrease blood flow to the kidney, triggering renin production and raising pressure. Each adrenal gland looks like a little triangular hat sitting atop the kidney below it. It is made up of two parts: the middle core, known as the medulla, and the outer layer, known as the cortex (cover). The medulla makes and stores adrenaline and couple closely related compounds, which quickly raise blood pressure in a crisis situation. The outer cortex of each adrenal gland makes a hormone called aldosterone. Aldosterone is a very powerful compound that travels by way of the blood to the kidney, where it tells the kidney to reabsorb sodium (salt) before it goes out in the urine. Nerve signals and hormones from the brain serve as messenger to raise blood pressure often through many steps. Pain or cold temperatures can do this too (Wilson & Childre 06: 25-29). The minimal criteria for the diagnosis of Systemic (Left-sided) Hypertensive Heart Disease (HHD) are: (1) left ventricular hypertrophy in the absence of other cardiovascular pathology and (2) a history of hypertension. The Framingham Heart Study established unequivocally that even mild hypertension (levels only slightly above 140/90 mm Hg), if sufficiently prolonged, induces left ventricular hypertrophy. The left ventricular wall thickness may exceed 2 cm and the heart weight 500 gm. Hypertrophy can lead to myocardial dysfunction, cardiac dilatation and ultimately congestive heart failure (CHF). Approximately 25% of the population of the United States suffers from hypertension of this degree, that could be detected on an ECG or echocardiograph, making systemic HHD the second most common form of cardiovascular disease. Depending on the severity of the hypertension, its duration, the adequacy of therapeutic control, and the underlying basis for the hypertension, the patient may enjoy normal longevity and die of unrelated causes, may develop progressive ischemic heart disease, may suffer progressive renal damage or cerebrovascular hemorrhagic stroke, particularly of the 10% hemorrhagic kind that is more than 50% fatal, or may experience progressive heart failure. The risk of sudden cardiac death is also increased. There is substantial evidence that effective control of hypertension can lead to regression of cardiac hypertrophy (Schoen 94: 541, 542). Cor Pulmonale, also known as Pulmonary (Right Sided) Hypertensive Heart Disease, constitutes the right ventricular enlargement secondary to pulmonary hypertension caused by disorders that affect the lungs or pulmonary vasculature. Acute cor pulmonale refers to the right ventricular dilatation that follows massive pulmonary embolism. Chronic cor pulmonale usually implies right ventricular hypertrophy (and later dilatation) secondary to prolonged pressure overload owing to obstruction of the pulmonary arteries or arterioles or compression or obliteration of septal capillaries (e.g. owing to emphysema). Chronic cor pulmonale is a surprisingly common condition because of its association with such widespread disorders as chronic bronchitis and emphysema (COPD), which affect perhaps 40 million or more Americans. Disorders which predispose the patient to cor pulmonale are such diseases of the lung as, chronic obstructive pulmonary disease (COPD), diffuse pulmonary interstitial fibrosis, extensive persistent atelectasis and cystic fibrosis; diseases of the pulmonary vessels such as pulmonary embolism, primary pulmonary vascular sclerosis, extensive pulmonary arteritis (e.g. Wegeners granulmonatosis), drug, toxin or radiation induced vascular sclerosis, or extensive pulmonary tumor micrometastases; disorders affecting chest movement such as, kyphoscoiosis, marked obesity (pickwicckian syndrome) or neuromuscular diseases and disorders inducing pulmonary arteriolar constriction such as, metabolic acidosis or hypoxemia, chronic altitude sickness, obstruction to major airways or idiopathic alveolar hypoventilation. In most instances, clinical effects of the pulmonary impairment overshadow those of the heart (Schoen 84: 542, 543). Malignant hypertension is relatively rare occurring in 1 to 5% of peope with high blood pressure. Before introduction of the new antihypertensive drugs, malignant hypertension was associated with a 50% mortality rate within 3 months of onset, progressing to 90% within a year. At present, however, about 75% of patients will survive 5 years, and 50% survive with precrisis renal function. The full blown syndrome of malignant hypertension is characterized by diastolic pressures greater than 130 mm Hg, papilledema retinopathy, encephalitis, cardiovascular abnormalities and renal failure sometimes encountered in "hypertensive crisis". At the onset of rapidly mounting blood pressure, ther is marked proteinuria and microscopic or sometimes macroscopic hematuria, but no significant alteration in renal function. Soon, however, renal failure makes its appearance and the patient is unable to urinate. The syndrome is a true medical emergency requiring the institution of aggressive and prompt antihypertensive therapy before the development of irreversible renal lesions (Saunders '94: 978). It wasnt until the 1940s and 50s that big changes in the treatment of hypertension took place, partly due to the fact that President Franklin Delano Roosevelt eventually died of a stroke, but also suffered from congestive heart failure and kidney failure, all complications of his long-standing hypertension. In the 1950s it was discovered that Reserpine and other Rauvolfia alkaloids, used in Ayurvedic medicine for the treatment of schizophremia, act on the sympathetic nervous system by depleting almost all the neurotransmitter substance, norepinephrine, from sympathetic nerve tissue. This neural blocking results in relaxation of the vessels and output of the heart, with subsequent reduction in blood pressure. Drug therapy can now control about 80% of all cases of hypertension. Drugs however do not cure, salt and meat elimination diets are necessary, but drug control of this disease marks a tremendous change in the outlook for patients who developed malignant hypertension whose inflexible fate until 1950 was a stroke, heart failure, or kidney failure (Elvin-Lewis 77). Although many drugs were tried in the early days of treatment, compounds began to be developed in the 1950s through the l970s that evolved into the new drugs classes currently in use. In the 1980s and 90s a couple more families of medications hit the scene. Today there are four basic classes of antihypertensive medications used in the treatment of high blood pressure diuretics, beta-blockers, angiotensin converting enzyme (ACE) inhibitors and calcium channel blockers; aldosterone blockers are for certain patients. Patients must be willing to persevere and deal with the art of medicine, often known as trial and error (Wilson and Childre 06: 41, 42). Modern cardiac drugs, including all hypertension medication are however the second leading cause of fatal drug overdose (Bronstein 11) and their prescription is rife with abuse (Moore 98). Doctors and nurses come out of medical school, able to rattle off these dangerous medicines, cardiologists are generally much more reluctant to prescribe these medicines than primary care doctors and these two offices, despite their disparate cardiac and hypertensive population, probably prescribe an equal amount of ACE inhibitors, beta-blockers, and calcium channel blockers. Among the many cardiotonic properties of Hawthorne Crataegus laevigata is the treatment of both high and low blood pressure (Gladstar 12)(Elvin-Lewis 77). Prescription Medicine for the Treatment of Hypertension Diuretics Generic NameDiuretics Trade NameBeta-blockers Generic NameBeta-blockers Trade NameBumetanideBumexAcebutololSectralChlorthalidoneHygrotonAtenololTenorminEthacrynic acidEdecrinCarvedilolCoregFurosemide LasixLabetalolNormodyne, TrandateHydrochlorothiazide (HCTZ)HydroDIURIL, MicrozideMetoprololLopressor, TroprolIndapamideLozolNadololCorgardMetolazoneZaroxolyn, MykroxPindololViskenTorsemideDemadexPropranololInderalACE Inhibitors Generic NameACE Inhibitors Trade NameARBs Generic NameARBs Trade NameBenazeprilLotensinCandesartanAtacandCaptoprilCapotenEprosartanTevetenEnalaprilVasotecIrbesartanAvaproFosinoprilMonoprilLosartenCozaarMoexiprilUnivascOlmesartanBenicarPerindoprilAceonTelmisartanMicardisQuinaprilAccuprilValsartan DiovanRamiprilAltaceAldosterone Blockers Generic NameAldosterone Blockers Trade NameTrandolarilMavikEplerenoneInspraCalcium Channel Blockers Generic NameCalcium Channel Blockers Trade NameSpironolactoneAldactoneAmlodipineNorvascAlpha Blockers Generic NameAlpha Blocker Trade NameDiltiazemCardizem, TiazacDoxazosinCarduraFelodipinePlendilPrazosinMinipressNicardipineCardeneTerazosinHytrinNifedipineProcardia, AdalatSympatholytic Drugs Generic NameSympatholytic Drugs Trade NameVerapamilCalan, Isoptin, VerelanClonidineCatapresDirect Vasodilators Generic NameDirect Vasodilators Trade NameGuanabenzWytensinHydralazineApresolineMethyldopaAldometMinoxidilLonitenRauwolfia alkaloids Generic NameRauwolfia alkaloids Trade NameRauwolfia serpentineRauwolfemmsReserpidine Oral Serpasil, Serpalan, Harmonyl, Novoreserpine, Raudixin, Rauval, Rauverid, Reserfia, Serpalan, WolfinaDeserpidine and Hydrochlorothiazide or Methyclothiazide Demi-Regroton, Diupres, Diurigen with Reserpine, Diutensen-R, Dureticyl, Enduronyl, Enduronyl Forte, Hydropres, Oreticyl, Oreticyl Forte, Rauzide, RegrotonSource: Wilson & Childre 06: Appendix Table I-VII pgs. 136-139 Arterial hypertension is the medical term for high blood pressure. Effective measures to improve blood pressure without drugs include weight loss, exercise, and avoidance of substance that aggravate blood pressure. The most important substance to avoid is salt but also aggravating are alcohol, licorice, decongestants, amphetamines, birth control and NSAIDs. With rare exceptions high blood pressure is related to the powerful hormone systems we need to survive that controls salt and water. The exceptions include tumors of the inner part of the adrenal gland (the adrenal medulla) called pheochromocytomas, and a congenital narrowing of the aorta called aortic coarctation. Much commoner is high blood pressure due to kidney problems or to enlargement of the outer part of the adrenal gland (the adrenal cortex). To control high blood pressure that is difficult the best way to sort out the cause is to measure the renin (a kidney enzyme) and aldosterone (an adrenal gland hormone) in the blood plasma (28, 29); this is most informative after the individual take a dose of diuretic to stimulate the production of renin and aldosterone. The kidney and adrenal gland have a central role in the long-term regulation of body salt and water. When it goes wrong, it causes high blood pressure. If the kidney senses that the body is too dry or the blood pressure is too low it puts out renin, the enzyme that activates a precursor to angiotensin I, a short chain of amino acids. Angiotensin I is converted to angiotensin II by an enzyme called angiotensin converting enzyme (ACE). Angiotensin II can raise blood pressure by itself because if constricts arteries by causing thickening of the arteries and heart muscle but it also goes to the outer part of the adrenal gland (the adrenal cortex) and causes the adrenal gland to release aldosterone. Aldosterone goes to the kidney, where it causes salt and water retention and excretion of potassium, magnesium and other ions (Spence '05: 120, 121, 132). Thiazine diuretics are the commonest and cheapest drug for treating high blood pressure is hydrochlorothizide, a drug that is particularly effective in the elderly and people with African ancestors, it acts first as a diuretic; after six weeks or so, iuts main effect is to relax the small artery branches, the arterioles. The main issue with this drug is determining the correct dose: for most indiviuals a dose of 12.5 mg daily is enough, and for others 12.5 mg every other day. Hydrochlorothizide is usually available in tablets of 25 mg or more, so half of the smallest tablet is the optimal dose (Spence '05: 127). Drug therapy can now control about 80% of all cases of hypertension. Drugs do not cure, but their control of this disease marks a tremendous change in the outlook for patients whose inflexible fate until 1950 was a stroke, heart failure, or kidney failure (Elvin-Lewis '77: 189). There are other categories of drugs that may be necessary in specific high blood pressure patients. Aldosterone blockers aldosterone is made in the adrenal gland and travels to the kidney to save sodium (salt) and water. It also acts as a constrictor of blood vessels. Blocking aldosterone may lower blood pressure by both mechanisms. These drugs are most often used in conjunction with other drugs, or may be used alone. High potassium is the most common side effect. Sympatholytic drugs are older drugs that decrease the outpouring of nervous system hormone with numerous side effects that are therefore rarely used. Direct vasodilators directly dilate the blood vessels and are used only in special situations (Wilson and Childre 06: 48-49). People taking long term diuretic therapy to rid their body of salt and water, often experience adverse effects related to the depletion of the number of ions. Often the rubric hypokalemia (low blood level of potassium) is used to characterize the problem. The problem is however not a low eve of potassium in the blood, it is potassium depletion in the cells throughout the body, including muscles, heart, brain, and elsewhere. Potassium supplements do not restore intracellular potassium unless magnesium is taken at the same time. Maintaining adequate intracellular potassium helps prevent toxicity of digoxin (a heart medication that can cause serious problems if the blood level is too high, or the potassium level in the cells is too low) and minimizes the adverse effects on diabetes and cholesterol. Taking diuretic causes the body to react by turning on hormone systems designed to retain salt and water. Aldosterone causes the kidney to retain sodium and excrete potassium and other ions; when potassium is eventually depleted, there is excretion of hydrogen ions, leading to an alkaline state in the blood (alkalosis). Most individuals with depleted potassium have a normal serum potassium. If taking a diuretic and feel tired, achy, have cramps in extremities, are impotent, and feel faint when standing up, presume depleted potassium. Usually when there is potassium depletion there is also depletion of magnesium, zinc, selenium, rubidium and other ions (Spence '05: 146). Drugs that reduce production of aldosterone by the adrenal gland also are magnesium and potassium sparing. Drugs that block activation of angiotensin by blocking angiotensin-converting enzyme, ACE inhibitors such as captopril, enalapril, lisinopril or any drug with a proper name ending in pril), or by blocking angiotensin II at its receptor (losartan irbesartan, candesartan, or other drug ending in sartan) will reduce urinary losses of potassium, magnesium and probably the other ions that are depleted by diuretics. Because potassium loss from the kidney is driven by exchange of potassium for sodium as regulated by aldosterone, salt intake is an important concern. The more salt eaten, the more potassium lost. Every sodium ion reabsorbed from the renal tubule leads to excretion of a potassium ion; high sodium intake aggravates potassium losses, and when potassium is depleted, potassium ions are exchanged for hydrogen ions, leading to acid urine with alkaline blood. Blocking the effect of high renin potassium and magnesiu depletion by blocking the effect of angiotensin II with angiotensin receptor blockers (ARBs) will prevent secondary hyperaldosteronism. This may be the best approach for people who have either congestive heart failure or secondary hyperaldosteronism from renal artery stenosis or other high-renin states. ACE inhibitors, also block formation of angiotensin II, but this effect wears off after a few weeks because there are other pathways for the formation of angiotensin II (Spence '05: 147, 148, 152). If potassium-sparing diuretics and ARBs or ACE inhibitors are used together, there is a real risk of seriously increased levels of potassium in the blood (hyperkalemia). For primary hyperaldosteronism the specific treatment is blockers of aldosterone such as spironolactone and eplerenone; amiloride can also be used and is the specific treatment for hypertension due to abnormalities of the renal tubule such as Liddles syndrome. The problem is not low levels of potassium in the blood (hypokalemia) but potassium/magnesium depletion; potassium supplements do not solve the problem because magnesium is required to restore intracellular potassium. A recommended approach is to: (1) reduce salt intake below 2-3 grams per day; (2) reduce the dose of diuretic, (3) use potassium/magnesium sparing diuretics to prevent losses or (4) use angiotensin blockers to reduce secondary hyperadlosteronism and thus prevent depletion of potassium and magnesium (Spence '05: 152). To minimize potassium losses, one can reduce salt intake; use angiotensin-receptor blockers (ARBs) to prevent angiotensin II from causing the adrenal cortex to release aldosterone; or block the effects of aldosterone on the kidney tubule by using potassium-magnesium sparing diuretics. A minority of patients with difficult to treat high blood pressure will require potassium and magnesium supplementation. Potassium depletion is usually managed by a combination of reducing salt intake, reducing the dose of diuretic and using either potassium/magnesium sparing diuretics or drugs that prevent excess aldosterone production such as angiotensin receptor blockers. For most individuals, particularly the elderly, a daily dose of 12.5 mg hydrochlorothiazide (HCTZ) is the commonest and cheapest drug for treating high blood pressure, is enough. Among that do not deplete the bodys potassium and magnesium, amiloride is generally preferred for men, because men who take spironolactone often have sore nipples and sometimes breast enlargement. This does not appear to be a problem with eplerenone, a new aldosterone antabgonist. Avoid triamterene, because half the people who take it develop an abnormality in the urine (triamterene casts) and it is implicated in kidney inflammation (interstitial mephritis) and kidney stones. If a small does of one of the thiazide family of diuretics if required, a common ratio might be HCTZ 12.5 mg to amiloride 10-20 mg, or spironolactone 100 mg. For people with secondary hyperaldosteronism, overproduction of aldosterone because of high levels of renin and angiotensin - angiotensin receptor blockers are more effective (Spence '05: 149, 150). Any ACE inhibitor will cause a cough in about 8 percent of people and swelling of the face and tongue (angiodedema) in about one in one thousand. One can avoid these adverse effects by switching to angiotensin blockers, which have benefits similar to those of ACE inhibitors. The first dose of any ACE inhibitor or angiotensin blocker can cause a severe drop in blood pressure, particularly in people taking diuretics. They can also cause acute kidney failure in people that have severe narrowing of both kidney arteries. This problem is rare except in very severe high blood pressure or heart failure. Among ACE inhibitors the main difference is due to the presence of a sulfhydryl group in captropril, which is responsible for the loss of taste and a characteristic generalized rash that looks like measles. Both of these problems will disappear if you switch to another ACE inhibitor or to an angiotensin blocker. Captopril is very short acting and must be taken two or three times per day to achieve desired effects in all but the least severe cases. Lisinopril, quinapril, and some of the other ACE inhibitors are long acting enough to work well when taken once a day. Captopril is also the most expensive of ACE inhibitors (Spence '05: 145). Beta-blockers block one of the two kinds of adrenaline receptor (a structure on the surface of cells that responds to adrenaline), the beta receptors. Beta receptors are of two types, beta-1 and bta-2. Stimulating beta-1 receptors causes the heart to speed up and beat more forcefullyl. Stimulating the beta-2 receptors causes the bronchi to dilate and the arteries that got to the muscles to dilate. Alpha-blockers block the second of the two kinds of adrenaline receptor, the alpha receptors: the alpha-1 receptor when stimulated causes the arteries to constrict, and the alpha-2 receptor when stimulated inhibits the sympathetic nervous system. Alpha-blockers are used selectively to block the alpha-1 receptors by preventing the arteries from constricting, they tend to lower blood pressure. They also have beneficial effects on cholesterol and diabetes, and are now commonly used for bladder symptoms from prostate gland enlargement. The main ones in use are prazosin, doxazosin, and terazosin. Compared with prazosin, the latter two are longer acting so can be taken less often, and they tend to cause less trouble with a faint feeling on standing. Doxazosin is the longest acting, and probably the best choice for that reason (Spence '05: 128, 129, 130). Beta-blockers have issues in the different ways individual bodies handle the drugs (pharmacokinetics) and the way the drugs interact with adrenaline receptors (pharmacodynamics). Concerns include how drugs metabolize, how long the drug action lasts, how the drugs are absorbed into various body tissues, and how tightly the drug binds to receptors. Propranolol undergoes extensive metabolism during its first pass through the liver (first-pass metabolism); about 70 percent of an oral dose is broken down in the liver and never makes to the rest of the body. Both propranolol and metoprolol have a twenty-fold range in the blood levels achieved with a given dose that in different people can lead to blood levels that range from five to one hundred units. If propranolol and metoprolol dont work well at the dose prescribed hypertension can be controlled, at a much lower cost, with a beta-blocker that is excreted by the kidney or metabolized in a different way. Nadolol and atenolol are two beta-blockers that are excreted by the kidney, creating special problems for the elderly and for people with impaired kidney function. They can build up in the blood-stream, causing relatively slow heart action (bradycardia), and aggravate heart failure, which in turn aggravates the kidney function. If the heart rate has been getting slower and slower switch to a beta-blocker that is not excreted by the kidney, but metabolized by the liver (Spence '05: 140, 141). The best and most convenient beta-blocker is pindolol, it has the most potent ISA, so it does not cause the adverse effects due to blockade of beta-2 receptors. (ISA, intrinsic sympathomimetic activity of drugs that block beta-1 receptors and stimulate beta-2 receptors.) Pindolol is also the best beta-blocker for people with diabetes, high cholesterol, or blocked arteries in the legs; it is less likely to aggravate cholesterol and diabetes, and less likely to cause fatigue and is the least likely to cause rebound hypertension if doses are missed. The downside of pindolol is that small proportion of people (about 5 percent) experience vivid dreams, tremor or anxiety because of the drugs greater penetration into the brain. Beta-blockers penetrate brain tissue to markedly varied extents because of difference in how well they dissolve in fat. These differences explain why pindolol, with its extreme penetration into brain tissue, is the most likely beta-blocker to cause anxiety, tremors and vivid dreams, and why propranolol, which is also concentrated in the brain, is the most likely to cause subjective tiredness and hallucinations. Selective blockade of beta-1 receptors that speed up the heart and cause it to beat harder and stimulation of beta-2 receptors that cause dilation of the large air tubes in the lung and of the arteries that go to muscles. Nonselective drugs such as propranolol, nadolol and timolol are more likely to cause adverse effects due to beta-2 blockade. Drugs that stimulate beta-2 receptors will have a different profile again; pindolol, a relatively potent beta-2 stimulator, had beneficial effects on cholesterol, may benefit diabetes, and is least likely to cause problems with cold extremities and asthma (Spence '05: 141, 142, 144). Calcium-channel antagonists, or calcium-channel blockers, dilate arteries by interfering with the channels that permit calcium to enter cells; they are useful for both hypertension and angina. Calcium-channel antagonists, or calcium-channel blockers, dilate arteries by interfering with the channels that permit calcium to enter cells. Trouble with constipation or shortness of breath or other symptoms of heart failure, is often helped by changing from verapamil or diltiazem to another type of drug, or changing to a dihydropyridine (the largest class of CCBs) such as nifedipine, felodipine, or amlodipine. If the problem is a slow heart rate from diltiazem, changing to a dihydropyridine or another class of drug should help; if it doesnt, check out a pacemaker. Consumers of both diltiazem and a beta-blocker, may need to reduce the dose of beta-blocker. Those having a lot of angina on a dihydropyridine such as felopidipine, are helped by adding a beta-blocker (or switching to diltiazem for those who cant take a beta-blocker). If it doesnt help, find out about endartectomy, angioplasty or bypass surgery, and make sure that all the risk factors are optimally controlled. If the problem is ankle swelling, flushing, or headache, switching from nifedipine or felodipine to amlodipine or another class of drug should help. Diltiazem and verapamil are not very strong and are extremely expensive, so are not advised for treating high blood pressure: the main reason to use them. Verapamil is good for heat-rhythm disturbances such as atrial fibrillation and diltiazem is good for angina (chest pain brought on by exertion, due to narrowing of the coronary arteries) (Spence '05: 139, 140). There are other categories of drugs that may be necessary in specific high blood pressure patients. Aldosterone blockers aldosterone is made in the adrenal gland and travels to the kidney to save sodium (salt) and water. It also acts as a constrictor of blood vessels. Blocking aldosterone may lower blood pressure by both mechanisms. These drugs are most often used in conjunction with other drugs, or may be used alone. High potassium is the most common side effect. Sympatholytic drugs are older drugs that decrease the outpouring of nervous system hormone with numerous side effects that are therefore rarely used. Direct vasodilators directly dilate the blood vessels and are used only in special situations (Wilson and Childre 06: 48-49). Drugs in the class called dihydropyridines, the largest group, tend to be the best at lowering blood pressure. Diltiazem is a somewhat weaker vasodilator in the peripheral arteries throughout the body, but it affects the coronary arteries and so may be better for angina. Verapamil is another relatively weak drug that may aggravate heart failure. The main dihydrpyrinidines are nifedipine, felodipine, amlodipine, nisodipine, and nicardipine. Nifedipine and felodipine are quite short acting, and the slow-release pills that have been developed are only partially effective in correcting the problem of peaks and troughs in blood pressure. Nifedipine is relatively expensive, but the best value is felodipine, and if it is causing too many side effects, amlodipine may be better. Nicardipine is very expensive and usually has to be taken several time a day, so it has little advantage. A special problem occurs when dihydropyridines are taken with grapefruit juice that reduce the metabolism of a number of drugs. Felodipine blood levels go up on average about 300 percent with grapefruit juice, nisodipine levels about 500 percent. A number of important interactions occur between grapefruit and other drugs such as cyclosporine, terfenadine (an antihistamine), and propafenone; based on the known metabolism of warfarin and the cholesterol-lowering drugs such as lovastatin and simvastatin, can be anticipated to be affected by grapefruit juice. As a rule of thumb any drug that should not be taken with erythromycin, ketoconazole or itraconazole, should not be taken with grapefruit juice (Spence '05: 162). Grapefruit juice inhibits the metabolism of a number of drugs, whereby a large proportion of the drug is metabolized by oxidation to form another chemical, in the wall of the intestine. This oxidation is performed by a specific form of the family of oxidative enzymes (Cytochrome P450) called CYP3A4. Drugs that are largely metabolized during oxidation are said to have low bioavailability, because a low proportion of the drug is available to the body. When the metabolism of these drugs in the intestinal wall is inhibited, a much larger proportion of the drug is absorbed unchanged, and the blood levels of the drug are much higher. Dihydropyridine calcium-channel antagonists) drugs with high bioavailability such as amlodipine are not much affected by grapefruit juice; nifedipine, which is 60 percent bioavailable, ahs a 30 percent rise in blood levels when taken with grapefruit juice, and nisoldipine, which is 8 percent bioavailbe, goes up on average fivefold up to ninefold. Interesting Florida orange juice has no such effect, although Seville orange juice and lime juice have some effect (though less powerful than grapefruit juice). Other drugs for which the grapefruit juice effect is important include the transplant antirejection drug cyclosporine (a tripling of blood levels); the AIDS drug squinovir (large effects); the sleeping pills midazolam and triazolam; and most importantly, the anti-histamine terfenadine. Both terfenadine and the gut-motility drug cisapride can cause serious heart-rhythm disturbances when their metabolism is inhibited, wherefore they are no longer on the market. Other drugs affected importantly by grapefruit include the anticoagulant warfarin and the heart-rhythm drug propafenone in some individuals, and the cholesterol-lowering drugs lovastatin and simvastatin. Blood levels of both lovastatin and simvastatin can be increased fifteen-fold by a glass of grapefruit juice. Atorvastatin is also affected by grapefruit, although to a much lesser degree, but pravastatin and rosuvastatin are not. A simple rule of thumb is that if a drug should not be taken with erythromycin, ketoconazole or itraconazole, it should not be taken with grapefruit juice. To be safe, don't drink grapefruit juice if taking one of the affected drugs (Spence '05: 162). Most high blood pressure is treated in primary care. Specialists are called in when blood pressure control is not achieved. When blood pressure isnt controlled by a low dose of one drug, doctors often will add a second (or third or fourth) medicine to the mix. This is because as higher doses of any one medication are taken, there is a greater chance for side effects to develop. In addition, there are often multiple and related problems contributing to increased blood pressure. So its common to see a diuretic combined with any of the other classes of hypertensive drugs. Some companies have developed combinations of these medications: ACE inhibitor with diuretic, ACE inhibitor with calcium channel blocker, alpha blocker combined with beta-blocker, and so forth (Wilson and Childre 06: 50). There are little clusters of nerves in the heart and along the arteries coming out of the heart that sense pressure. These sensors relay information in to the area of your brain that regulates a lot of basic automatic functions: breathing rate, heart rate and blood pressure. The reflex that involves sensing pressure and then responding with instructions to change your heart rate and relax or constrict the blood vessels is referred to as the baroreceptor reflect. The concept of neutral in Heart Math , which has been taught to 50,000 people worldwide and reduced hospital employee turnover from 27 to 4 percent in one hospital, in one year, is useful for stepping back, neutralizing your emotions and see the options with clarity. Heart focus shift attention to the area of the heart and breathe slowly and deeply. Heart breathing keep focus in the heart by gently breathing five seconds in and five seconds out through the heart. Do this two or three times. Heart feeling activate and sustain a genuine feeling of appreciation or care for someone or something in life. Focus on the good heart feeling while continuing to breathe through the area of the heart (Wilson and Childre 06: 75, 97, 98, 104). 8. Kidney Disease Human kidneys serves to convert more than 1700 liters of blood per day into about 1 liter of a highly specialized concentrated fluid called urine. In so doing the kidney excretes the waste products of metabolism, precisely regulates the body's concentratin of water an dsalt, maintains the appropriate acid balance of plasma, and serves as an endocrine organ, secreting such hormones as erythropoietin, renin and prostaglandins. Renal disease is responsible for a great deal of morbidity by, fortuneately, are not equally major causes of mortality. Approximately 45,000 deaths are attributed yearly to renal disease in the United States, in contrast to about 650,000 to hart disease, 560,000 to cancer, and 145,000 to stroke. Millions of people are affected annually by nonfatal kidney diseases, most notably infections of the kidney or lower urinary tract, kidney stones and urinary obstruction. Twenty percent of all women suffer from infections fo the urinary tract or kidney at some time in their lives, and as many as 5% of the U.S. population develops renal stones. Modern treatment, notably dialysis and transplantation, keep many [atoients alive who earlier would ave died of renal failure. People with even mild chronic kidney disease have a greatly enhanced risk for cardiovascular disease. The study of kidney disease is facilitated by dividing them up in those that affect the four basic morphologic components: glomeruli, tubules, interstitium and blood vessels. Most glomerular disease are immunologically mediated, whereas tubular and interstitial disorders are frequently caued by toxic or infectious agents. Damage to one kidney invariably affects the other. Disease primarily in the blood vessels, for example, inevitably affects all the structures that depend on this blood supply. Severe glomerular damage impairs the flow through the peritubular vascular system and also delivers potentially toxic products to tubules; conversely, tubular destruction, by increasing intraglomerular pressure, may induce glomerular injury. Whatever its origin there is a tendency for all forms of chronic kidney disease ultimately to destroy all four components of the kidney, culminating in chronic renal failure and what has been called end-stage kidneys. The functional reserve of the kidney is large and much damage may occur before there is evident functional impairment (Saunders-Elsevier; Alpers '10: 906). Pyelonephritis is a renal disorder affecting the tubules, interstitium and renal pelvis and is one of the most common diseases of the kidney. It can be acute renal lesion caused by bacterial infection. Chronic pyelonephritis is more complex, bacterial infection plays a dominant role, but other factors such vesicoureteral reflux, where the reflux of urine allows bacteria to ascend the ureter and obstruction by a tumor or enlarged prostate are involved. Pyelonephritis is a serious commplication of urinary tract infections that affect the bladder (cystitis). The dominant etiologic agents, accounting for more than 85% of cases of urinary tract infection are the gram-negative bacilli that are normal inhabitants of the intestinal tract, most commonly Escherichia coli, followed by Proteus, Klebsiella and Enterobacter. Streptococcus feacalis, also of enteric origin, staphylocooci and virtually every other bacterial and fungal agent, (e.g. Candida) can also cause lower urinary tract and renal infection that destroys the glomeruli (Alper '10: 939). Bactrim monopolizes the drug monograph for E. coli although it may be the drug and not the disease that so often causes malabsorption, that manifests as a post-infectious auto-immune disease in the kidneys or intestines, particularly in vegans without adequate vitamin B12 and probiotic supplementation. Metronidazole (Flagyl ER) is preferred for the treatments of all fecal coliform and although it is contraindicated with alcohol causes such minimal vitamin B12 deficiency exhibited by chronic consumption of all other antibiotics more research is needed for the FDA to verify in the impressive metronidazole monograph, that it is effective against E. coli. Because the effective oral antifungal Sporanox (itraconazole) is highly contraindicated for congestive heart failure patients due to adverse reactions with almost all hypertension medicine natural anticandidal remedies and vigilance with athletes foot crme (clotrimazole), rather than the antifungal foot powder (prescribed for elders) spray (Toftate) that causes diffuse pain and chest pain, are all available over-the-counter. The glomerular filtration barrier allows discrimination among various protein molecules, depending on their size (the large, the less permeable) and charge (the more cationic, the more permeable). Most cases of human glomerulonephritis are a consequence of deposits of discrete immune complexes. Microbial antigens that have been implicated are bacterial products (streptococci), appearing 1 to 4 weeks post-streptococcal infection of the pharynx or skin, but only certain strains of groups A -hemolytic streptococci are nephritogenic, as well as the surface antigen of hepatitis B and C virus antigens, and antigens of Treponema pallidum, Plasmodium falciparum and several other viruses. More than 95% of children and 60% of adults recover but fewer than 1% of childen and 40% of aduts become severely oliguric, and develop a rapidly progressive glomerulonephritis; prolonged and persistent heavy proteinuria and abnormal GFR mark patients with an unfavorable prognosis (Alpers '10: 940, 941, 907, 910, 914, 919). In chronic interstitial nephritis there is infiltration with predominantly mononuclear leukocytes proment interstitial fibrosis and widespread tubular atrophy. Defects in tubular function may cause impaired ability to concentrate urine, evidenced by polyuria or nocturia, salt wasting, diminished ability to excrete acides (metabolic acidosis), and isolated defects in tubular reabsorption or secretion. In immunocompromised persons, particularly those with transplanted organs, viruses such as Polyomavirus, cytomegalovirus and adenovirus can also cause renal infection. In most patients with urinary tract infections, the infecting organisms are derived from the patient's own fecal flora that has reached the kidney through the bloodstream (hematogenous infections) or from the lower urinary tract (ascending infection) the most common cause of clinical pyelonephritis. Chronic pyelonephritis at one time accounted for 10-20% of patients in renal transplant or dialysis units, until predisposing conditions such as reflux became better recognized. The clinical manifestations of renal disease can be grouped into well defined syndromes. Azotemia is a biochemical abnormality that refers to an elevation of the blood urea nitrogen (BUN) and creatinine levels, and is related largely to a decreased glomerular filtration rate (GFR). Azotemia is a consequence of many renal disorders, but also arises from extrarenal disorders. Prerenal azotemia is encountered when there is hyperfusion of the kidneys (e.g. hemorrhage, shock, volume depletion and congestive heart failure that impairs renal function in the absence of parenchymal damage. Postrenal azotemia is seen whenever urine flow is obstructed beyond the level of the kidneys. Relief of the obstruction is followed by correction of the azotemia. Uremia is characterized by a host of metabolic and endocrine alterations resulting from renal damage. Nephritic syndrome onset present grossly visible hematuria (red blood cells in urine), mild to moderate proteinuria (>3.5 gm/day), hypoalbuminemia (plasma albumin <3 gm/dL), severe edema, hyperlipidemia and lipiduria (lipid in the urine) is due to glomerular disease classically acute poststreptococcal glomerulonephritis. Glomerular disease is often associated with such systemic disorders as diabetes mellitus, SLE, vasculitis, amyloidosis and endocarditis. Rapidly progressive glomerulonephritis includes a rapid decline (hours to days) in GFR) (Alpers '10: 906-907). Acute renal failure is dominated by oliguria or anuria (reduced or no urine flow), and recent onset of azotemia that can result from glomerular, interstitial or vacular injury or acute tubular injury. Chronic renal failure is characterized by prolonged symptoms and signs of uremia, it is the end result of all chronic renal parenchymal diseases. Renal tubular defects are dominated by polyuria (excessive urine formation), noctuira and electrolyte disorders (e.g. metabolic acidosis). Defects in specific tubular functions can be inherited (e.g., familial nephrogenic diabetes, cystinuria, renal tubular acidosis) or acquired (e.g. lead nephropathy). Urinary tract infection is characterized as bacteriuria and pyuria (bacteria and leukocytes in the urine). The infection may be symptomatic or asymptomatic and may affect the kidney (pyelonephritis) or the bladder (cystitis). Nephrolithiasis (renal stones) manifest as severe spasma of pain (renal colic) and hematuria, often with recurrent stone formation. Urinary tract obstruction and renal tumors have varied clinical manifestations based on the specific anatomic location and nature of the lesion. Nephrotic patients are particularly vulnerable to infection especially staphylococcal and pneumococcal. Thrombotic and thromboembolic complications are also common due in part to oss of endogenous anticoagulants (e.g. antithrombin III) and antiplasmins in the urine. Renal vein thrombosis may result (Alpers '10: 907-908, 922). Chronic renal failure progresses through four stages that merge into one another. In stage 1 there is a diminished renal reserve the GFR is about 50% of normal. Serum BUN and creatinine values are normal, and the patient is asymptomatic. However, they are more susceptible to developing azotemia with an additional renal insult. Stage 2 is known as renal insufficiency the GFR is 20-50% of normal. Azotemia appears, usually associated with anemia and hypertension. Polyuria and nocturia can occur as a result of decreased concentrating ability. Stage 3 chronic renal failure, GFR is less than 20-25% of normal. The kidneys cannot regulate volume and solute composition, and patients develop edemia, metabolic acidosis, and hyperkalemia. Overt uremia may ensue, with neurologic, gastrointestinal and cardiovascular complications. Stage 4 end-stage renal disease GFR is less than 5% of normal; this is the terminal stage of uremia. The major characteristic of normal glomerular filtration are an extraordinarily high permeability to water and small solutes, and impermeability to proteins, such as molecules of the size of albumin (~3.6 nm radius; 70 kilodaltons [kD] molecular weight or larger (Alpers '10: 907, 910). A century ago, two French investigators reported that small amounts of plasma from anemic rabbits injected into normal animals caused an increase in red blood cell production (erythropoiesis) within a few hours. They referred to this activity as hemopoietine. Over time, as investigators became more convinced that this red-blood-cell stimulating activity was caused by a single protein in the blood plasma, they gave it a variety of names erythropoietic-stimulating activity, erythropoietic-stimulating factor, and, ultimately, erythropoietin. Refining the work of the French scientists in the 1950s and 60s, American investigators conclusively showed that a hormone stimulated red cell production, and that the kidneys were the primary source of erythropoietin, and that low oxygen was the main driver of erythropoietin production. Soon, researchers found that patients with anemia responded by increasing their levels of erythropoietin to stimulate increased red blood cell production. Patients who required an increase in red blood cells in order to make up for low oxygen levels in the blood (such as patients with lung disease living at high altitudes, or smoking more than a pack of cigarettes a day) also had elevated erythropoietin levels. In the early 1960s came the development of hemodialysis, a method of removing waste products from the blood when the kidneys are unable to perform this function, to sustain the lives of patients with end-stage kidney disease. As a result of this treatment advance, these patients were able to survive the underlying disease, but their damaged kidneys could no longer make erythropoietin, leaving them severely anemic and in desperate need of Epo therapy. In 1983, scientists discovered a method for mass producing a synthetic version of the hormone. Experiments were conducted to test the safety and effectiveness of the new drug, Epo, for treating anemia in patients with kidney failure. The results of these early clinical trials were dramatic. Patients who had been dependent on frequent blood transfusions were able to increase their red blood cell levels to near-normal within just a few weeks of starting therapy. Patients appetites returned, and they resumed their active lives. It was the convergence of two technologies long-term dialysis and molecular biology that set the stage for anemia management in this group of patients. Since then, millions of patients worldwide have benefited from Epo therapy (Adamsom '08). In some patients with rapidly progressive (crescentic) glomerulonephritis, exhibiting hematuria with red blood cell casts in the urine, variable hypertension and edema, antibodies produce the clinical picture of pulmonary hemorrhage associated with renal failure known as Goodpasture syndrome treated with plasmapheresis to remove the pathogenic circulating antibodies and immunosuppression. Exposure to viruses and hydrocarbon solvents has been implicated. Crescentic glomuleronephritis can also be caused by immune complex deposition or pauci-immune type with circulating antineutrophil cytoplasmic antibodies (ANCAs). 1 to 7% of patients treated for rheumathoid arthritis with drugs such as penicillamine, captopril, gold, develop membranous glomerulopathy. Underlying malignant tumors are present in as many as 5-10% of adults with membranous glomerulopathy that can be caused by chronic hepatitis B or C, syphilis, schistosomiasis, malaria, Systemic Lupus Erythomatous (SLE), or autoimmune disorders such as thyroiditis but in 85% of patients no associated condition is discovered and the condition is considered idiopathic. Although proteinuria persists in more than 60% of patients, only about 10% die or progress to renal failure within 10 years. Minimal-change disease can be caused by nonsteroidal anti-inflammatory drugs (NSAIDs), and although there are no immune deposits, tends to respond well to corticosteroids and other immunosuppressive therapies. Focal segmental glomerulonephrosis is characterized by sclerosis of some but not all, glomeruli and can be a primary disease or secondary disease due to HIV infection, sickle-cell disease, massive obesity, scarring and accounts for 10-35% of cases of neophrotic syndrome in children and adults in the United States particularly in Hispanic and African-American patients, there is a poor response to corticosteroid therapy, and 50% develop end-state renal disease in 10 years. 20% of patients follow an unusually rapid course, with intractable massive proteinuria ending in renal failure within 2 years. Recurrences are seen in 25% to 50% of patients receiving allografts. Membranoproliterative glomerulonephritis (MPGN) accounts for 10-20% of cases of nephrotic syndrome in children and young adults. Glomerular immune deposits are thought to derive from infections by hepatitis B and C viruses. About 50% develop chronic renal failure within 10 years. Treatment with steroids, immunosuppressive agents and antiplatelet drugs have not proved to be effective, There is a high incidence of recurrence in transplant recipients, particularly in dense deposit disease recurrence happens in 90% of patients although renal failure in the allograft is much less common. Secondary MPGN can result from SLE, hepatitis B and C, cryoglobulinemia, endocarditis, infected ventriculoatrial shunts, chronic visceral abscesses, HIV infection, schostosomiasis, 1-Antitrypsin deficiency, malignant diseases such as chornic lymphocytic leukemia and lymphoma and hereditary deficiencies of complement regulatory proteins (Alpers '10: 920, 922, 925). IgA Nephropathy (Berger Disease) has prominent IgA deposits that occur with increased frequency with Henoch-Schnlein purpura, gluten enteropathy (celiac disease) and liver disease. The disease affects people of any age, but older children and young adults are most commonly affected. The hematuria typically lasts for several days and then subsides, only to return every few months. Many patients maintain normal renal function for decades. Slow progression to chronic renal failure occurs in 15-40% of cases over a period of 20 years. Recurrence of IgA deposits in transplanted kidneys is frequent and 15% develop another progressive disease. Alport Syndrome is a hereditary nephritis that is manifest by hematuria with progression to chronic renal failure, accompanies by nerve deafness and various eye disorders, including lens dislocation, posterior cataracts and corneal dystrophy. The disease is inherited as an X-linked trait in 85% of cases with males expressing the full syndrome and females as carriers limited to hematuria although autosomal recessive and autosomal dominant pedigrees exist. Symptoms appear at ages 5 to 20 years, and the onset of overt renal failure is between the ages of 20 and 50 years in men. Thin basement membrane lesion (Benign Familial Hematuria) is a fairly common hereditary entity manifested clinically by familial asymptomatic hematuria and diffuse thinning of the GBM to between 150 and 250 nm (compared with 300-400 nm in normal adults) renal function is normal and prognosis is excellent but most patients are heterozygous for the defective gene and may be carriers, homozygotes or compound heterozygotes may progress to renal failure (Alpers '10: 929-933). Chronic glomerulonephritis is best considered a pool of end-stage glomerular disease fed by several streams of specific types of glomerulonephritis. Patients with crescentic glomerulonephritis, if they survive the acute episode, usually progress to chronic glomerulonephritis, membranous nephropathy, MPGN, IgA nephropathy and FSDS all may progress to chronic renal failure, but there are unexplained cases of obliteration of the glomeruli. Because hypertension is an accompaniment of chronic glomerulonephritis, arterial and arteriolar sclerosis may be conspicuous. Kidneys from patients with end-stage disease on long-term dialysis show a variety of changes that are unrelated to the primary disease, including arterial intimal thickening, extensive deposition of calcium oxalate crystals, acquired cystic disease and uremic complications such as uremic pericarditis, uremic gastroenteritis, secondary hyperparathyroidism and left ventricular hypertrophy due to hypertension. Patients often present with such nonspecific complaints as loss of appetite, anemia, vomiting or weakness. In some, renal disease is suspected with the discovery of proteinuria, hypertension or azotemia on routine medical examination. In others, the underlying renal disorder is discovered in the course of investigating edema. Most patients are hypertensive and sometimes the dominant clinical manifestations are cerebral or cardiovascular. Advanced or end-stage kidney disease occurs in as many as 40% of both insulin-dependent type 1 diabetics and type 2 diabetics. The term diabetic nephropathy describes the conglomerate of lesions that occur on the glomeruli. Deposits of amyloid, typically light-chain (AL) or AA type, Congo red-positive, eventually obliterate the glomerulus completely and the kidney may increase in size. Goodpasture syndrome, microscopic polyangiitis, Wegener granulomatosis, essential mixed cryoglobulinemia, plasma cell dyscrasias and multiple myeloma are commonly associated with glomerular lesions (Alper '10: 933-935) treated as neoplasms, probably of fungal origin. Acute kidney injury (AKI) is a reversible renal lesion that causes 50% of case of acute renal failure in hospitalized patients and can be caused by ischemic or toxic tubular injury and acute renal failure or inflammatory reaction of the tubules and interstitium (tubulointerstitial nephritis). In AKI there is a rapid reduction of renal function and urine flow, falling within 24 hours to less than 400 mL per day. It can be caused by ischemia, direct toxic injury by drugs, such as gentamicin and other antibiotics, poisons (heavy metals such as mercury), organic solvents (e.g. carbon tetrachloride), pancreatitis, radiocontrast dyes, myoglobin, hemoglobin, radiation or urinary obstruction by tumors, prostatic hypertrophy or blood clots. The clinical course of AKI is variable but he classic case may be divided into (1) initiation phase lasting about 36 hours dominated by the inciting medical, surgical or obstetric event with a slight decline in urine output and rise in BUN, declining GFR and blood flow explaining oliguria; (2) maintenance phase with sustained decreases in urine output to between 40 to 400 mL/day (oliguria), salt and water overload, rising BUN concentrations, hyperkalemia, metabolic acidosis and other manifestations of uremia. With appropriate attention to the balance of water and blood electrolytes, including dialysis, the patint can be supported through this oliguric crisis; and (3) the recovery phase has a steady increase in urine volume that may reach up to 3 L/day. The tubules are still damaged, so large amounts of water, sodium and potassium are lost in the flood of urine. Hypokalemia, rather than hyperkalemia becomes a clinical problem and there is a peculiar increased vulnerability to infection at this stage. Eventually, renal tubular function is restored and concentrating ability improves, BUN and creatinine levels return to normal. Tubular functional impairment may persist for months, but most patients who reach this phase recover completely. The prognosis of AKI depends on the clinical setting, recovery is expected with nephrotoxic AKI when the toxin has not caused serious damage to other organs, such as the liver or heart. With current supportive care, 95% recover but with shock related to sepsis, extensive burns, or other causes of multi-organ failure, the mortality rate can rise to more than 50%. Up to 50% of patients with AKI do not have oliguria and instead have increased urine volumes and tend to follow a more benign clinical course. (Alper '10: 935-938). An increasing number of drugs are known to be nephrotoxic. First reported after the use of sulfonamides, acute tubulointerstitial nephritis and renal papillary necrosis most frequently occurs with synthetic penicillins (methicillin, ampicillin) other synthetic antibiotics (rifampin), diuretics (thiazides), allopurinol, cimetidine, aristolochic acid found in some herbal remedies, NSAIDs, analgesics mixtures including phenacetin, aspirin, caffeine, acetaminophen and codeine. Selective COX-2 inhibitors, while sparing the gastrointestinal tract, affect the kidneys. Acute uric acid nephropathy can be caused by the precipitation of uric acid crystals in the renal tubes particularly in individuals with leukemias and lymphomas who are undergoing chemotherapy whereas the drugs induce death of tumor cels and uric acid is produced as relased nucleic acids are broken down. Gouty nephropathy is often precipitated by the consumption of moonshine whiskey contaminated with lead. Papillary necrosis is readily induced experimentally by a mixture of aspirin and phenacetin, usually combined with water depletion. The disease begins about 15 days (2-40) after exposure to the drug and characterized by fever, eosinophilia, a rash in 25% of patients and renal abnormalities in the form of hematuria, mild proteinuria and lukocyturia (often including eosinophils). A rising serum creatinine level or acute renal failure with oliguria develops in about 50% of cases, particularly older patients. Withdrawal from the offending drug is followed by recovery, although it may take several month, and irreversible damage occurs occasionally in older subjects. While drugs are the leading cause of acute interstitial nephritis in 30-40% of patients no offending drug or mechanism can be found. Urinary tract infections complicate 50% of cases (Alper '10: 944-946). Disorders associated with hypercalcemia, such as hyperparathyroidism, multiple myeloma, vitamin D intoxication, metastatic cancer, or excess calcium intake (milk-alkali syndrome) may induce the formation of calcium stones and deposition of calcium in the kidney (nephrocalcinosis) which can lead to chornic tubulointerstitial disease and renal insuffieincy. The earliest functional defect is an inability to concentrate the urine. Other tubular defects, such as tubular acidosis and salt-losing nephritis, mayalso occur. Extensive accumulations of calcium phosphate crystals can occur in patients consuming high doses of oral phosphate solutions in preparation for colonoscopy, presenting as renal insufficiency several weeks after exposure. Nonrenal malignant tumors, particularly those of hematopoietic origin, affect ht ekidneyas in several ways. The most commn involvements are tubulointerstitial, causd by complicatinos of the tumor (hypercalcemia, hyperuricemia, obstruction of ureters) or therapy (irradiation, hyperuricemia, chemotherapy, inections in immunosuppressed patietns). As the survival rate of persons with malignant neoplasms increases, so do these renal complications. Overt renal insuffiency occurs in half of those with multiple myeloma and related lymphoplasmacytic disorders. The main cause of renal dysfunction is related to the Bence Jones (light-chain) proteinuria. Amyloidosis formed from free light chains occur in 6-24% of individuals with myeloma. Light-chain deposition disease can cause glomerulopathy or tubulointerstitial nephritis. Hypercalcemia and hyperuricemia are often present in these patients. In the most common form, chornic renal failure develops insidiously and usually progresses slowly during a period of several months to years. Another form occurs suddenly and is manifested by acute renal failure with oliguria. Precipitating factors in these patients include dehydration, hypercalcemia, acute infection and treatment with nephrotoxic antibiotics, mistakenly used to treat myeloma of fungal origin (Alper '10: 947, 948). Nearly all diseases of the kidney involve the renal blood vessels secondarily. Hypertension is intimately linked to the kidneys because kidney disease can be both the cause and consequence of increased blood pressure. There are benign and malignant nephrosclerosis and renal artery stenosis, lesions associated with hypertension and sundry lesions involving mostly smaller vessels of the kidney. Benign nephrosclerosis is associated with the sclerosis of renal arterioles and small arteries causing focal ischemia of parenchyuma supplied by vessels with thickened walls and narrowed lumens. Nephrosclerosis at autopsy is associated with increasing age, more frequent in blacks than whites, and may be seen in the absence of hypertension. Kidneys are often moderately reduced in size, with average weights of 110 to 130 gm. It is unusual for uncomplicated benign nephrosclerosis to cause renal insuffiiecy or uremia. Although there is usually a moderate reduction in renal bood fow, the GFR is normal or only slightly reduced and occasionally there is mild proteinuria. Hypertension and diabetes mellitus, however, increase the incidence and severity of the lesions. Malignant nephrosclerosis is the form of renal disease associated with the malignant or accelerated phase of hypertension. It is relatively uncommon, occurring in 1-5% of all people with elevated blood pressure. In its pure form is usually affects younger individuals and occurs more often in men and in blacks. The turn for the worse seems to result from some sort of vascular damage to the kidneys. Fibrinoid necrosis of the arterioles and small arteies cause the kidneys to become markedly ischemic, and patients with malignant hypertension nhave markedly elevated levels of plasma renin which causes angiotensin II to cause intrarenal vasoconstriction. Aldosterone levels are also elevated, and salt retention contributes to the elevation of blood pressure. The consequences of the markedly elevated blood pressure on the blood vessels throughouth the body are known as malignant arteriosclerosis and the renal disorder is malignant nephrosclerosis. The full blown syndrome is characterized by a systolic pressure greater than 200 mm Hg and diastolic pressures greater than 120 mm Hg, papilledema, retinal hemorrhages, encephalopathy, cardiovascular abnormalities and renal failure. Early symptoms are related to increased intracranial pressure and include headaches, nausea, vomiting and visual impairment, particularly scotomas or spots before the eyes. Hypertensive criss are sometime encountered, characterized by loss of consciousness or convulsions. Soon however, renal failure makes its appearance. The syndrome is a true medical emergency requiring the institution of aggressive and prompt antihypertensive therapy to prevent the development of irreversible renal lesions. Before the introduction of current antihypertensive drugs, malignant hypertension was associated with a 50% mortality rate within 3 months of onset, progressing to 90% within a year. At present, however, 75% of patietns survive 5 years, and 50% survive with restoration of pre-crisis renal function (Alper '10: 949-950). Unilateral renal artery stenosis is a relatively uncommon cause of hypertension, responsible for 2-5% of cases, but it is important becaue it represents a potentially curable form of hypertension with surgical treatment. 70% of cases of renal artery stenosis involve an occlusion by an aatheromatous plaque at the origin of the renal artery, that are more common in men, the remaining 30% are caused by fibromuscular dysplasia of the renal artery, which are more common in women. The hypertensive effet is, at least initially, due to stimulation of renin secreting cells of the juxtaglomerular apparatus and the subsequent production of vasoconstrictor angiotensin II. Many patients with renovascular hypertension have elevated plasma or renal vein renin levels, and almost all show a reduction of blod pressure when givne drugs that block the activity of angiotensin II. Unilateral renal renin hypersecretion can be normalized after renal revascularization, usually resulting in a decrease of blood pressure. Other factors, however, may contribute to the maintenance of renovascular hypertension after the renin-angiotensin system has initiated it, including sodium retention and possibly endothelin and loss of nitric oxide. Bilateral renal artery disease, usually diagnosed definitively by arteriography, seems to be a fairly common cause of chronic ischemia with renal insufficiency in older individuals, sometimes in the absence of hypertension, that is reversible with surgical revascularization. Atheroembolic renal disease involving embolization of fragments of atheromatous plaques from the aorta or renal artery into intraparenchumal renal vessels occurs in elderly patietns with severe atherosclerosis, especially after surgery on the abdominal aorta, aortography, or intra-aortic cannulization. These emboli can be recognized in the lumens and walls of arcuate and interlobular arteries by their content of cholesterol crystals, which appear as rhomboid clefts. Frequently they have no clinical significance, however, acute renal failure may develop in elderly patients in whom renal function is already compromised, principally after abdominal surgery or atherosclerotic aneurysms. Sickle cell nephropathy can occur in homozygous people with the disease or heterozygous people with the trait. The most common clinical abnormalities are hematuria and diminished concentrating ability (hyposthenuria). Patchy papillary necrosis may occur associated with cortical scarring. Mild to moderate proteinuria is also common, occurring in about 30% of patients. Diffuse cortical necrosis is an uncommon condition that occurs most frequently after obstetric emergency, such as abrupti placentae (premature separation of the acenta), septic shock, or extensive surgery, giving rise to sudden anuria, terminating rapidly in uremic death. When bilateral and symmetric, it is fatal in the absence of supportive therapy, unilateral or patchy involvement is compatible with survival. Renal infarcts are predisposed by the extensive blood flow to the kidneys (one fourth of the cardiac output), and end-organ nature of the arterial blood supply. Most infarcts are due to embolism. A major sourc of such emboli is mural thrombosis of the left atrium and ventricle as a result of myocardial infarction. Vegetative endocarditis, aortic aneurysms and aortic atherosclerosis are less frequence sources of emboli. Most renal infarcts are of the white anemic variety. They may be solitary lesions or may be multiple and bilateral. Within 24 hours infarcts become pale, yellow-white areas tat may contain small irregular foci of hemorrhagic discoloration, usually ringed by a zone of intense hyperemia. Many renal infarcts are clinically silent. Sometimes pain with tenderness occurs. Large infarcts of one kidney are probably associated with narrowing of the renal artery or one of its major branches, which in turn may be a cause of hypertension (Alper '10: 953-955). About 10% of all people are born with potentially significant malformations of the urinary system. Renal dysplasias and hypoplasias account for 20% of chornic renal failure in children. Congenital renal disease can be hereditary but is most often the result of an acquired developmental defect that arises during gestation. Genetic abnormalities may also cause enzymatic or metabolic defets in tubular transport, such as syctinuria and renal tubular acidosis. All except horseshoe kidney are uncommon. Horseshoe kidney is caused by fusion of the upper or lower poles of the kidneys produces a horsehoe-shaped structure that is found in 1 in 500 to 1,000 autopsies. Ninety percent tof such kidneys are fused atht hlower pole and 10% are fused ath the upper pole. Agenesis of the kidney can be bilateral, which is incompatible with life, usually encountered in stillborn infants, and is often associated with other congential disorders and leads to early death. Unilatera agenesis is compatible with normal life if no other abnormalities exist. The opposite kidney is usually enlarged as a result of compensatory hypertrophy. Some patients eventualy develop progressive glomerular sclerosis in the remaining kidney. Hypoplasia refers to a failure o fhte kidneys to develop to a normal size. This anomaly may occur bilaterally, resulting in renal failure in early childhood, but it is more commonly encountered as a unilateral defect. Most cases probably represent acquired scarring but a truly hypoplastic kidney shows no scars and has a reduced numer of renal lobes and pyramids, usually six or fewer. In one form of hypoplastic kidney, oligomeganephronia, the kidney is small with fewer nephrons that are markedly hypertrophied. Ectopic kidneys lie either just above the pelvic brim or within the pelvis. They are usualy normal or slightly small in size but otherwise not remarkable, because of their abnormal position, kinking or tortuosity of the ureters may cause some obstruction to urinary flow, which predisposes to bacterial infection. Multicystic renal dysplasia is characterized by the persistence in the kidney of abnormal structures-cartilage, undifferentiated mesenchyme and immature collecting ductures, and by abnormal lobar organization. Most cases are associated with ureteropelvic obstruction, ureteral agenesis or atresis and other anomalies of the lower urinary tract. Dysplasia, enlargement of the kidney, can be unilateral or bilateral and is almost always cystic. When unilateral surgical nephrectomy is performed, when bilateral renal failure may ultimately result (Alper '10: 954-956). Cystic diseases of the kidney may be hereditary, developmental or acquired disorders. Besides Multicystic renal dysplasia, explained above, polycystic kidney disease is a hereditary disorder. Polycystic kidney disease can be autosomal-dominant (adult) polycystic disease (ADPKD) or autosomal-recessive (childhood) polycystic disease (ARPKD). ADPKD is characacterized by multiple expanding cysts of both kidneys that ultimately destroy the renal parenchyma and cause renal failure. It is a common condition affecting roughly 1 of every 400 to 1000 live births and accounting for 5-10% of cases of chronic renal failure requiring transplantation or dialysis. The likelihood of developing renal failure with a PKD1 mutation is less than 5% by 40 years of age, rising to more than 35% by 50, more than 70% at 60 and m ore than 95% by 70. With a PKD2 mutation the odds of renal failure are less than 5% by 50, 15% at 60, and about 45% at 70. Progression is accelereated in blacks (largely correlated with the sickle cell trait), in males, and in the presence of hypertension. Individuals with PKD tend to have extrarnal congenital anomalies and about 40% have one to several cysts in the liver (polycystic liver disease) that are usually asymptomatic. Cysts are derived from biliary epithelium. Cysts occur much less frequently in the spleen, pancreas, and lungs. Intracranial berry aneurysms arise in the circle of Willis, and subarachnoid hemorrhages from these account for death in about 4-10% of inviduals. Mitral valve prolapse and other cardiac valvular anomalies occur in 20-25% of patients, but most are asymptomatic. Patients may survive for many yars with azotemia slowly progressing to uremia. Ultimately, about 40% of adult patients die of coronary or hypertensive heart disease, 25% of infection, 15% of a ruptured berry aneurysm or hypertensive intracerebral hemorrhage, and the rest of other causes. ARPKD is genetically distinct. Patients who survive infancy may develop a peculiar type of congential hepatic fibrosis. In older children the hepatic disease is the predominant clinical concern. Such patients may develop portal hypertension with splenomegaly (Alper '10: 956- 959). The three major types of medullary cystic disease are medullary spong kidney, a relatively common and unusually innocuous structural change, and nephronophthisis and adult-onst medullary cystic disease, which are almost always associated with renal dysfunction. Medullary sponge kidney is restricted to lesions consisting of multiple cystic dilations of the collecting ducts in the medulla. The condition occurs in adults and is usually discovered radiographcially. The papillary ducts in the medulla are dilated, and small cysts may be present. The cysts are lined by cuboidal epithelium or occasionally by transitional epithelium. Nephronophthisis and Adult-onset medullary cystic disease is a group of progressive renal disorders. The common characteristic is the presence of a variable number of cysts in the medulla, usually concentrated at the corticomdullary junction, cortical tubulointerstitial damage is the cause of the eventual renal insufficiency. Some forms are inherited as autosomal recessive traits and usually bcome manifest in childhood or adolescence. As a group, the nephronophthisis complex is now thought to be the most common genetic cause of end-stage renal disease in children and young adults. Adult-onset medullary cystic disease has an autosomal dominant pattern of transmission and is now considered a distinct entity. Affected children present first with polyuria and polydipsia, reflecting a defecft in the concentrating ability of the renal tubules. Sodium wasting and tubular acidosis are also prominent. The kidneys are small and show cysts in the medulla and small cysts in the cortex. The epected course is progression to terminal renal failure during a period of 5 to 10 years (Alper '10: 959, 960). The kidneys from patients with end-stage renal disease who have undergone prolonged dialysis sometimes show numerous cortical and medullary cysts, a condition known as acquired (dialysis associated) cystic disease. The cysts measure 0.5 to 2 cm in diameter, contain clear fluid, are lined by either hyperplastic or flattened tubular epithelium, and often contain calcium oxalate crystals. The probably form as a result of obstruction of tubules by interstitial fibrosis or by oxalate crystals. Most are asymptomatic, but sometimes the cysts bleed, cuasing hematuria. The most ominous complication is the development of renal cell carcinoma in the walls of these cysts occurin gin 7% of dialyzed patients observed for 10 years. Simple cysts may occur as multiple or single, usually cortical, cystic spaces that vary widely in diameter. They are commonly 1 to 5 cm but may reach 10 cm or more in size. They are translucent, lined bya gray, glistening, smototh membrane, and filed with clear fluid. Simple cysts are a common postmortem finding without clinical significance. The main importance of cysts lies in their differentiation from kidney tumors when they are discovered either incidentally or because of hemorrhage and pain. Radiologic studies show that in contrast to renal tumors, renal cysts have smooth contours, are almost always avascular, and give fluid rather htan solid signals on ultrasonography (Alper '10: 960). Urinary tract obstruction increases susceptibility to infection and to stone formation, and unrelieved obstruction amost always leads to permanent renal atrophy, termed hydronephrosis or obstructive uropathy. Fortuneately many causes of obstruction are surgically correctable or medically treatable. Congenital anomalies can cause posterior urethral valves and urethral strictures, meatal stenosis, bladder neck obstruction, ureteropelvic junction narrowing or obstruction or severe vesicouretera reflux. Urinary calculi, benign prostatic hypertrophy, tumors, carcinoma of the prostate, bladder tumors, retroperitoneal lymphoma and carcinoma of the cervix or uterus, inflammation, prostatitis, ureteritis, urethritis, retroperitoneal fibrosis, sloughed papillae or blood cots, pregnancy, uterine prolapse and cystocele and functional disorders such as spinal cord damage or diabetic nephropathy and other functional abnormalities of the ureter or bladder can all cause obstructive uropathy. Hydronephrosis is the term used to describe dilation of the renal pelvis and clayces associated with progressive atrophy of the kidney due to obstruction of the outflow of urine. Even with complete obstruction, glomerular filtration persists for some time because the filtrate subsequently diffuses back into the renal interstitium and perirenal spaces, where it ultimately returns to the lymphatic and venous systems. Affected calyces and pelvis become dilated. The high pressure in the pelvis transmitted back through the collecting ducts into the cortex, causing renal atrophy, and diminution in inner medullary blood flow. Obstruction also triggers an interstitial inflammatory reaction leading eventually to interstitial fibrosis. In far advanced cases the kidey may become transformed into a thin-walled cystic structure having a diameter of up to 15 to 20 cm. Acute obstruction may provoke pain. Unilateral complete or partial hyronephrosis may remain silent for long periods, since the unaffected kidney can maintain adequate renal function. In bilateral partial obstruction the earliest manifestation is inability to concentrate urine, reflected by polyuria and nocturia. Hypertension is common in such patients. Complete bilateral obstruction results in oliguria or anuria and is incompatible with survival unless the obstruction is relieved. After relief of complete urinary tract obstruction, postobstructive diuresis occurs, this can be massive, with the kidney excreting large amounts of urine that is rich in sodium chloride (Alper '10: 961, 962). Stones may form at any level in the urinary tract, but most arisein the kidney. Urolithiasis is a frequent clinical problem affecting 5-10% of Americans in their lifetime. Men are affected more often than women, and the peak age at onset is between 20 and 30 years. Familial and hereditary predisposition has long been known. Many inborn errors of metabolism, such as gout, cystinuria and primary hyperoxalulria, provide examples of hereditary disease characterized by excessive production and excretion of stone-forming substances. There are four ain types of calculi (1) calcium stones (about 70%), composed largely of calcium oxalate or calcium oxalate mixed with calcium phosphate, (2) another 15% are triple stones or struvite stones, composed of magnesium ammonium phosphate formed largely after infections by bacteria (e.g. Proteus and stome staphylococci) and can get huge (3) 5 to 10% are uric acid stones, common in people with hyperurecemia, like gout, and radioluscent (4) 1 to 2% are made up of cystine caused by genetic defects it eh renal reabsorption of amino acids, including cysteine, leading to cystinuria. An organic mucoprotein matrix, making up 1 to 5% of the stone by weight, is present in all calculi. Although there are many causes for the formation of stones the most important is an increased urinary concentration of the stones' constituents, such that it exceeds their solubility (supersaturation). Stones are of importance when they obstruct urinary glow or produce ulceration and bleeding and may cause significant renal damage. In general smaller stones are most hazardous, because they may pass into the ureters, producing colic, one of the most intense forms of pain. Larger stones cannot enter the ureters and are more likely to remain silent within the renal pelvis first manifesting by hematuria. Stones also predispose to superimposed infection (Alper '10: 962, 963). Most kidney stones won't require invasive treatment. A small stone may be passed by: Drinking water.Drinking as much as 2 to 3 quarts (1.9 to 2.8 liters) a day may help flush out the urinary system. Unless a doctor tells you otherwise, drink enough fluid mostly water to produce clear or nearly clear urine, orange juice is even more effective but loses its effectiveness after two cups a day. To relieve mild pain, pain relievers such as ibuprofen (Advil, Motrin, others), acetaminophen (Tylenol, others) or naproxen sodium (Aleve) may be helpful. A doctor may prescribe an alpha blocker, to relax the muscles in the ureter, helping to pass the kidney stone more quickly and with less pain. Large and symptomatic kidney stones that can't be treated with conservative measures either because they're too large to pass on their own or because they cause bleeding, kidney damage or ongoing urinary tract infections may require more invasive treatment. Procedures may include: Using sound waves to break up stones.For certain kidney stones depending on size and location a doctor may recommend a procedure called extracorporeal shock wave lithotripsy (SWL). SWL uses sound waves to create strong vibrations (shock waves) that break the stones into tiny pieces that can be passed in your urine. The procedure lasts about 45 to 60 minutes and can cause moderate pain, so sedation or light anesthesia is administered to make the patient comfortable. SWL can cause blood in the urine, bruising on the back or abdomen, bleeding around the kidney and other adjacent organs, and discomfort as the stone fragments pass through the urinary tract. A procedure called percutaneous nephrolithotomy (nef-row-lih-THOT-uh-me) involves surgically removing extremely large kidney stone(s) using small telescopes and instruments inserted through a small incision in your back. General anesthesia is administered during the surgery and the patient is hospitalized for one to two days to recover. A doctor may recommend this surgery if SWL was unsuccessful or if the stone is very large. Using a scope to remove stones is done to remove a smaller stone in the ureter or kidney. A doctor may pass a thin lighted tube (ureteroscope) equipped with a camera through the urethra and bladder to the ureter. Once the stone is located, special tools can snare the stone or break it into pieces that will pass in your urine. The doctor may then place a small tube (stent) in the ureter to relieve swelling and promote healing. The patient may need general or local anesthesia during this procedure. Parathyroid gland surgery is performed if some calcium stones are caused by overactive parathyroid glands, which are located on the four corners of your thyroid gland, just below your Adam's apple. When these glands produce too much parathyroid hormone (hyperparathyroidism), calcium levels can become too high and kidney stones may form as a result. Hyperparathyroidism sometimes occurs when a small, benign tumor forms in one of the parathyroid glands or another condition leads these glands to produce more parathyroid hormone. Removing the growth from the gland stops the formation of kidney stones. Or a doctor may recommend treatment of the condition that's causing your parathyroid gland to overproduce the hormone. Surgery is the most common treatment for primary hyperparathyroidism and provides a cure in at least 90 percent of all cases. A surgeon will remove only those glands that are enlarged or have a tumor (adenoma). If all four glands are affected, a surgeon will likely remove only three glands and perhaps a portion of the fourth leaving some functioning parathyroid tissue. Surgery may be done as an outpatient procedure. Medications to treat hyperparathyroidism include: Calcimimetics, a drug that mimics calcium circulating in the blood. Therefore, the drug may trick the parathyroid glands into releasing less parathyroid hormone. This drug is sold as cinacalcet (Sensipar). The Food and Drug Administration approved cinacalcet to treat hyperparathyroidism caused by chronic kidney disease or parathyroid cancer. Some doctors may prescribe it to treat primary hyperparathyroidism, particularly if surgery hasn't successfully cured the disorder or a person isn't a good candidate for surgery. Hormone replacement therapy, for women who have gone through menopause and have signs of osteoporosis, hormone replacement therapy may help bones retain calcium and is also reported to reduce the risk of heart disease, but five to ten years of regular use are apparently needed to gain these benefits. This treatment, usually a combination estrogen and progestin, doesn't address the underlying problems with the parathyroid glands. Prolonged use of hormone replacement therapy can increase the risk of cardiovascular disease and some cancers. Bisphosphonates.Bisphosphonates also prevent the loss of calcium from bones and may lessen osteoporosis caused by hyperparathyroidism. Both benign and malignant tumors occur in the kidney. With the exception of oncocytoma, the benign tumors rarely cause clinical problems. Renal papillary adenoma are small, discrete adenomas arising from the renal tubular epithelium and are found commonly in 7 to 22% at autopsy. Angiomyolipoma consists of vessels, smooth muscle and fat and are present in 25 to 50% of patients with tuberous sclerosis, a disease cuase by loss-of-function mutationsi nt he TSC1 or TSC2 tumor suppressor genes. It is characterized by lesions of the cerebral cortex that produce epilepsy and mental retardation, a variety of skin abnormalities and unusual benign tumors at other sites, such as the heart and kidneys. They are susceptible to spontaneous hemorrhage. Oncocytoma is an epithelial tumor composed of large eosinophilic cells having small, round, benign-appearing nuclei that have large nucleoli. It is not an uncommon tumor, accounting for approximately 5 to 15% of surgically resected renal neoplasms. The tumors are tan or mahogany brown, and well encapsulated, however, they may achieve a large size (up to 12 cm in diameter). Malignant tumors on the other hand, are of great significance. The most common of these malignant tumors is renal cell carcinoma, followed by Wilms tumor, which is found in children and urothelial tumors of the calyces and pelves. Renal cell carcinoma (adenocarcinoma of the kidney) represent about 3% of all newly diagnosed visceral cancers in the United States and accont for 85% of renal cancers in adults. There are approximately 30,000 new cases per year and 12,000 deaths. The tumors occur most often in older individuals, usually in the sixth and seventh decades of life and show a 2:1 male preponderance. Tobacco is the most significant risk factor an dcigarette smokers have double the incidence of renal cell carcinoma. Additional risk factors incude obesity (particularly in women), hypertension, unopposed estrogen therapy and exposure to asbestos, petroleum products, and heavy metals. There is an increased incidence in patiens with chronic renal failure and acquired cystic disease and in tuberous sclerosis. Although they account for only 4% of renal cancers, familial variants are instructive and include: (1) Von Hippel-Lindau (VHL) syndrome with half to two thirds developing renal cysts and bilateral, often multiple renal cell carcinomas; (2) hereditary (familial) clear cell carcinoma, and (3) hereditary papillary carcinoma an autosomal dominant form manifested by multiple bilateral tumors with pappilary histology, cytogenic abnormalities and mutations in the MET proto-oncogene. Clear cell carcinoma is the most common type accounting for 70 to 80% of renal cell cancer. Papillary carcinoma accounts for 10 to 15% of renal cancers. The three classic diagnostic features of renal cell carcinoma are costovertebral pain, palpable mass and hematuria, but these are seen in only 10% of cases. Hematuria is the most reliable, but may be microscopic and tumors may reach 10 cm before being discovered. Renal cell carcinoma is classified as one of the great mimics in medicine because it tends to produce a diversity of systemic symptoms not related to the kidney. In addition to fever and constitutional symptoms, renal cell carcinomas produce a number of paraneoplastic syndromes ascribed to abnormal hormone production, including polycythemia, hypercalcemia, hypertension, hepatic dysfunction, feminization or masculinization, Cushing syndrome, eosinophilia, leukemoid reactions and amyloidis. One of the common characteristics of this tumor is its tendency to metastasize widely before giving rise to any local symptoms or signs. In 25% of new patients with renal cell carcinoma, there is radiologic evidence of metastases at the time of presentation. The most common locations of metastasis are the lungs (more than 50%) and bones (33%) followd by the regional lumph nodes, live adrenal and brain. The average 5-year survival rate of persons with renal cell carcinoma is about 45% and as high as 70% in the absence of distant metastases. With renal vein invasion or extension into the perinephric fat, the figue is reduced to approximately 15 to 20%. Nephrectomy has been the treatment of choice but partial nephrectomy to presever renal function is being done with increasing frequency and similar outcome. Approximately 5 to 10% of primary renal tumors originate from the urothelium of the renal pelvis and are known as urothelial carcinomas of the renal pelvis. These tumors span the range from apparently benign papillomas to invasive urothelial (transitional cell) carcinomas. Urothelial tumors may occasionally be multiple, involving the pelvis, ureters and bladder. In 50% of renal pelvic tumors there is a preexisting or concomitant bladder urothelial tumor. There is an increased risk of urothelial carcinomas of the renal pelvis and bladder in individuals with analgesic nephropahty and Balkan nephropathy. Infiltration of the wall of the pelvis and calyces is common. The prognosis for these tumors is not good. 5 year survival rates vary from 50 to 100% for low-grade non-invasive lesions to 10% with high-grade infiltrating tumors (Alper '10: 963-967). Immunotherapy is considered one of the standard treatment options for kidney cancer patients with advanced metastatic disease. Well-documented, but very rare, cases of spontaneous regressions in kidney cancer patients with metastatic disease suggest that the immune system can play an important role in the control and potential treatment of this disease. The building blocks of immunotherapy are biologic response modifiers (BRMs). They are substances that enhance the bodys immune system and improve its ability to fight cancer. BRMs do their work by regulating the intensity and duration of immune responses. A BRM can be either a manmade drug or a natural substance produced by the body. Several BRMs can boost the bodys natural immune defenses. The cytokines are an important family of BRMs that include Interleukin-2 (IL-2) and Interferons. Used either alone or in combination, they have represented the standard in the treatment of kidney cancer. Interleukin-2 is a biologic response modifier (BRM) available for the treatment of advanced kidney cancer. It stimulates the growth of two types of white blood cells: T cells and natural killer (NK) cells. T cells are very important in your bodys fight against cancer because they recognize cancer cells and set off an alarm to the body. The NK cells respond to this alarm and are transformed into lymphokine-activated killer (LAK) cells, which are capable of destroying cancer cells. Proleukin(interleukin-2) was approved by the FDA in 1992 for the treatment of metastatic renal cell carcinoma. A genetically engineered product, recombinant IL-2, is available for use in various therapeutic regimens. Several different routes of administration may be used: IV bolus, subcutaneous (SC), and continuous IV infusion (CIV). Interferons are widely used to treat kidney cancer, alone or in combination with other drugs. Interferon therapy is typically self-administered by injection under the skin several times per week. Interferons work by interfering with the life processes within the cancer cell, preventing its growth and making the cell more susceptible to attack by other elements of the immune system. There are three major types of interferons alfa, beta, and gamma but interferon alfa has been most widely studied in the treatment of kidney cancer. Several interferon alfa products are available in the United States and have been used in the treatment of kidney cancer. INTRON* A, a product of Schering Corporation (Kenilworth, NJ), has been designated as interferon alfa-2b. Roferon*-A is manufactured by Roche Laboratories (Nutley, NJ) and has been designated as interferon alfa-2a. These drugs are very similar, and kidney cancer may be treated with either. Most insurance companies recognize the value of interferon alfa in treating kidney cancer and reimburse for this therapy. In several dozen clinical trials, an overall response rate of about 13% has been achieved with interferon alfa.29 However, in patients with high performance status (i.e., lack of symptoms related to their disease), previous nephrectomy, and metastases predominantly in the lung, the major response rate (complete plus partial responses) with interferon alfa treatment is usually from 6 to 10%. It is also recognized that patients who receive interferon alpha, when compared with those who are treated with hormones or chemotherapy, have improved survival rates. Response to interferon alfa is characterized by slow regression of tumors; the average time from start of treatment to objective response is three to four months. The most common side effects of interferon therapy are flu-like in nature. Though it is not considered a primary form of therapy, radiation can be used in the treatment of kidney cancer that has metastasized to the bone, brain or spine. Although chemotherapy is the standard treatment for most solid tumors, kidney cancer is generally resistant to chemotherapy.35 The reason for the resistance of kidney cancer cells to chemotherapy is not completely understood. However, it is now known that kidney cancer cells produce an overabundance of multidrug-resistance-associated protein, which acts to repel various chemotherapeutic agents away from the cancer cell. 5-Fluorouracil (5FU) appears to be the most effective conventional chemotherapeutic agent currently available for kidney cancer, but response rates are only in the range of 5% to 8%. In 2005 and 2006, the U.S. Food and Drug Administration (FDA) approved the first new medications to treat kidney cancer in more than a decade: sorafenib tosylate and sunitinib malate. Both of these new drugs disrupt the angiogenesis process. Known as tyrosine kinase inhibitors, they interfere with the proteins inside cancer cells, thus interfering with certain cell functions. These drugs are also known as multi-kinase inhibitors because they target both the tumor cell and the tumor blood vessel structures. They work by interfering with reproduction of cancer cells as they attempt to grow and divide uncontrollably. They also have the advantage of being administered orally. The goal of treatment with these newer medications is to slow the rate of growth of the cancer and, if possible, shrink the size of existing tumors. Some patients may experience a significant decrease in the amount of cancer in their body. Some patients may not experience shrinkage in the size of their tumors, but have long periods of stable disease. A physician will discuss how the cancer is responding to treatment, and will have additional options to consider for treatment when necessary. It should be noted that some patients will not receive any benefit from a medication. In some cases, a medication that was effective in treating a patients cancer stops working and other treatment options must be considered. Sutent(sunitinib malate) claims to reduce tumor size and is not only seems to be the most highly recommended chemotherapy for kidney cancer, but is available in capsule form for oral consumption, but hepatoxicity and cardiotoxicity has been deadly, it is prescribed once a day for four weeks and two weeks off. Nexavar(sorafenib tosylate) is a medication that targets the blood supply of a tumor, depriving it of the oxygen and nutrients it needs for growth. By blocking the vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF), Nexavar can interfere with the tumor cells ability to increase its blood supply. By blocking the Raf-kinase pathway, Nexavar can also interfere with tumor cell growth and proliferation. Clinical studies show that it can significantly slow the progression of tumors. In the Phase III trial which led to the FDA approval of Nexavar, the median time for tumor progression was doubled for patients taking Nexavar, compared with patients taking a placebo. Sutent(sunitinib malate) also deprives tumor cells of the blood and nutrients needed to grow by interfering with VEGF and PDGF signaling pathways. Sutent was approved by the FDA in 2006 for kidney cancer patients because of its ability to reduce the size of tumors. Clinical studies showed a favorable response rate in patients with metastatic kidney cancer whose tumors had progressed following immunotherapy. Torisel(temsirolimus) is another recently approved kidney cancer drug. It was designed to inhibit the mTOR (mammalian target of rapamycin) kinase, which is important in cell growth and cell survival. By blocking the mTOR pathway, Torisel can interfere with the tumors ability to multiply as well as reducing its ability to stimulate angiogenesis. Afinitor(everolimus), approved by the FDA in March 2009, is an orally administered mTOR inhibitor. Afinitor works by blocking a specific protein known as the mammalian target of rapamycin (mTOR) and acts as a multifunctional inhibitor of cell growth and proliferation, angiogenesis, and cell metabolism. The drug is intended for those patients with advanced renal cell cancer who have already tried a kinase inhibitor, such as Sutent or Nexavar. Votrient(pazopanib), the sixth drug to be approved for kidney cancer since 2005, is an oral medication that interferes with angiogenesis, the growth of new blood vessels needed for solid tumors to grow. It is a kinase inhibitor indicated for the treatment of patients with advanced renal cell carcinoma. Inlyta(axitinib), approved by the FDA in January 2012, is a prescription medicine used to treat advanced kidney cancer (advanced renal cell carcinoma or RCC) when one prior drug treatment for this disease has not worked. As with antibiotics chemotherapeutic drugs require probiotic supplementation to avoid vitamin B12 deficiency, chronic diarrhea, pernicious anemia and dental cavities. Curing cancer always requires a vegan diet, no lipids, with little or no protein, because protein is the primary dietary cancer growth factor, as well as pesticides. A very high level of athletic performance is exhibited by many cancer survivors and cardiovascular exercise and/or strength exercises are absolutely necessary to metabolize neoplasms and atherosclerotic plaques. 9. Anemia and Bleeding Disorders The hemoglobin and hematocrit (H&H) levels are used to determine the presence and severity of anemia. Normal hemoglobin and hematocrit values (H&H) vary. For adolescents normal is a hemoglobin value of 130 g/L and hematocrit of 40. For adult males it is 160 (+/- 20) and 47 (+/-6). For adult women it is 130 (+/- 20) and 40 (+/- 6). For postmenopausal women it is 140 (+/- 20) and 42 (+/- 6). For pregnant women in the 3rd trimester it is 120 (+/- 20) and 37 (+/-6). Higher normal values may be established for adults who live at a high altitude or smoke more than 1 pack of cigarettes a day. Heavy smokers can show an increase in the hemoglobin level of 5 to 10 g/L secondary to carbon monoxide binding to hemoglobin. When the hemoglobin value falls below 100 to 120 g/L (10 to 12 g/dL) new cells are recruited and erythropoietin levels increase logarithmically according to the severity of the anemia. This stimulates erythroid production severalfold but requires normal renal function, healthy marrow and an adequate supply of key nutrients, especially iron (Hillman 98: 334-336). Anemia may be defined as a reduction in the oxygen transport capacity of the blood, usually resulting from a deficiency of red cells, diagnosed when ablood testshows a hemoglobin value of less than 13.5 gm/dl in a man or less than 12.0 gm/dl in a woman. Normal values for children vary with age. Plasma volume and fluid loss may create abnormalities in clinical measurements. The skin is pale and usually becomes thin and inelastic as the epidermis and dermis atrophy. Frequently, the nails become brittle and lose their normal convexity to assume a concave spoon-shape (koilonychia), particularly in iron deficiency anemia. Weakness, malaise, dyspnea (shortness of breath) and fatigue are common complaints. Cells that are vulnerable to hypoxia may undergo fatty change or ischemic necrosis, usually in the myocardium, convoluted tubules of the kidney, the centrilobular hepatic cells, and the sensitive ganglion cells of the cortex and basal ganglia. Angina pectoris, and cardiac failure may develop and compound the respiratory difficulty caused by reduced oxygen transport. The increased demand for erythropoiesis in anemia causes the fatty marrow to become active and red if the marrow is capable of response. When the need is great extramedullary hematopoiesis ensues. With acute blood loss and shock, oliguria and anuria may develop in the shock kidney. Central nervous system hypoxia may be evidenced by headache, dimness of vision and faintness (Saunders 94: 586, 587). With acute blood loss, the alterations reflect principally the loss of blood volume rather than the loss of hemogloblin. Shock and death may follow. If the patient survives, the blood volume is rapidly restored by sift of water from the interstitial fluid compartment. The resulting hemodilution lowers the hematocrit. Reduction in the oxygenation of tissues triggers the production of erythropoietin, and the marrow responds by increasing erythropoietin, and the marrow responds by increasing erythropoiesis. When the blood is lost internally, as into the peritoneal cavity, the iron can be recaptured, but if the blood is lost externally, the adequacy of the red cell recovery may be hampered by iron deficiency when insufficient reserves are present. Mobilization of platelets and granulocytes from the marginal pools leads to thrombocytosis and leukocytosis in the period immediately following acute blood loss. Soon after acute blood loss the red blood cells appear normal in size and color, however, as the marrow begins to regenerate, changes occur in the peripheral blood. Most striking is an increase in reticulocyte count, reaching 10 to 15% after 7 days. Chronic blood loss induces anemia only when the rate of loss exceeds the regenerative capacity of the erythroid precursors or when iron reserves are depleted. In addition to chronic blood loss, any cause of iron deficiency such as malnutrition, malabsorption states, or an increased demand above the daily intake as occurs in pregnancy will lead to an identical anemia. (Saunders 94: 587). Blood transfusions are the transfer of blood, its components, or products from one person (donor) into another persons bloodstream (recipient). Every year in the U.S., more than 20 million units of red blood cells, platelets, and plasma are transfused to treat hematologic conditions such as severe anemia, leukemia, and sickle cell disease. Transfusions have long been associated with some risk to patients. The HIV epidemic during the 1980s was a major cause of fear; regular transfusions, especially of clotting factor concentrates, spread the virus quickly and nearly undetected. That outbreak prompted the developmentof biovigilance or hemovigilance: tracing and tracking transfusion-related adverse events and incidents, both infectious and non-infectious, that affect blood donors and recipients. Another of the most significant issues complicating transfusion safety has been bacterial contamination of blood products, particularly of platelets. However, steps have been taken in the last decade to avoid, detect, and eliminate this complication through improved donor selection, specialized preparation of the arm before needle insertion, and special screening techniques. Blood is regularly tested for infectious disease transmission, particularly for viruses such as Hepatitis B and C, HIV, and West Nile Virus. Serum tests have been replaced by molecular testing called nucleic acid amplification testing (NAT), which finds active viruses in the donors blood to determine infection risk. If an active virus is found, the donor unit is discarded. Experts anticipate that new methods, including new molecular and microarray testing, which can identify many infectious agents rapidly and accurately, will replace or augment serum studies and NAT in the near future. Blood transfusion has never been safer from known infectious risk than it is today (Luban '08). Potential post-transfusion reactions include transfusion-related lung injury (TRALI), during which the donors immune antibodies cause breathing problems in the recipient; transfusion associated cardiac overload (TACO), which is swelling caused by the increased blood volume; and post-transfusion iron overload, which is a buildup of iron in the body, usually caused by multiple or regular transfusions. Immune reactions, which happen when the bodys immune system is affected by the donor blood, also pose several risks to transfused patients. Alloimmunization occurs when the recipient develops an allergic reaction to the donors red blood cells: transfusion-related immune modulation (TRIM) can lead to increased risk of infections and cancer recurrence, post-transfusion graft-versus-host disease (GVHD, when the donors immune system attacks the recipients blood cells), and microchimerism (when a small amount of donor blood persists in the recipients body, causing ongoing low-grade GVHD). Removing white blood cells or radiating blood to prevent white blood cell growth can reduce the likelihood that the recipient will reject the donor blood.New techniques can isolate specialized cell populations from blood most importantly, hematopoietic progenitor cells (HPCs) that are used for stem cell transplantation. Because HPCs are easier to extract and the process is safer for donors, HPC transplantation has replaced bone marrow transplantation for many cancers and other diseases. Researchers are also using umbilical cord stem cells (UCSCs) as a source of HPCs. UCSCs are collected and processed in a method similar to whole blood and are a rich resource for transplantation therapy in pediatric and some adult patients. In the future, these cells may be grown and expanded for clinical use. Furthermore, researchers have isolated specialized cell types other than HPCs that play an important role in cellular therapy because they can modify proliferation and immune responses during the engraftment of transplanted cells (Luban '08). The hemolytic anemias are all characterized by (1) shortening of the normal red cell life span, premature destruction of red cells; (2) accumulation of the products of hemoglobin catabolism; and (3) a marked increase in erythropoiesis within the bone marrow, in an attempt to compensate for the loss of red cells. In general, hereditary disorders are due to intracorpuscular defects and the acquired disorders to extrinsic factors such as autoantibodies. The leading cause of kidney failure in US and Canadian children is hemolytic uremic syndrome of which 85 percent of cases are caused by E. coli 0157:H7. Incidence of hemolytic uremic syndrome in the US is 7,500 and in the Netherlands 25 (Robbins 01: 133). Hereditary spherocytosis (HS) is an inherited disorder (autosomal recessive) characterized by an instrinsic defect in the red cell membrane that renders erythrocytes spheroidal, less deformable and vulnerable to splenic sequestration and destruction. The prevalence of HS is highest in people of northern European extraction, in whom rates of 1 in 5000 have been reported. Although a deficiency of any one of the membrane skeletal proteins could adversely affect the red cells, a deficiency of spectrin seems to be the most common abnormality in patients with all forms of HS. Moderate splenic enlargement is characteristic of HS (500 to 1000 mg), in few other hemolytic anemias is the spleen enlarged as much or as often. The clinical features are anemia, splenomegaly and jaundice. The severity of the disease varies. A hemolytic crisis may develop, a sudden onset of a wave of massive hemolysis accompanied by fever, abdominal pain, increasing jaundice, low blood pressure and even shock. Alternatively, an aplastic crisis (triggered usually by parvovirus infection of the marrow red cell precursors) may appear. Transfusions may be necessary to support the patient, but eventually both these crises remit in most instances. Gallstones may also produce symptoms so diagnosis is usually based on family history and evidence of spherocytosis. The cardinal role of the spleen in the premature demise of the spherocytes is proved by the invariably beneficial effect of splenectomy. The spherocytes persist, but the anemia is corrected (Saunders 94: 589-591). Hemolytic disease can be due to erythrocyte enzyme defects: glucose-6-phosphate dehydrogenase deficiency (G6PD). The erythrocyte and its membrane are vulnerable to injury by exogenous and endogenous oxidants. Normally, intracellular reduced glutathione (GSH) inactivates such oxidants. Abnormalities in the hexose monophosphate shunt or in glutathione metabolism resulting from deficient or impaired enzyme function reduce the ability of red cells to protect themselves against oxidative injuries and lead to hemolytic disease. Several hundre G6PD genetic variants have been identified, but only two variants, designated G6PDA- and G6PD Mediterranean (more severe anemia), lead to significant hemolysis. Infection or exposure to oxidant drugs causes oxidation by means of the production hydrogen peroxide which accumulates and causes oxidation leading to denaturation of hemoglobin and formation of precipitates (Heinz bodies) within the cell. Macrophages pluck out the Heinz bodies giving rise to red cells that appear to have a bite of cytoplasm removed which leads to further membrane damage and induces the formation of spherocytes. After lag period of 2 to 3 days, acute intravascular hemolysis, characterized by hemoglobinemia, hemogobinuria and decreased hematocrit levels, is triggered. Since only senescent red cells lysed, the episode is self-limited and hemolysis stops when only the younger red cells remain in the circulation despite continued administration of the oxidant drug). The recovery phase is heralded by reticulocytosis, as in the case of other hemolytic anemias (Saunders 94: 591, 592). Sickle cell disease is the prototype of hereditary hemoglobinopathies, characterized by the production of structurally abnormal hemoglobin, HbS. If an individual is homozygous for the sickle mutation, almost all hemoglobin in the erythrocyte is HbS. In the heterozygote, only about 40% is HbS, the remainder being normal hemoglobins. Where malaria is endemic, as many as 30% of black Africans are heterozygous. This protection may be related to the slight protection against falciparum malaria imparted by HbS. On deoxygenation the changes that occur in the HbS molecules convert hemoglobin from a freely flowing liquid to a vicious gel, leading ultimately to distortion of the red cells, which acquire a sickle or holly-leaf shape. Sickled cells lose potassium and water and at the same time gain calcium, which normally is rigorously excluded. The formation of HbS has two major consequences (1) a chronic hemolytic anemia, and (2) occlusion of small blood vessels, resulting in ischemic tissue damage. Irreversibly sickled cells (ISC) have a very rigid non-deformable cell membrane and have difficulty negotiating the splenic sinusoids. They become sequestered in the spleen, where they are destroyed by the mononuclear phagocyte system. Some intravascular hemolysis may also occur due to the increased mechanical fragility of the sickle cells. The average red cell survival correlates with the percentage of ISC in circulation and is shortened to approximately 20 days. In children, the continued scarring caused by this disease often causes a progressive shrinkage of the spleen so that by adolescence or early adulthood only a small nubbin of fibrous tissue may be left, this is called autosplenectomy, which predisposes to septicemia and meningitis by Streptococcus pneumoniae and Haemophilus influenzae, the most common causes of death in children with sickle cell anemia. Chronic hemolysis in a fairly severe anemia exhibits hematocrit values ranging between 18 and 30%. Vaso-occlusive crises, also called painful crises, represent episodes of hypoxic injury and infarction with extreme pain in abdomen, chest or joints, and may produce a seizure or stroke. Aplastic crisis represents a temporary cessation of bone marrow activity, usually triggered by parvovirus infection of erythroid progenitor cells causing reticulocytes to disappear from the peripheral blood and there is sudden and rapid worsening of anemia. A sequestration crisis may appear in children with splenomegaly caused by massive sequestration of deformed red cells and sometimes shock. Despite improvement in therapy sickle cell anemia shortens longevity and many patients die within the first 3 years owing to overwhelming infections, and those who cross these hurdles may live up to the fourth or fifth decade (Saunders 94: 592-596). The thalassemia syndromes are a heterogeneous group of mendelian disorders characterized by a lack of or decreased synthesis of either the alpha or the beta-globin chain of hemoglobin A (22).   thalassemia is characterized by deficient synthesis, or total lack, of the beta chain, whereas   thalassemia is characterized by deficient synthesis of the alpha chain. The hematologic consequences of diminished synthesis of one globin chain derive not only from the low intracellular hemoglobin (hypochromia) but also from the relative excess of the other chain.  thalassemia syndromes can be classified into two categories (1) 0- thalassemia associated with total absence of beta-globin chains in the homozygous state and (2) +-thalassemia with a reduced (but detectable) beta-globin synthesis in the homozygous state. Sequencing reveals approximately 100 different mutations responsible for these two disorders. Cell membrane damage, caused by unbound  chain aggregation, leads to a loss of K+, excessive absorption of dietary iron, and impaired DNA synthesis. The net effect is destruction of the red cell precursors within the bone marrow, 70 to 85% of marrow normoblasts are destroyed in severely affected patients. In general, individuals who are homozygous for the   thalassemia genes (0 or +) have a very severe transfusion dependent anemia and are said to have   thalassemia major. Thalassemia major is most common in Mediterranean countries and parts of Africa and Southeast Asia. The anemia is very severe and first manifests 6 to 9 months after birth. In untransfused patients Hb levels range between 3 and 6 gm/dl. The spleen may increase up to 1500 gm. Unless supported by transfusion, children suffer from growth retardation and die at an early age from anemia. In those who survive the face is overlarge and somewhat distorted with malocclusion. Cardiac disease resulting from progressive iron overload and secondary hemochromatosis is an important cause of death even in patients who can otherwise be supported by transfusion. To reduce iron overload most patients receive iron chelators. Many patients survive into the third decade. Bone marryow transplantation from an HLA-identical sibling is the only therapy that offers a cure. The presence of one normal gene in the heterozygotes usually leads to enough normal beta-globin chain synthesis so that the affected individuals are usually asymptomatic with only a mild anemia, referred to as   thalassemia minor or   thalassemia trait, or for intermediate cases   thalassemia intermedia, predominantly in the same ethnic groups. Because the non-alpha chains in general form more soluble and less toxic aggregates than those derived from alpha chains, the hemolytic anemia and ineffective erythropoiesis tend to be less severe in   thalassemia. The most common cause of reduced alpha-chain synthesis seems to be the deletion of alpha-globin genes.   thalassemia is classified on the basis of the number and position of the alpha-globin genes deleted, which determine the clinical syndrome. The silent carrier state is characterized by the deletion of a single alpha-globin gene and barely detectable reduction in alpha-globin chain synthesis. These individuals are completely asymptomatic and do not have anemia. -thalassemia trait is characterized by deletion of two alpha-globin genes and although they have minimal or no anemia and no abnormal physical signs, the position of the deleted genes makes a big difference to the likelihood of severe forms of the disease such as HbH disease or hydrops fetalis. Hemoglobin H disesase is associate with deletion of three of the four alpha-globin genes. HbH is seen mostly in Asians and rarely in Africans. Patients have a moderately severe anemia. Hydrops fetalis is the most severe form of   thalassemia, resulting from the deletion of all four alpha-globin genes. Severe tissue anoxia associated with the total failure to deliver oxygen to the tissues, invariably leads to intrauterine fetal death (Saunders 94: 596-601). Paroxysmal nocturnal hemoglobinuria (PNH) is a rare but fascinating acquired clonal disorder of disorder, involving a somatic mutation affecting a pluripotent stem cell; that sometimes evolves into other stem cell disorders, such as aplastic anemia and acute leukemia. The clonal progeny of the mutant stem cell (red cells, white cells, platelets) are deficient in a family of proteins that are attached to the cell membrane by a glycosyl phosphatidyl inositol (GPI) anchor and their absence renders blood cells unusually sensitive to lysis by endogenous complement. Patients classically have intravascular hemolysis, which is paroxysmal and nocturnal in only 25% of cases. Most of the remaining patients have chronic hemolysis without dramatic hemoglobinuria. Over the long course, hemosiderinuria with loss of iron eventually leads to iron deficiency. Multiple episodes of venous thrombosis in the hepatic, portal or cerebral veins, are fatal in 50% of cases. The course of this disease is chronic with a median survival of 10 years (Saunders 94: 601). Immunohemolytic anemia is caused by extracorpuscular mechanisms, sometimes the immune reaction is initiated by ingestion of drugs such as penicillin, cephalosporins, quinidine, phenacetin or -methyldopa. Differentiation of immunohemolytic anemias form other forms of hemolytic anemias depends on demonstration of anti-red cell antibodies in the Coombs antiglobulin test. Warm antibody hemolytic anemia is the most common form of immune hemolytic anemia. In about 60% of patients the condition is idiopathic and primary and in the remaining 40% there is an underlying predisposing condition or some drug exposure. Ig-G coated red cells are bound to Fc receptors on monocytes and splenic macrophages and undergo spheroidal transformation. The spherocytes are then sequestered and removed in the spleen, the major site of red cell destruction, and moderate to severe splenomegaly manifests. Cold agglutinin immune hemolytic anemia is caused by IgM antibodies that bind avidly to red cells at low temperatures (0 to 4C). These antibodies occur acutely during the recovery phase of certain infectious disorders such as mycoplasmal pneumonia and infectious mononucleosis, and is self-limited and rarely induces hemolysis. Chronic cold agglutinins occur with lymphoproliferative disorders and as an idiopathic condition. The clinical symptoms result from agglutination of red cells and fixation of complement in distal body parts, and the IgM bound to red cells is released when it reaches 37C, leaving the cell vulnerable to phagocytosis by mononuclear phagocytes in the liver and spleen. The hemolytic anemia is of variable severity. Vascular obstruction cause by red cell agglutinates results in pallor, cyanosis of the body parts exposed to cold temperatures and Raynauds phenomenon. Cold hemolysin hemolytic anemia autoantibodies are characteristic of the disease paroxysmal cold hemoglobinuria wich is noted for acute intermittent massive hemolysis, often with hemoglobinuria, following exposure of the affected patient to cold. When the temperature is elevated, the hemolysis due to IgG antibodies occur. The antibody is also known as the Donath-Landsteiner (DL) antibody, previously associated with syphilis. Most cases of PCH follow various infections such as mycoplasmal pneumonia, measles, mumps and some ill-defined viral and flu symptoms (Saunders 94: 601-603). Red cell trauma can cause fragmentation of red blood cells, such as by the insertion of valve prostheses and diffuse deposition of fibrin in the microvasculature, may be severe enough to cause significant intravascular hemolysis. Hemolysis due to narrowing or obstructions in the microvasculature is called microangiopathic hemolytic anemia. This form of anemia is encountered in disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura (TTP), the hemolytic uremic syndrome, malignant hypertension, renal cortical necrosis, systemic lupus erythematosus (SES) and metastatic adenocarcinoma. The common denominator is the presence of some vascular lesion. In patients with prosthetic heart valves, particularly aortic valves, the red cells are damaged by the sheer stress resulting from the turbulent blood flow and abnormal pressure gradients. Diminished erythropoiesis may result from a deficiency of some vital substrate necessary for red cell formation, such as iron deficiency anemias, in which heme synthesis is impaired and anemia of vitamin B12 and folate deficiency, characterized by defective DNA synthesis (megaloblastic anemias). Other causes of decreased erythropoiesis include anemia of chronic disease and marrow stem cell failure that occurs in such conditions as aplastic anemia, pure red cell aplasia and anemia of renal failure (Saunders 94: 603). Megaloblastic anemias constitute a diverse group of entities, having in common impaired DNA synthesis and distinctive morphologic changes in the blood and bone marrow. The erythroid precursors and erythrocytes are abnormally large, thought to be related to impairment of cell maturation and division. Vitamin B12 and folic acid are coenzymes in the DNA synthetic pathway. A deficiency of these vitamins or impairment in their utilization results in deranged or inadequate synthesis of DNA that may lead to megaloblastic anemia and usually presents in the form of chronic diarrhea. Vitamin B12 is a complex organometallic compound known as cobalamin, for the cobalt atom attached to a corrin ring, therapeutically synthesized as stable cyanocobalamin. Vitamin B12 is required for methylcobalamin to convert homocysteine to methionine and to metabolize polyglutamate forms of folate. Under normal circumstances, human are totally dependent on dietary animal products for the vitamin B12. Strictly vegan or macrobiotic diets do not provide enough of this essential nutrient. The daily requirement is 2 to 3 g daily and the normal balanced diet contains significantly larger amounts which takes years of vegan diet to deplete (Saunders 94: 603-607). A vitamin B12 deficiency normally manifests as chronic post-infectious diarrhea, about once a day, and is highly susceptible to food borne pathogens, neurological symptoms may manifest. The symptoms tend to go away temporarily with vitamin B12 supplementation but strict vegans will need to regularly eat some animal products (i.e. cheese aged more than two months contains no more lactose and good live culture yoghurt contains more than 100 billion probiotic organisms per serving) daily or be in chronic need for the medicinal constipating quality of meat or loperamide (Immodium). The benefits of regularly eating animal products extend further to Phosphorus, found in all animal products, mung and soy beans, that is necessary to protect the teeth against frequent cavities)(Sanders 12). The hypothesis that lack of folate is the proximate cause of anemia in vitamin B12 deficiency is supported by the observation that the anemia improves with the administration of folic acid. Folate is most necessary for (1) the synthesis of purines.; (2) the synthesis of methionine from monocysteine, a reaction that also requires vitamin B12; and (3) the synthesis of deoxythymidylate monophosphate (dTMP). Folic acid deficiency results in megaloblastic anemia without the neurological changes, but is not common, except with a very marginal diet, without adequate green vegetables. Despite their abundance in raw foods folate is sensitive to heat and cooking foods for 5 to 10 minutes destroy up to 95% of the folate. Folic acid antagonist drugs such as methotrexate, 6-mercaptopurine and cyclophosphamide inhibit folate function leading to ulcerative lesions in the gastrointestinal tract as well as megloblastic anemia. Human require 50 to 200 g of folate daily especially due to the increased demand for folate during pregnancy and dietary inadequacies found in chronic alcoholics, the indigent and very elderly. Megaloblastic anemia resulting from folic acid and vitamin B12 deficiency are identical (Saunders 94: 605-610). Dark leafy greens and brown rice, seem to be the most effective vegan staple, before diarrhea calls for animal products. The feature that sets pernicious anemia apart from dietary vitamin B12 deficiency is that the cause of the malabsorption is atrophic gastritis with failure of the production of intrinsic factor (IF). Chronic atrophic gastritis is marked by a loss of parietal cells, a prominent infiltrate of lymphocytes and plasma cells, and megaloid and atypical changes to the mucosal cells. It is an auto-immune disorder resulting from the presence of blocking, binding and gastric antibodies. Absorption of vitamin B12 requires IF, which is secreted by the parietal cells with HCl. Diagnostic features include (1) a marked to severe megalobastic anemia; (2) leukopenia with hypersegmented granulocytes; (3) mild to moderate thrombocytopenia; (4) neurologic changes related to involvement of the posterolateral spinal tracts; (5) achlorhydria even after histamine stimulation; (6) inability to absorb an oral dose of cobalamin (assessed by urinary excretion of radiolabeled cyanocobalamin given orally, called the Schilling test; (7) low serum levels of vitamin B12 ; (8) excretion of methymalonic acid in the urine; and (9) a striking reticulocytic response and improvement in hematocrit levels following parenteral administration of vitamin B12 (Saunders 94: 605, 608). Iron deficiency is probably the most common nutritional disorder in the world. Although more common in developing countries this form of anemia is also common in the United States. Normally, the total body iron content is in the range of 2gm in women and up to 6 gm in men. Approximately 80% of the functional iron is found in hemoglobin, myoglobin and iron-containing enzymes such as catalase and the cytochromes contain the rest in pools of hemosiderin and ferritin containing approximately 15 to 20% of total body iron. Because women have substantially smaller stores of iron than males they have a much more precarious iron balance and are vulnerable to excessive loss or increased demands associated with menstruation and pregnancy. In iron deficiency, serum ferritin is always below 12 g/liter, whereas in iron overload very high values approaching 5000 g/liter may be obtained. With liver damage and inflammatory states, serum ferritin levels may be high despite normal body stores. Storage iron pool is readily mobilized in the event of an increase in body iron requirements, as may occur following loss of blood. Iron is transported by transferrin which delivers iron to the cells, including erythroid precursors, where iron is required for hemoglobin synthesis. Immature red cells possess high-affinity receptors for transferrin. The most active site of iron absorption is the duodenum, but the stomach, ileum, and colon may also participate to a small degree. Approximately 25% of the heme iron derived from hemoglobin, myoglobin, and other animal proteins is absorbed, but only 1 to 2% of nonheme iron is absorbed. Daily losses of iron range between 1 and 1.5 mg. Thus to maintain a normal iron balance, approximately 1 mg of iron must be absorbed from the diet every day. Because only 10 to 15% of the ingested iron is absorbed, the daily iron requirement for adult males is 5 to 10 mg and for adult females 7 to 20 mg. The average daily dietary intake of iron in the Western World is about 15 to 20 mg. An iron deficiency may result from (1) dietary lack; (2) impaired absorption; (3) increased requirement; or (4) chronic blood loss. Dietary inadequacy is found in the elderly, very poor, infants because milk contains very small amounts of iron and children who need dietary iron to accommodate growth and expansion of blood volume. Impaired absorption is encountered in sprue, intestinal steetorrhea and chronic diarrhea. Chronic blood loss is the most important cause of iron deficiency in the Western world. Bleeding within the tissues or cavities of the body may be followed by total recovery and recycling of iron, however, external hemorrhage depletes the reserves of iron. Iron deficiency induces a hypochromic microcytic anemia and may cause other changes, including koilonychias, alopecia, atrophic changes in the tongue and gastric mucosa and intestinal malabsorption. The diagnosis of iron deficiency anemia rests on laboratory studies. Both hemoglobin and hematocrit are depressed, usually to moderate levels, and are associated with hypchromia, microcytosis and some poikilocytosis. The serum iron and serum ferritin are low, and the total plasma iron-binding capacity is high. Low serum iron with increased iron-binding capacity results in a reduction of transferrin saturation levels to below 15%. Reduced heme synthesis leads to elevation of free erythrocyte protoporphyrin. Unexplained iron deficiency anemia can be caused by an occult lesion or cancer (Saunders 94: 610-613). Marrow failure can be occupied by myelophthisic anemia caused by (1) space-occupying lesions, usually metastatic cancer, that destroy a significant amount of bone marrow or disturb the marrow architecture depressing its productive capacity, (2) diffuse liver disease with the contributing factors of folate deficiency and iron deficiency due to gastrointestinal blood loss or (3) chronic renal failure is almost always associated with anemia in proportion to the severity of the uremia, often with iron deficiency secondary to a tendency to bleeding, resulting in reduced red cell production although there is increased demand, with inadequate formation of erythropoietin. Recombinant erythropoietin results in significant improvement of anemia in patients with renal failure. Impaired red cell production associated with chronic disease is perhaps the most common cause of anemia among hospitalized patients in the United States. It is associated with defective iron utilization and may mimic iron deficiency but this anemia is instead caused by chronic illness from chronic microbial infections, such as osteomyelitis, bacterial endocarditis and lung abscess; chronic immune disorders, such as rheumatoid arthritis and enteritis; or neoplasms, such as Hodgkins disease and carcinomas of the lung and breast. The common features of anemia in these clinical settings is a low serum iron and reduced total iron-binding capacity in association with abundant stored iron in the mononuclear phagocytic cells, and there seems to be a defect in the reutilization of iron. The anemia is usually mild and treatment of the underlying condition corrects the anemia (Saunders 94: 615, 613). Polycythemia, or erythrocytosis, denotes an increased concentration of red cells, usually with a corresponding increase in hemoglobin levels. Such an increase may be relative, when there is hemococoncentration due to decreased plasma volume, or absolute, when there is an increase in total red cell mass. Relative polycythemia results from any cause of dehydration or stress polycythemia, called Gaisbocks syndrome. Absolute polycythemia is said to be primary when the increase in red cell mass results from an intrinsic abnormality of the myeloid stem cell and secondary when the red cell progenitors are normal but proliferate in response to increased levels of erythropoietin. Primary polycythemia is one of several expressions of clonal, neoplastic proliferation of myeloid stem cells. Aplastic anemia refers to pancytopenia characterized by (1) anemia; (2) neutropenia and (3) thrombocytopenia as the result of a suppression of multipotent myeloid stem cells, with inadequate release of differentiated cell lines. Most cases of aplastic anemia follow exposure to chemicals and drugs. With some agents the marrow damage is predictable and reversible when the use of the offending agent is stopped, usually benzene, chloramphenicol, alkylating agents, and antimetabolites (e.g. 6-mercaptopurine, vincristine and busulfan) or idiosyncratically with chloramphenicol, phenylbutazone, methylphenylethylhydantoin, streptomycin and chlorpromazine. Whole body irradiation causes dose related destruction of hematopoietic stem cells. Some forms of marrow insult cause genetic damage that results in the generation of stem cells with poor proliferative and differentiative capacity. If one such altered stem cell dominates, the resultant picture is one of aplastic anemia. The occasional transformation of aplastic anemia into acute leukemia lends further credence to this hypothesis. Although aplastic anemia may appear following a variety of infections (including HIV), it most commonly follows viral hepatitis of the non-A, non-B type. Anemia may cause the progressive onset of weakness, pallor and dyspnea. Splenomegaly is characteristically absent. Diagnosis rests on examination of bone marrow biopsy and peripheral blood. It is important to distinguish aplastic anemia from other causes of pancytopenia, such as aleukemic leukemia and myelodysplastic syndromes. Fanconis anemia is a rare autosomal recessive disorder characterized by defects in DNA repair causing marrow hypofunction in early life accompanied by multiple congential anomalies. The idiopathic form has a poor prognosis and there is increasing use of bone marrow transplantation to replace defective stem cells and in selected cases this is effective. Benefit may also be derived from immunosuppressive therapy with antithymocyte globulin, which presumably neutralize the marrow-suppressive effect of immune cells (Saunders 94: 616, 614-615). Hemorrhagic diatheses, excessive bleeding, may result from (1) increased fragility of vessels, (2) platelet deficiency or dysfunction, (3) derangements in the coagulation mechanisms and (4) combinations of these. Bleeding disorders caused by vessel wall abnormalities, called nonthrombocytopenic purpuras, do not usually cause serious bleeding problems most often they induce small hemorrhages (petechieae and purpura) in the skin or mucous membranes, particularly the gingivae, however occasionally more significant hemorrhages can occur into joints, muscles and subperiosteal locations or take the form of menorrhagia, nosebleeds, gastrointestinal bleeding or hematuria. The platelet count, bleeding time and coagulation time are usually normal. Many infections induce petechial and purpuric hemorrhages, but expecially implicated are meningococcemia, other forms of septicemia, severe measles and several rickettsioses. Drug reactions may induce abnormal bleeding. Scurvy and Ehlers-Danlos syndrome impair the formation of the collagenous support of vessel walls predisposing to hemorrhage. Henoch-Schnlein purpura is a systemic hypersensitivity disease of unkown cause characterized by a purpuric rash, colicky abdominal pain (presumably due to gastrointestinal hemorrhage), polyarthralgia and acute glomerulonephritis. Hereditary hemorrhagic telangiectasia is an autosomal dominant disorder characterized by dilated, tortuous blood vessels that have thin walls and hence bleed readily anywhere in the body but most commonly under the mucous membranes of the nose (epistaxis) tongue, mouth and eyes (Saunders 94: 616, 617). Thrombocytopenia, reduced platelet number, constitutes an important cause of generalized bleeding. Platelet counts normally range between 150,000 to 300,000/mm3 and a count below 100,000/mm3 is generally considered to constitute thrombocytopenia. However spontaneous bleeding does not become evident until the count falls below 20,000/mm3. Platelet counts in the range of 20,000 to 50,000/mm3 are associated with post-traumatic bleeding. Rarely thrombocytopenia can be caused by diseases of the bone marrow, ineffective megakaryopoiesis in megaloblastic anemias resulting from a deficiency of folate or vitamin B12; increased destruction of platelets following drug ingestion or infection most commonly quinine, quinidine, methyldopa, thiazide diuretics and heparin; most common hematological manifestation of AIDS; acute postviral thrombocytopenia, may appear in children following recovery from viral exanthema or upper respiratory tract infection, but resolves spontaneously in 4 to 6 weeks; mechanical injury, such as by prosthetic heart valves or hypertense arteries; hypersplenism, normally sequestering 30 to 40% of the mass of circulating platelets, sequestrates as much as 90% of all platelets; and massive transfusions with blood stored for longer than 24 hours that contains virtually no viable platelets. Neonatal and post-transfusion (Isoimmune) thrombocytopenia results from the development of antibodies. In addition to HLA an ABO antigens, platelets possess several antigenic determinants not present in other blood cells including Duzo, PL and Bak antigen systems. PLA1 antigen is believed to be the cause of both the purpura associated with post-transfusion and neonatal thrombocytopenia. Idiopathic thrombocytopenic purpura (ITP) is a chronic autoimmune disorder in which lesions are found in the spleen and bone marrow and platelets are destroyed by the formation of antiplatelet IgC antibodies targeting two platelet glycoprotein complexes IIb/IIIa and Ib/IX, that can be demonstrated in 80% of patients. ITP occurs most commonly in adults, particularly in women of childbearing age. About 75 to 80% of patients are remarkably improved or cured following splenectomy but a diagnosis of ITP should be made only after all the possible known causes for platelet deficiencies have been ruled out. Thrombotic microangiopathies encompass a spectrum of clinical syndromes that include thrombotic thrombocytopenic purpura (TTP) and hemolytic-uremia syndrome (HUS). TTP traditionally occurs in adult females with fever, thrombocytopenia, microangiopathic hemolytic anemia, transient neurologic deficits and renal failure. HUS is also associated with microangiopathic hemolytic anemia and thrombocytopenia but is distinguished from it by the absence of neurologic symptoms, the dominance of acute renal failure and onset in childhood. At one time these conditions were uniformly fatal, but with recent improvements in treatment, including plasma exchange, approximately 80% survival can be expected (Saunders 94: 617, 620). Qualitative defects of platelet function may be congenital or acquired. Congenital disorders are rare and can be classified into three groups on the basis of the predominant functional abnormality (1) defects of adhesion, (2) defects of aggregation and (3) disorders of platelet secretion (release reaction). Defective adhesion is best illustrated by the autosomal recessive Bernard Soulier syndrome in which there is an inherited deficiency of platelet membrane glycoprotein complex (GpIb/IX) that is a receptor for von Willebrands factor which is essential in normal platelet adhesion to collagen. Defective platelet aggregation is exemplified by the autosomal recessive trait thrombasthenia in which platelet fail to aggregate with ADP, collagen, epinephrine, or thrombin, owing to a deficiency of GpIIb/IIIa, the fibrinogen receptor. Disorders of platelet secretion are characterized by normal initial aggregation with collagen or ADP, but the subsequent responses, such as secretion of prostaglandins and release of granulebound ADP, are impaired causing storage pool disease. There are two clinically significant acquired defects of platelet function (1) related to aspirin and other NSAIDs, which may significantly prolong bleeding time and lead to bruising, with ingestion of as little as 1g in 10% of normal healthy subjects and (2) uremia (Saunders 94: 619, 620). A deficiency of every one of the known clotting factors has been reported at one time or another as the cause of a bleeding disorder. The bleeding differs somewhat from that encountered in platelet deficiencies. The bleeding manifests as large ecchymoses or hematomas following an injury, or as prolonged bleeding after a laceration or any form of surgical procedure. Acquired disorders are usually characterized by multiple clotting abnormalities. Vitamin K deficiency results in depressed synthesis of factors II, VII, IX and X and protein C. Since the liver makes virtually all the clotting factors, severe parenchymal liver disease may be as associated with hemorrhagic diathesis. Hereditary deficiencies have been identified for each of the clotting factors. Deficiencies of factor VIII (hemophilia A) and of factor IX (Christmas disease, or hemophilia B) are transmitted as sex-linked recessive disorders that are usually autosomal. In most cases four screening procedures will localize the hemostatic abnormality, (1) bleeding time, (2) platelet count, (3) the prothrombin time, and (4) the partial thromboplastin time (Saunders 94: 620, 621). Hemophilia A and von Willebrands disease, are two of the most common inherited disorders of bleeding, both caused by qualitative or quantitative defects involving the factor VIII-vWF complex. Plasma factor VIII-vWF is a complex made up of two separate proteins. Synthesized separately through noncovalent bonds, factor VIII is linked to a much larger protein called von Willebrands factor (vWF) which forms approximately 99% of the complex, which circulates in the plasma to promote clotting and the platelet vessel wall interactions necessary to ensure hemostatis. Von Willebrands factor binds to several other proteins involved in hemostasis, most importantly subendothelial collagens, but also heparin and platelet membrane glycoproteins (GpIb and IIb/IIIa). The half-life of factor VIII in the circulation is 12 hours if vWF is present but only 2.4 hours if the latter is lacking. vWF can be assayed with a ristocetin aggregation test. With an estimated frequency of 1% von Willbrands disease (vW) is one of the most common inherited disorders of bleeding in humans. It manifests as sponataneous bleeding from mucous membranes, excessive bleeding from wounds, menorrhagia and a prolonged bleeding time in the presence of a normal platelet count. More than 20 variants have been described, most are autosomal dominant. Types I and III vWD are associated with a reduced quantity of circulating vWF. Type I, an autosomal dominant disorder, accounts for approximately 70% of these cases and is relatively mild. Type III, an autosomal recessive disorder is associated with extremely low levels of vWF and correspondingly clinical manifestations are severe, but is much less common. Type II vWD involves a qualitative defect in vWF, that is inherited as an autosomal dominant disorder, where the vWF that is formed is abnormal, and intermediate multimers, the most active forms of vWF are missing from plasma. Type II vWD accounts for 10 to 15% of all cases and is associated with mild to moderate disease. Patients with von Willebrands disease have a compound defect involving platelet function and the coagulation pathway. However, except in the most severely affected (e.g. homozygous) patients, effects of factor VIII deficiency such as bleeding into the joints, which characterizes hemophilia, are uncommon (Saunders 94: 621, 622). Hemophilia A is the most common hereditary disease with serious bleeding caused by a reduction in the amount or activity of factor VIII. Hemophilia A is inherited as an X-linked recessive trait, and thus occurs in males and in homozygous females. However, excessive bleeding has been described in heterozygous females. Approximately 30% of patients have no family history presumably because the disease is caused by new mutations. Those with less than 1% of normal activity develop severe disease, levels between 2 to 5% of normal are associated with moderate disease and patients with 6 to 50% of activity develop mild disease. Typically patients wit hemophilia A have normal bleeding time and platelet counts, with prolonged partial thromboplastin time. Factor VIII assays are required for diagnosis. Treatment of hemophilia A involves infusion of factor VIII, currently derived from human plasma. Replacement therapy however carries the risk of transmission of viral diseases. Until the mid-1980s, before routine screening of blood for HIV antibodies, thousands of hemophiliacs received factor VIII concentrates containing HIV and many developed AIDS. Although blood bank standards have improved the only safe factor VIII will be a recombinant factor VIII derived from cloned factor VIII gene. Hemophilia B, also known as Christmas disease, involves a severe factor IX deficiency that is clinically indistinguishable from hemophilia A, the partial thromboplastin time is prolonged and bleeding time is normal. It is also inherited as an X-linked recessive trait and may occur asymptomatically or with associated hemorrhage. In about 14% of these patients, factor IX is present but nonfunctional. Identification of Christmas disease, named after the first patient) is possible only by assay of the factor levels (Saunders 94: 622, 623). Disseminated intravascular coagulation (DIC), sometimes referred to as consumption coagulopathy, is an acute, subacute or chronic thrombohemorrhagic disorder occurring as a secondary complication in a variety of diseases, it is not a primary disease. It is characterized by activation of the coagulation sequence that leads to the formation of microthrombi throughout the microcirculation of the body, but often in a quixotically uneven distribution. DIC may present with signs and symptoms relating to tissue hypoxia, and infarction caused by the myriad mirothrombi, or as a hemorrhagic disorder related to depletion of the elements required for hemostasis. DIC occurs in the course of a variety of clinical conditions. Clotting can be initiated by either of two ways (1) the extrinsic pathway, with is triggered by the release of tissue factor (tissue thromboplastin) and (2) the intrinsic pathway, which involves the activation of factor XII by surface contact with collagen or other negatively charged substances. Both pathways result in the generation of thrombin, which in turn converts fibrinogen to fibrin. This process is regulated by clot-inhibiting influences which include the activation of fibrinolysis involving generation of plasmin, the clearance of activated clotting factor by the mononuclear phagocyte system or by the liver and activation of endogenous anticoagulants such as protein C. There are two major mechanisms which trigger DIC (1) release of tissue factor thromboplastic substance such as the placenta into the circulation and (2) widespread injury to the endothelial cells which causes the release of tissue factor activating the intrinsic coagulation pathway. DIC is most likely to follow obstetric complications, malignancy, sepsis and major trauma. Infections, particularly those caused by gram-negative bacteria, endotoxins released by the bacteria may activate both the intrinsic and extrinsic pathways producing endothelial cell injury, furthermore endotoxins inhibit the anticoagulant activity of protein C. Endothelial cell damage may also be caused by meningococci, rickettsiae and viruses. Among cancers acute promyelocytic leukemia and carcinomas of the lung, pancreas, colon and stomach are most frequently associated with DIC. The consequences of DIC are twofold. First there is widespread deposition of fibrin with the microcirculation which may lead to ischemia and to hemolytic anemia from the fragmentation of red cells as they squeeze through the narrowed microvasculature (microangiopathic hemolytic anemia). A hemorrhagic diathesis may dominate the clinical picture resulting from consumption of platelets and clotting factors as well as activation of plasminogen by plasmin which can not only cleave fibrin but also digest factors V and VIII. Thrombi are found in decreasing order of frequency in the brain, heart, lungs, kidneys, adrenals, spleen and liver. In giant hemangiomas thrombi are localized to the neoplasm. The onset may be fulminant, as in endotoxic shock or amniotic fluid embolism, or may be insidious and chronic, as in the cases of carcinomatosis or retention of a dead fetus. About 50% of individuals with DIC are obstetric patients having complications with pregnancy this disorder tends to be reversible with delivery of the fetus. About 33% of patients have carcinomatosis. Acute DIC associated for example with obstetric complications or major trauma, is dominated by bleeding diathesis, whereas chronic DIC, such as may occur in patients with cancer, tends to present initially with thrombotic complications. It is usually necessary to monitor the fibrinogen, platelets, prothrombin time, partial thromboplastin time and fibrin degradation products for a laboratory confirmed diagnosis. The prognosis is highly variable and depends on the underlying disorder. The management of these cases requires meticulous maneuvering between the Scylla of the thrombotic tendency and the Charybdis of the bleeding diathesis. Thus is posed the dilemma of whether or not to attempt to block coagulation or to control bleeding by the administration of anticoagulants such as heparin and antithrombin III or coagulants in the form of fresh-frozen plasma may be administered. Platelet transfusion may sometimes be necessary (Saunders 94: 623-626). A blood clot is called a thrombus, and formation of a clot is called thrombosis; because platelet clumps are white, they are sometimes called white thrombus. A red thrombus forms when strands of fibrin, a blood-clotting protein, grow longer and longer, forming a mesh like fiberglass wool. The mesh entraps red blood cells and platelets and tends to keep growing. The red blood cells give the clot a red appearance. The drugs used to prevent red thrombus act by reducing the levels of blood-clotting proteins, thus preventing the coagulation of blood, so they are called anticoagulants. Acetylsalicylic acid (ASA, or Aspirin) and new drugs that prevent platelet clumping are called antiplatelet agents (blood thinners). The two main types are heparin, which is given by injection and warfarin (Coumadin, which is taken in pill form (Spence 06: 6, 7). Dissolution of a clot in an unwanted location, thrombolysis, was originally used for the treatment of deep vein thrombosis and pulmonary embolism but is now also used for treating acute peripheral arterial thrombosis and embolism and for thrombosed prosthetic heart valves, catheters and shunts. Thrombolytic agents used currently act directly or indirectly as plasminogen activators. Thrombolytic therapy with various fibrinolytic agents such as streptokinase or tissue-type plasminogen activator (tPA) is used in about 15% of myocardial infarcts, in an attempt to dissolve the thrombus that initiated the infarct, to re-establish blood flow to the area at risk for infarction, and possibly to rescue the ischemic heart muscle. Thrombolysis re-establishes the patency of the occluded coronary artery in about 70% of cases, and significantly improves survival rates. Reperfusion of the myocardium with blood, sufficiently early, within 15 to 20 minutes, after onset of ischemia may prevent all necrosis. Reperfusion after a longer interval can salvage at least some myocytes that would have died with more prolonged or permanent ischemia. However, reperfusion injury can cause cell death of myocytes that were still viable before reperfusion. Persistance of total occlusion with failure of clot lysis occurs in approximately 30% of patients undergoing thromblytic therapy. The major complications of thrombolytic therapy that lessen enthusiasm for its use in patients with occlusive vascular disorders include hemorrhage due to the systemic fibrinolytic state (15% of patients) and thrombotic reocclusion (15 to 35% of patients). Reocclusion is related to the continued presence of the factors, responsible for the original thrombus initiation (Schoen 94: 535, 537, 512). Because platelet aggregation has been strongly implicated in the pathogenesis of unstable angina pectoris and myocardia infarction, Aspirin, a platelet inhibitor, shows a 51% lower incidence of myocardial infarction and death in the aspirin group (324 mg/day) than the placebo group, although it is generally conceded that lower doses (1mg/kg) work as well and are less inhibitory to the arterial endothelium's production of prostacyclin than higher doses. Aspirin causes irreversible acetylation of platelet cyclooxygenase, thereby preventing the formation of thromboxane A2 an extremely potent vasoconstrictor and platelet activator. The thienopyridine drugs ticlopidine and clopidogrel (Plavix) are also effective antiplatelet drugs used to prevent stent cosure, generally, clopidogrel is preferred, because it is safer, more potent, and faster acting and can be taken once a day. Plavix is used with acetylsalicylic acid (aspirin) after placement of a stent to prevent the stent and coronary artery from occluding. Glycoprotein (GB) IIb/IIIa Receptor Antagonists prevent fibrinogen binding and platelet aggregation and is used by paitents at high risk and those undergoing percutaneous coronary intervention. Three GP IIb/IIIa receptor antagonists are currently available abciximab (long lasting 12 hours affect on platelets) an, eptifibatide, and tirofiban that have short half live of 2 to 3 hours. Severe thrombocytopenia (less than 20,000/mL) is seen in 0.5% of patients. Unfractionated heparin (UFH) reduces the risk of sudden cardiac death, myocardial infarction and recurrent ischemic events when combined with ASA in the setting of unstable angina pectoris. Unless there is a contraindication, full-dose heparin anticoagulation appears to be a logical therapy in the earl coronary care unit setting followed by chronic low-dose aspirin in patients with intermediate or high risk unstable angina pectoris. Most of the benefit is short term and most trials have limited heparin use to 2 to 5 days. Severe thrombocytopenia (less than 100,000/mL) occurs in 1 to 2% UFH auto-immune induced thrombocytopenia with thrombosis occurs in less than 0.2% of cases. Low-molecular-weight heparin (LMWH) is safer and alleviates the need for partial thromboplastin time testing (Heger et al '04: 124-126). Clinical trials testing three new drugs appear to offer some promise to heart patients. Two of the drugs, cangrelor and inclacumab, might improve outcomes for patients undergoing cardiac interventions such as angioplasty or stenting, while a third drug, Inspra, seems to lower heart patients odds for death and heart failure following a heart attack. All three trials were funded by the respective drugs makers, and all three were presented Sunday at the annual meeting of the American College of Cardiology (ACC) in San Francisco. In the first trial, researchers compared an as-yet approved blood thinner called cangrelor against the current standard medication, Plavix (clopidogrel), for patients who have recently had a stent implanted in an artery to help improve blood flow. According to the ACC, more than 600,000 coronary artery stent procedures are conducted in the United States each year, but doctors have long sought safer alternatives to Plavix to help prevent clots. Plavix comes with one big drawback for patients rushed to the hospital with suspected heart attack: It is taken in pill form, and its anti-clotting effects (with accompanying bleeding risk) may not wear off for up to a week. Cangrelor may help get around that issue. Even though it is delivered intravenously and begins acting quickly, its anti-clotting effects also fade quickly within an hour should any bleeding complications occur. So, doctors might feel free to give heart patients cangrelor upon admittance to the hospital and then send them immediately for angioplasty a minimally invasive procedure to reopen clogged vessels or stenting, if needed. In the trial, which was funded by cangrelors maker, New Jersey-based The Medicines Company, researchers compared short-term outcomes for 11,000 patients who underwent stent placement at one of 153 centers around the world. Some of the patients got cangrelor, while others got Plavix. The research team reported that cangrelor reduced by 22 percent the odds of a patient dying, having a heart attack or having a clot develop in the stented vessel within two days of the procedure, compared to patients who took Plavix. Safety profiles were similar: Severe bleeding at 48 hours after the stenting procedure occurred in 0.16 percent of those on cangrelor and 0.11 percent of those given Plavix. More than 1 million Americans each year undergo angioplasty. But angioplasty can also trigger damage to heart tissues, and it was thought that the new drug might help minimize that risk. cangrelors price has not yet been set, but it likely will carry a much higher price tag than Plavix. A second study focused on the drug eplerenone, marketed by Pfizer as Inspra. The drug is currently FDA-approved to help lower high blood pressure and to ward off heart failure after heart attack. In the new Pfizer-funded trial, slightly more than 1,000 patients who had had a heart attack caused by complete blockage of an artery took either Inspra or a placebo in addition to standard treatments. Patients were followed for an average of a bit more than 10 months. Those taking Inspra were 38 percent less likely than those on a placebo to have outcomes such as death by cardiovascular causes, rehospitalization due to heart failure, irregular heart rhythms or other indicators of heart failure. A third and smaller trial, published simultaneously online in theJournal of the American College of Cardiology, looked at another still-unapproved drug, the anti-inflammatory agent inclacumab, for use in patients undergoing angioplasty. More than 1 million Americans each year undergo angioplasty. But angioplasty can also trigger damage to heart tissues, and it was thought that the new drug might help minimize that risk. In the study, which involved 322 patients with a common form of heart attack, participants got either various doses of inclacumab or a placebo about an hour before their angioplasty. The research team assessed changes in levels of troponin I a protein found in the blood that indicates heart damage as a means of telling whether the drug was effective or not. The researchers reported that 24 hours after the procedure, patients who had gotten the highest dose of inclacumab saw their troponin I levels drop by more than 24 percent compared to those on a placebo indicating less heart tissue damage. Levels of another marker of heart tissue damage, called CK-MB, fell by more than 17 percent over 24 hours compared to placebo, the team added. There was also no bad signal [from the data] in terms of increased rates of bleeding or infection with the use of inclacumab (Mundell '13). Decade-old heart attack scars healed after being injected with stem cells from a patients' own bone marrow. So far, eight patients have received the experimental treatment in an ongoing clinical trial. All eight had suffered heart attacks an average of 5 1/2 years prior; one of the patients had his heart attack 11 years earlier. All had dangerously enlarged hearts, with areas of scar tissue from their heart attacks. The researchers harvested bone marrow progenitor cells from four patients and adult stem cells from another four patients. Using a catheter, they then injected the cells into the walls of the patients' hearts. Within three months, the scarred areas of the patients' hearts began to work again. About six months after treatment, and for a year later -- the length of the study so far -- all eight hearts regained a more normal size. They shrank 15% to 20%, three times more than current treatments can achieve. Whether just plain old bone marrow or [adult stem] cells, injected into the scar, and three months later, the area that was completely dead started to contract again. Stem cells are being explored in the treatment of people with recent heart attack damage -- but the "landmark area" is the use of stem cells to treat end-stage heart failure. Stem cells actually reverse the enlargement and their propensity to get worse (DeNoon 11). 9. Leukopenia, Lymphoma, Leukemia and Myeloma Disorders of white cells may be classified into two broad categories, proliferative and leukopenias characterized by a deficiency of leukocytes. Proliferations of white cells and lymph nodes can be reactive or neoplastic. Reactive proliferation in response to an underlying microbial disease is fairly common. Neoplastic disorders, although less frequent, are much more severe. Leukopenia is an abnormally low white cell count usually resulting from reduced numbers of neutrophils (neutropenia, granulocytopenia). Lymphopenias are much less common, and in addition to the congenital immunodeficiency diseases, they are associated with specific clinical syndromes (e.g Hodgkins disease, nonlymphocytic leukemias, following corticosteroid therapy and occasionally in chronic diseases. Neutropenia, a reduction in the number of granulocytes in the peripheral blood may be seen in a wide variety of circumstance. A marked reduction in neutrophil count predisposes to infection. Inadequate or ineffective granulopoiesis may be encountered with (1) suppression of myeloid stem cells as occurs in aplastic anemia, a variety of leukemias and lymphomas, where granulocytopenia is accompanied by anemia and thrombocytopenia; (2) suppression of the committed granulocytic precursors, which occurs after exposure to certain drugs such as alkylating agents and antimetabolites used in cancer treatment which produce neutropenias in a dose-related fashion and other drugs in an idiosyncratic reaction with aminopyrine, chloramphenicol, sulfonamides, chlorpromazine, thiouracila and phenylbutazone; (3) megloblastic anemias due to vitamin B12 or folate deficiency and (4) monoclonal proliferations of CD8+ large granular lymphocytes. Ulcerating necrotizing lesions of the gingiva, floor of the mouth, buccal mucosa, pharynx, or anywhere within the oral cavity (agranulocytic angina) are characteristic of agranulocytosis. The ulcers are typically deep, undermined and covered by gray to green black necrotic membranes for which numerous bacteria or fungi can be isolated. Similar ulcerations may occur less frequently in the skin, vagina, anus, or gastrointestinal tract. In many instances the bacteria and fungi grow in colony formations. The regional lymph nodes draining these infections are enlarged and inflamed but the spleen and liver are rarely enlarged. The symptoms and signs of neutropenias are those of bacterial infections malaise, chills, and fever, followed by weakness and fatigability. In severe agranulocytosis with virtual absence of neutrophils, these infections may become so overwhelming as to cause death within a few days. Characteristically the total white cells count is reduce to 1000 cells per mm3 of blood, and when counts fall below 500 per mm3 serious infections tend to occur. In addition to control of bacterial infections with antibiotics, treatment efforts are aimed toward increasing the production of neutrophils by administration of recombinant human granulopoietic factors such as granulocyte-macrophage colony stimulating factor (GM-CSF) and G-CSF (Saunders 94: 630, 631). Leukocytosis is a common reaction to a variety of inflammatory states. Pyogenic infections are common causes of neutrophilic leukocytosis, but it may as a result from nonmicrobial stimuli, such as tissue necrosis caused by burns or myocardial infarctions. In patients with severe, live-threatening sepsis, in addition to leukocytosis there may be morphologic changes in the neutrophils, such as toxic granulations and cytoplasmic vacuoles. Eosinophilic leukocytosis is characteristic of allergic disorders, such as bronchial asthma, hay fever, parasitic infections and some diseases of the skin. The skin diseases include pemphigus, eczema and dermatitis herpetiformis. In hospitalized adult patients the most likely cause of eosinophilia is an allergic drug reaction. Elevations in monocyte may be seen in several chronic infections including tuberculosis, bacterial endocarditis, brucellosis, rickettsiosis, and malaria. Certain collagaen vascular diseases, such as systemic lupus erythematosus (SLE) and rheumatoid arthritis are associated with monocytosis, as are inflammatory bowel diseases such as ulcerative colitis and Crohns disease. Lymphocytosis may accompany monocytosis in chronic inflammatory states such as brucellosis and tuberculosis. The lymphocyte count may also be increased in acute viral infections such as viral hepatitis, in cytomegalovirus infections and particularly infectious mononucleosis. In most instances, reactive leukocytosis is easy to distinguish from neoplastic proliferation of the white cells (i.e. leukemias) by the rarity of immature cells in the blood. However, in some inflammatory states, many immature white cells may appear in the blood and a picture of leukemia may be simulated (leukemoid reaction). Infections and other inflammatory stimuli may not only cause leukocytosis but also involve the lymph nodes, which act as defensive barriers (Saunders 94: 63, 632). Malignant proliferative disorders constitute the most important part of white cell disorders. Malignant lymphomas take the form of cohesive tumorous lesions, composed mainly of lymphocytes and rarely of histiocytes, that arise in lymphoid tissue anywhere in the body, most commonly within lymph nodes. Leukemias and myeloproliferative disorders are neoplasms of the hematopoietic stem cells arising in the bone marrow that secondarily flood the circulating blood or other organs with transformed cells. Plasma cells dyscrasias and related disorders usually arising in the bones, take the form of localized or disseminated proliferations of antibody forming cells. Thus, this category is marked by the appearance in the peripheral blood of abnormal levels of complete immunoglobulins or the light or heavy chains of the immunoglobulins. The histiocytoses represent proliferative lesions of histiocytes that include rare histiocytic neoplasms that present as malignant lymphomas,. A special category of histiocytes referred to as Langerhans cell histiocytes gives rise to a spectrum of disorders, some of which behave disseminatd malignant tumors and others as localized benign proliferations (Saunders 94: 633, 634). The concept that myeloproliferative disorders result from clonal neoplastic proliferations of the multipotent myeloid stem cells is well established. Several environmental factors have been implicated in the causation of leukemias and lymphomas. Well-established influences include ionizing radiation, chemicals and alkylating agents used in chemotherpy. Two viruses, HTLV-2 and EBV, have been associated with acute T-cell leukemia/lymphoma and Burkitts lymphoma respectively. Recent studies have implicated HTLV-1 and HTLV-2 in the causation of mycosis fungoides as well (Saunders 94: 658, 656). That is however too much for poet to tolerate; if mycosis fungoides is truly caused by a virus the term mycosis fungoides should go into general circulation to describe tumors that are treatable with antifungal drugs alone, and a new name to describe the HTLV-1 and 2 tumor. Patients must not be dissuaded from self-medicating neoplasms with antifungals but for the protection of health care professionals from drug resistant pathogens, such as viruses that are implicated in 18% of cancers, and need to dissolve tumors effectively, the clinical treatment of neoplasms should involve appropriate chemotherapeutic drugs, which are available in oral prescription drug form or hospitalization and IV chemotherapy, often in conjunction with radiation treatment and any necessary surgeries, is grossly about 80% effective at curing cancer. Multiple myeloma is plasma cell cancer that originates in the bone marrow and is characterized by involvement of the skeleton at multiple sites with peak incidence between 50 and 60 years. Infiltration of bone is manifested by pain and stress fractures. Multiple myeloma presents most often as multifocal destructive bone lesions throughout the skeletal system vertebral column 66%, ribs 44%, skull 41%, pelvis 28%, femur 24% clavicle 10% and scapula 10%. Focal lesions beign in the medullary cvity, erode the cacellous bone and progressively destroy the cortical bone. Fractures are often produced by plasma cell lesions. On section, the bony defects are typically filled with soft, red, gelatinous tissue. Most commonly the lesions appear radiographicaly as punched out defects, usually 1 to 4 cm in diameter. Increased numbers of plasma cells in the marrow constituting 10 to 90% of total. Renal involvement, generally called myeloma nephrosis, causes abnormal plasma cells to be encountered or at least proteinaceous casts surrounded by giant cells, and hypercalcemia and pyelonephritis may occur. Hypercalcemia resulting from bone resportion may give rise to neurologic manifestations such as confusion, weakness, lethargy, constipation and polyuria. Recurrent infections with bacteria such as Streptococcus pneumonia, Staphylococcus aureus and E. coli resulting from severe suppression of normal immunoglobulins, also pose a major clinical problem. In 99% of patients with multiple myeloma, electrophoretic analysis reveals increases levels of immunoglobulins in the blood and/or light chains (Bence Jones proteins) in the urine. It may also spread to extraosseous sites. Renal insufficiency is the second leading cause of death after infection. The neoplastic plasma cells synthesize complete or incomplete immunoglobulins. Diagnosis rests on radiographic and laboratory findings. The lesions appear as sharply punched out defects having a rounded soap-buble appearance on x-ray film, but generalized osteoporosis may be seen. Marrow examination revels aggregates of plasma cells that suppress and replace normal hematopoietic elements. The resultant marrow failure gives rise to a normocytic normochromic anemia, sometimes accompanied by moderate leukopenia and thrombocytopenia. Rarely plasma cells flood the peripheral blood, giving rise to plasma cell leukemia. Prognosis depends on the stage at the time of diagnosis. Patients with multiple bony lesions, if untreated, rarely survive for more than 6 to 12 months. Chemotherapy in the form of alkylating agents induces remission in 50 to 70% of patients, bu the median survival is still a dismal 3 years. Autologous and allogeneic bone marrow transplantation after intensive chemotherapy offers the promise of cure. High serum levels of cytokine IL-6 is associated with a poor prognosis. Loss of bone is in large part due to osteoclastic reabsorption induced by the tumor. Solitary myeloma (plasmacytoma) lesion occurs in 3 to 5% of monoclonal gammopathies. Estaosseous lesions are often located in the lungs, oronaspharynx, or nasal sinuses. Progression to classic multiple myeloma becomes manifest in most patients with osseous plasmacytoma, whereas extaosseous primaries rarely disseminate. Solitary plamacytoma involving the bones is an early stage of multiple myeloma, but in some individual sit may be present for 10 to 20 years without progression. Extraosseous plasmacytomas, particularly involving the upper respiratory tract, are limited disease that can usually be cured by local resection (Saunders 94: 663-665). Home treatment of bone pain, myeloma, usually starts with the application of antifungal foot crme (clotrimazole), if bacteria is presumed in which case metronidazole (Flagyl ER) is the most effective antibiotic for bone and joint infections and Sporanox (itraconazole) is the most effective antifungal. Care must be taken when treating myeloma with chemotherapeutic agents because many defective antineoplastic drugs that cause deterioration of the bone and athletic performance. Cancer is an idiopathic disorder. Drug info removed the explanation that antineoplastic cancer drugs are antibacterial, antiviral and antifungal. Initial necrosis is usually caused by exposure to toxic chemicals, such as benzene, or physical trauma to the bone. Untreated with basic antibiotics and antifungals, the necrotic tissue becomes septic and doesn't heal and the diseases progresses and becomes worse, and the mycotic infection of the necrotic tissue breaks through the bone and induces mutations distorting the peripheral complete blood count and white blood cell differential, although there is no more exposure to the toxic substance. The patient may be quite confused about their disease due to an affinity for the well-documented mind altering affects of fungi such as brewer's yeast and psychedelic mushrooms. The pathogenesis of neoplastic white cell disease relies heavily upon the failure to treat the large fungal cells causing neoplastic mutation in human cells sensed by the patient as painful bone infections known as myelomas as well as lymphoma. Although the bacteria and virus would happily infiltrate any crack in the bone to get at the marrow where they can cause hematopietic disorders, fungus cells are the most likely to break through the bone, and induce mutations by releasing the enzymes that drive their two stage sexual fungal life cycle. Their large size however gives them away and fungal infections often cause excruciating bone pain and can lead to white cell disease if the infection breaks through the bone and eats the marrow. Athletes foot crme (clotrimazole) is generally effective at keeping the cripple able to jog, used twice daily for three weeks, is likely to completely eliminate the fungal infection causing the arthritis anywhere the topical preparation can penetrate, it can however be a frustrating 3 weeks chasing multiple myelomas as the fungi translocate from one location to another to escape the topical cream. Another antifungal foot powder spray (toftate), powder being prescribed for elders, however caused a diffuse pain to occur, and elders are definitely recommended to use clotrimazole (athlete's foot cream) as their basic antifungal, Athlete's foot cream (clotrimazole) can be purchased for $1 and lasts about one of three weeks recommended for the treatment of athlete's foot, jock itch and bone pain. There are several oral antifungal drugs such as Lamisil and Grifulvin V available for the treatment of athlete's foot and toenail and fingernail onchymycosis but a scientist cannot be sure they have used an effective antifungal for the treatment of invasive pulmonary and extrapulmonary Aspergillosis, sold to academic laboratories as A. niger, and other insidious fungal pathogens until they have tried a fingernail pulse of Sporanox (itraconazole), a highly effective broad spectrum oral antifungal used in the treatment of both pulmonary and extra pulmonary invasive aspergillus as well as the common onchymycosis and histoplasmosis - 200 mg 3 times daily for 3 days, then 200 mg twice daily until no longer immune-compromised. For primary prophylaxis of aspergillosis in immunocompromised individuals at high risk of invasive disease such as neutropenic patients with acute myelogenous leukemia (AML) or myelodysplastic syndrome (MDS) or hematopoietic stem cell transplant (HSCT) recipients with graft-versus-host disease (GVHD). IDSA considers posaconazole the drug of choice; alternatives are itraconazole or micafungin. The prophylaxis of invasive Aspergillus and Candida infections in patients, 13 years of age and older, who are at high risk due to being severely immunocompromised, such as hematopoietic stem cell transplant (HSCT) recipients with graft-versus-host disease (GVHD) or those with hematologic malignancies with prolonged neutropenia from chemotherapy and also fororopharyngeal candidiasis. Sporanox is hepatoxic and liver enzymes must be monitored on a monthly basis and is highly contraindicated in heart failure due to adverse drug reactions with antihypertensive drugs. IV amphotericin B is the preferred alternative to oral Sporonox (itraconazole). The effectiveness of oral antifungals is 60-80%. There is still a chance of re-infection after finishing the course of the medication. The re-infection rate is 15% but can be as high as 25% in diabetics. Serious adverse reactions are less than 0.5%. There are some interactions between these medication and other drugs such as cyclosporine, cimetidine, rifampin, terfenadine, and caffeine (Debrowolski 04: 14-16). Swift and effective treatment of bone infections is the best way of preventing invasive neoplasms from breaking through the bone to the marrow causing hematopoietic proliferative disorders better treated with modern chemotherapeutic agents. Plasma cell dyscrasias account for 15% of all deaths from malignant white cell disease. Plasma cell myeloma is the most important and most common syndrome characterized by multiple neoplastic tumorous masses of plasma cells scattered throughout the skeletal system. Waldenstrms macroglobulinemia associated with lymphadenopathy and hepatosplenomegaly, but the lytic bone lesions are not present. Heavy-chain disease is rare gammopathy infiltrating plasma cells and precursors that synthesize only heavy chains. Primary or immunocyte associated amyloidosis is a monoclonal proliferation of plasma cells, with excessive production of free light chains that are deposite as amyloid. Monoclonal gammopathy of undetermined significant. Expansion of incomplete monoclonal immunoglobulin secreting cells in the plasma and/or urine called dyscracias, gammopathies, monoclonal gammopathies, dysproteinemias, and paraproteinemias (Saunders 94: 662, 663). Normocytic, normochromic anemia is present in 60% of patients at diagnosis. It is due primarily to the decreased production of red blood cells by marrow, infiltration with plasma cells, and the suppressive effect of various cytokines. Patients with renal failure may also have decreased levels oferythropoietin (Drug information on erythropoietin), which can worsen the degree of anemia. Among newly diagnosed patients, up to 20% have hypercalcemia (corrected serum calcium level > 11.5 mg/dL) secondary to progressive bone destruction, which may be exacerbated by prolonged immobility, especially in the context of fracture. Hypercalcemia should be suspected in patients with myeloma who have nausea, fatigue, confusion, polyuria, or constipation. It may also suggest high tumor burden. It should be considered an oncologic emergency and requires prompt treatment with aggressive hydration, use of bisphosphonates, calcitonin, and antimyeloma therapy, including steroids. Approximately 20% of patients present with renal insufficiency and at least another 20% to 40% develop this complication in later phases of the disease. Light-chain cast nephropathy is the most common cause of renal failure. Additional causes include hypercalcemia, dehydration, and hyperuricemia. Less commonly, amyloidosis, light-chain deposition disease, nonsteroidal anti-inflammatory agents taken for pain control, intravenous radiographic contrast administration, and calcium stones may contribute to renal failure. Bisphosphonate therapy has been associated with the kidney problem azotemia, which is usually reversible with treatment cessation. Common Laboratory Features of Plasma Cell Dyscracias and Myeloma DiseaseLaboratory FeaturesMultiple MyelomaMarrow plasmacytosis >10% Clonal immunoglobulin peak > 3.0 g/dL Presence of Bence-Jones protein Lytic bone lesions and/or diffuse osteopenia Related organ or tissue impairmentSmoldering myelomaMonoclonal immunoglobin level > 3.0 g/dL No symptoms due to plasma cell dyscracia No lytic bone disease Normal calciu and renal function No anemiaSolitary plasmocytoma of boneSolitary lesion due to plasma cell tumor Normal skeletal survey and MRI of skull, spine and pelvis Normal bone marrow plasmacytosis No anemia, hypercalcemia or renal disease Preserved levels of uninvolved immunoglobulinsMonoclonal gammopathy of unkown significance (MGUS)Monoclonal immunoglobin level < 3.0 g/dL Bone marrow plasma cells < 10% No bone lesions No symptoms due to plasma cell dyscracia Usualy preserved levels of uininvolved immunoglobulins No related organ or tissue impairmentSource: Jagannath. Cancernetwork '11 Oral Thalidomide, used in conjunction with dexamethsaome, a corticosteroid, are the first FDA approved drugs usually taken by people diagnosed with multiple myeloma and plasma cell dyscracias. Others include: Bortezomib, Carfilzomib, Clafen (Cyclophosphamide), Cyclophosphamide, Cytoxan (Cyclophosphamide), Doxil (Doxorubicin Hydrochloride Liposome), Doxorubicin Hydrochloride Liposome, Dox-SL (Doxorubicin Hydrochloride Liposome), Evacet (Doxorubicin Hydrochloride Liposome), Kyprolis (Carfilzomib), Lenalidomide, LipoDox (Doxorubicin Hydrochloride Liposome), Mozobil (Plerixafor), Neosar (Cyclophosphamide), Plerixafor Pomalidomide (Pomalyst), Pomalyst HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/plerixafor" , Revlimid (Lenalidomide), Synovir (Thalidomide), Thalidomide, Thalomid (Thalidomide), Velcade (Bortezomib), Zoledronic Acid Zometa (Zoledronic Acid). Radiation therapy may be done to relieve bone pain or treat abone tumor. Two types of bone marrow transplantation may be tried: Autologous bone marrow or stem cell transplantation makes use of ones own stem cells. Allogeneic transplant makes use of someone elses stem cells. This treatment carries serious risks but offers the chance of improved survival. Many patients with myeloma develop bacterial infections that may be serious, and infectious complications remain the most common cause of death in myeloma patients. In the past, gram-positive organisms (eg,Streptococcus pneumoniae, Staphylococcus aureus) andHaemophilus influenzaewere the most common pathogens. More recently, however, infections with gram-negative organisms, anaerobes, and fungi have become frequent. The increased susceptibility of patients with multiple myeloma to bacterial infections, specifically with encapsulated organisms, has been attributed to impairments of host-defense mechanisms, such as hypogammaglobulinemia, qualitative deficiency in immunoglobulin function, granulocytopenia, decreased cell-mediated immunity, and the prolonged use of steroids and a prescription to metronidazole (Flagyl ER) is needed to treat bacterial infection of the bone. Waldenstrm macroblobulinemia, constituting about 5% of monoclonal gammopathies, is a disease of old age, usually the sixth and seventh decades. Half of atients have lymphadenopathy, hepatomegaly and splenomegaly. Visual impairment from distention and hemorrhage of retinal veins, neurologic problems such as headaches, dizziness, dafness and stupor, from sluggish blood flow; bleeding , cryoglobulinemia from precipitation of macroglobulins at low temperatures produces symptoms such as Raynauds phenomenon and cold urticarial. It is marked by a diffuse, leukemia-like infiltration of the bone marrow by lymphocytes, plasma cells and hybrid forms that synthesize a monoclonal IgM immunoglobulin, leading to macroglobulinemia. The tumor cells diffusely infiltrate the lymphoid tissues, including bone marrow, spleen and lymph nodes. Heavy chain disease is an extremely rare monoclonal gammopathy characterized by elevated levels in the blood or urine of specific heavy chain immunoglobulins. Gamma-chain disease is found most often in the elderly, and resembles malignant lymphoma, manifesting in lymphadenopathy, anemia, and fever, often accompanied by malaise, weakness and hepatomegaly or splenomegaly. The course can be rapidly downhill to death within a few months or protracted for years. Alpha-chain disease is most common occurring mostly in young adults in the Mediterranean area. Mu-chain disease is the rarest, most often encountered in patients with chronic lymphocytic leukemia, hepatomegaly and splenomegaly are usually present but peripheral lyumphadenopahty is inconspicuous. M proteins can be identified in the serum of 1% of asymptomatic healthy persons older than 50 years of age and in 3% older than 70 years. To this dysproteinemia without associated disease, the term monoclonal gammopathy of undetermined significance (MGUS) is applied. MGUS is the most common monoclonal gammopathy. Approximately 20% of patients develop well-defined plasma cell dyscrasia (myeloma, Waldenstrms macroglubinemia or amyloidosis) over a period of 10 to 15 years. In general patients with MGUS have less than 3 gm/dl of monoclonal protein in the serum and no Bence Jones proteinuria. Whether a given patient will follow a benign course, as most do, or develop well-defined plasma cell neoplasm cannot be predicted wherefore periodic assessment of serum M component levels and Bence Jones proteinuria is warranted (Saunders 94: 665, 666). In recent years, the drugsFludara (fludarabine) andLeustatin(cladribine) have become the first chemotherapy drugs given to people with Waldenstroms macroglobulinemia. SometimesCytoxan(cyclophosphamide) is added. Other commonly used chemotherapy drugs areLuekeran(chlorambucil) and prednisone, usually given together, or Adriamycin (doxorubicin). Sometimes an individual may start with one combination of drugs, then switch to another combination that is more effective. Another drug used to treat Waldenstroms macroglobulinemia isRituxan(rituximab). Some doctors may use this drug for hard-to-treat disease; others may combine it with chemotherapy drugs at the start of treatment.Campath(alemtuzumab) has also been an effective treatment, as has Velcade (bortezomib). The term histiocytosis is an umbrella designation for a varity of proliferative disorders of histiocytes of macrophages. Some histiocytic lymphomas are clearly malignant but reative histiocytic proliferations in the lymph nodes are benign. The Langerhans cell histiocytoses are associated with tumor like proliferations, but they are not truly neoplastic. The proliferating cell is the Langerhans cell of marrow origin which is normally found in the epidermis. Langerhans cell histiocytosis presents as three clincopathoogic entities. Acute disseminated Langerhans cell histiocytosis (Letterer-Siwe disease) occurs most frequently before two years of age but occasionally may affect adults. Cutaneous lesions resemble a seborrheic eruption secondary to to infiltration of Langerhans histiocytes over the front and back of the trunk and on the scalp. Most patients have hepatosplenomegaly, lymphadenopathy, pulmonary lesions and eventually destructive osteolytic bone lesions. Extensive infiltration of the marrow often leads to anemia, thrombocytopenia, and predisposition to recurrent infections such as otitis media and mastoiditis. The course of untreated disease is rapidly fatal with intensive chemotherapy 50% of patients survive 5 years. Unifocal lesions usually affect the skeletal system, they may be asymptomatic or cause pain and tenderness predisposing to stress fracture. It may heal spontaneously or be cured by local excision or irradiation. Multifocal Langerhans cell histiocytosis usually affects children who present with fever, diffuse eruptions, particularly on the scalp and in the ear canals, and frequent bouts of otitis media, mastoiditis and upper respiratory tract infections. An infiltrate of Langerhans cells may lead to mild lymphadenopathy, hepatomegaly, and splenomegaly. In about 50% of patients, involvement of the posterior pituitary stalk of the hypothalamus leads to diabetes insipidus,which does not seem to be treated with chemotherapy. The combination of calvarial bone defects, diabetes insipidus and exophthalmos is referred to as the Hand-Schller-Christain triad. Many patients experience spontaneous regression, others can be treated with chemotherapy (Saunders 94: 666, 667). Langerhans cell histiocytoses is treated with oral methotrexate (20 mg/m2) weekly for 6 months or oral thalidomide 50 mg to 200 mg nightly, with prednisone are taken for low risk disease or vinblastine IV and prednisone for patients with more complicated cases requiring radiation and surgery. The infections that lead to lymphadenitis are numerous. Lymph nodes undergo reactive changes whenever challenged by microbiologic agents or their toxic products, or by cell debris and foreign matter introduced into wounds or into the circulation, as in drug addiction. Acutely inflamed nodes are most commonly caused by direct microbiologic drainage and are seen most frequently in the cervical area in association with infections of the teeth or tonsils, or in the axillary or inguinal regions secondary to infections in the extremities. Generalized acute nonspecific lymphadenopathy is characteristic of viral infections and bacteremia. The nodal reactions in the abdomen may induce acute abdominal symptoms resembling acute appendicitis. The nodes become swollen, gray-red and engorged to the unaided eye. Clinically, nodes with acute nonspecific lymphadenitis are enlarged because of the cellular infiltration and edema. As a consequence of the distention of the capsule, they are tender to touch. When abscess formation is extensive, they become fluctuant. The overlying skin is frequently red, and sometimes penetration of the infection to the skin surface produces draining sinuses, particularly when the nodes have undergone suppurative necrosis. Healing of such lesions is associated with scarring (Saunders 94: 631, 632). Chronic nonspecific lymphadenitis assumes one of three patterns depending on their causation (1) follicular hyperplasia, (2) paracortical lymphoid hyperplasia and (3) sinus histiocytosis. Characteristically, lymph nodes in chronic reactions are not tender, because they are not under increased pressure. Chronic lymphadenitis is particularly common in inguinal and axillary nodes. Both groups drain relatively large areas of the body. Follicular hyperplasia is caused by chronic infections with microbes that activate B cells such as rheumatoid arthritis, toxoplasmosis, and early stages of human immunodeficiency virus (HIV) infection. It is distinguished by prominence of the large germinal centers, which appear to bulge against the surrounding collar of small B lymphocytes. There is generally striking hyperplasia of the mononuclear phagocytic cells lining the lymphatic sinuses. The lymph node architecture is preserved with normal lymphoid tissue between germinal centers, there is variation in the size and shape of lymphoid nodules and a mixed population of lymphocytes in different stages of differentiation. Paracortical lymphoid hyperplasia is characterized by reactive changes within the T-cell regions of the lymph node that encroach on, and sometimes efface the germinal follicles. There is hypertrophy of the sinusoidal and vascular endothelial cells and a mixed cellular infiltrate, principally of macrophages. Such changes are encountered with drugs such as Dilantin or following smallpox vaccination or other vaccine. Sinus histiocytosis refers to distention and prominence of the lymphatic sinusoids, encountered in lymph nodes draining cancers, particularly carcinoma of the breast. The lining endothelial cells are markedly hypertrophied, and the sinuses may be engorged with histiocytes. This pattern of reaction has been thought to represent an immune response on the part of the host against the tumor or its products (Saunders 632, 633). Lymphomas are malignant neoplasms characterized by the proliferation of cells native to the lymphoid tissues lymphocytes, histiocytes and their precursors and derivatives. There are no benign lymphomas. Among the broad group of malignant lymphomas, Hodgkins lymphoma is segregated from all other forms, which constitute the non-Hodgkins lymphomas. Although both have their origin in the lymphoid tissues, Hodgkins disease is set apart by the presence of a distinctive morphologic feature, the Reed-Sternberg giant cell. In addition the nodes contain non-neoplastic inflammatory cells, which in most cases outnumber the neoplastic element represented by the Reed-Sternberg cell. Non-Hodgkins lymphomas (NHL) presents as a localized or generalized lymphadenopathy. Lymph node enlargement due to lymphomatous disease must be differentiated from that caused by the more frequent infectious and inflammatory disorders. Although variable, all forms of lymphoma have the potential to spread from their origin in a single node or chain of nodes to other nodes, and eventually disseminate to the spleen, liver and bone marrow when it creates a leukemia-like picture in the peripheral blood. The vast majority of NHLs (80-85%) are of B cell origin, the remainder are in large part T cell tumors. Growth patterns are either clustered into identifiable nodules or spread diffusely throughout the node. Nodular or follicular architecture has a superior prognosis to that of diffuse pattern. Divided into three prognostic groups, NHLs are designated as low, intermediate and high grade lymphomas with 10 years survival rates of 45, 36 and 23% respectively (Saunders 94: 634-636). Drug for the treatment of Non-Hodgkin's lymphoma are Abitrexate (Methotrexate), Adcetris (Brentuximab Vedotin), Adriamycin PFS (Doxorubicin Hydrochloride), Adriamycin RDF (Doxorubicin Hydrochloride), Ambochlorin (Chlorambucil), Amboclorin (Chlorambucil), Arranon (Nelarabine), Bendamustine Hydrochloride, Bexxar (Tositumomab and Iodine I 131 Tositumomab), Blenoxane (Bleomycin), Bleomycin, Bortezomib, Brentuximab Vedotin, HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/bortezomib"  Chlorambucil, Clafen (Cyclophosphamide), Cyclophosphamide, Cytoxan (Cyclophosphamide), Denileukin Diftitox, DepoCyt (Liposomal Cytarabine), Doxorubicin Hydrochloride, DTIC-Dome (Dacarbazine), Folex (Methotrexate), Folex PFS (Methotrexate), Folotyn (Pralatrexate), Ibritumomab Tiuxetan, Intron A (Recombinant Interferon Alfa-2b) HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/ibritumomabtiuxetan" , Istodax (Romidepsin), Leukeran (Chlorambucil), Linfolizin (Chlorambucil), Liposomal Cytarabine, Matulane (Procarbazine Hydrochloride), Methotrexate, Methotrexate LPF (Methotrexate), Mexate (Methotrexate), Mexate-AQ (Methotrexate), Mozobil (Plerixafor), Nelarabine, Neosar (Cyclophosphamide), Ontak (Denileukin Diftitox), Plerixafor Pralatrexate, Recombinant Interferon Alfa-2b HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/pralatrexate" , Rituxan (Rituximab), Rituximab, Romidepsin, Tositumomab and Iodine I 131 Tositumomab, Treanda (Bendamustine Hydrochloride), Velban (Vinblastine Sulfate), Velcade (Bortezomib), Velsar (Vinblastine Sulfate), Vinblastine Sulfate, Vincasar PFS (Vincristine Sulfate), Vincristine Sulfate, Vorinostat, Zevalin (Ibritumomab Tiuxetan), Zolinza (Vorinostat) and combinations CHOP, COPP, CVP, EPOCH, ICE, R-CHOP. Non-Hodgkins Lymphomas Lymphoma type% of CasesMorphologyImmuno-phenotypeCommentsSmall lymphocytic Lymphoma3-4Small unstimulated lymphocytes in a diffuse pattern>95% B cellsOccurs in old age; generalized lymphadenopathy with marrow involvement and blood picture resembling CLLFollicular lymphomas40Germinal center cells arranged in follicular patternB cellsFollicular small cleaved cell type most common; occur in older patients; generalized lymphadenopathy; difficult to cureDiffuse lymphomas40-50Various cell types; predominantly large germinal center cells, some mixed with smaller cells; others with immunoblastic morphology~80% B cells ~20% post-thymic T cellsOccur in older patients as well as pediatric age group; greater frequency of extranodal, visceral disease; marrow involvement and leukemia very uncommon at diagnosis and poor prognostic sign; aggressive tumors but up to 60% are curable.Lymphoblastic lymphoma4Cells somewhat larger than lymphocytes; in many cases nuclei markedly lobulated; high mitotic rate>95% immature intrathymic T cellsOccurs predominantly in children (40% of all childhood lymphomas); prominent mediastinal mass; early involvement of bone marrow and progression to T-cell ALL, very aggressiveSmall noncleaved (Burkitts) Lymphoma<1Cells intermediate in size between small lymphocytes and immunobasts; prominent nucleoli; high mitotic rateB cellsEndemic in Africa, sporadic elsewhere; predominantly affects children; extranodal visceral involvements presenting features; rapidly progressive but responsive to therapy; translocation characteristicMycosis fungoides and Szary SyndromeUncommonMedium to large cells with markedly convoluted (cerebriform) nucleusCD4+ T cellsOccur in older males; proclivity for involvement of skin in both forms; tumorous masses in mycosis fungoides; Szary syndrome is a leukemic variantAdult T-cell leukemia lymphomaRareVery variable; cells may have cerebriform nucleiCD4+ T cellsAssociated with HTLV-1 infection; endemic in Japan and the Caribbean;cutaneous lesions, leukemia, spleen and lymph node involvement; rapidly fatalSource: Saunders 94: Table 14-4, 644 Hodgkins lymphoma is characterized by the presence of distinctive neoplastic giant cells called Reed-Sternberg (RS) cells, admixed with a variable inflammatory infiltrate and fever. It accounts for 0.7% of all new cancers in the United States (7,400 new cases). It is one of the most common forms of malignancy in young adults, with an average age of at diagnosis of 32 years. It is now considered to be curable in most cases. There are four subtypes of Hodgkins disease (1) lymphocyte predominance, (2) mixed cellularity, (3) lymphocyte depletion and (4) nodular sclerosis. The staging of Hodgkins disease is of great clinical importance, since the course, choice of therapy and prognosis all are intimately related to the distribution of the disease that must be investigated with lymphangiography or computed tomography of abdomen and pelvis, chest radiograph, biopsy of bone marrow and ultrasonography of liver and spleen. Hodgkins disease presents with a painless enlargement of lymph nodes. Younger patients tend to present in clinical stage I or II and are usually free from systemic manifestations. Patients with disseminated disease (stages III and IV) are more likely to present with systemic complaints, such as fever, unexplained weight loss pruritus and anemia. Cutaneous anergy resulting from depressed cell-mediated immunity is seen in most cases. The 5- year survival rate of patients with stages I and IIA is close to 90% and many can be cured. Even with advanced disease (stages IVA and IVB), 60 to 70% 5 year disease free survival can be achieved. Long-term survivors of chemotherapy and radiotherapy have an increased risk of developing second cancers. Acute nonlymphocytic leukemia and lung cancer lead the list of second malignancies, but also include NHL, breast cancer, gastric cancer and malignant melanoma. The many therapeutic steps forward in the light of this unhappy byproduct, may involve a few steps backward (Saunders 94: 643, 644, 647, 648). Drug treatments for Hodgkin's Lymphoma include Adcetris (Brentuximab Vedotin), Adriamycin PFS (Doxorubicin Hydrochloride), Adriamycin RDF (Doxorubicin Hydrochloride), Ambochlorin (Chlorambucil), Amboclorin (Chlorambucil), HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/BEACOPP"  Blenoxane (Bleomycin), Bleomycin, Brentuximab Vedotin, HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/bleomycin"  Chlorambucil, Clafen (Cyclophosphamide), Cyclophosphamide, Cytoxan (Cyclophosphamide), Dacarbazine, Doxorubicin Hydrochloride, DTIC-Dome (Dacarbazine), Leukeran (Chlorambucil), Linfolizin (Chlorambucil), Lomustine, Matulane (Procarbazine Hydrochloride), Neosar (Cyclophosphamide), Procarbazine Hydrochloride, Velban (Vinblastine Sulfate), Velsar (Vinblastine Sulfate), Vinblastine Sulfate, Vincasar PFS (Vincristine Sulfate), Vincristine Sulfate, combinations; ABVD, ABVE, ABVE-PC, BEACOPP, COPP, ICE, MOPP, STANFORD and VAMP. The cure of Hodgkin lymphoma in the 20th century is another one of cancers biggest success stories. Breakthroughs in radiation therapy and chemotherapy paired with surgical removal of metastatic tumors and careful clinical research transformed an invariably fatal disorder into one that is routinely cured.The recognition of late adverse effects from radiation therapy and chemotherapy in the form of second cancers, heart and blood vessel disease, and sterility shaped subsequent research efforts to maintain or improve cure rates with fewer complications, an important goal in a disease that primarily affects individuals in their 20s and 30s. Today, as more than 80 percent of patients are cured after primary treatment. Sir Thomas Hodgkin is credited with the initial description of the clinical disorder that bears his name. In 1832, he reported on a group of patients with enlargement of lymph nodes and spleen that differed from the major known maladies of the day. The introduction of the linear accelerator (a radiation machine used to treat cancer) in the treatment of Hodgkin lymphoma at Stanford University resulted in cures of early-stage lymphoma. Meanwhile, a team at the National Cancer Institute safely combined four chemotherapy drugs (mustard, vincristine, procarbazine, and prednisone) known as the MOPP regimen and reported the first cures of advanced Hodgkin lymphoma in 1964. Steadily improving techniques for defining the extent and location of disease (staging) has allowed appropriate modalities of treatment to be selected for individual patients. The late 1970s and 80s presented new challenges in the recognition of adverse effects associated with MOPP and radiation therapy, some of which were not apparent for decades after treatment. This time period also featured another major advance in an alternative four-drug chemotherapy regimen (doxorubicin, bleomycin, vinblastine, and dacarbazine), known as ABVD, that proved to be more effective than MOPP in treating advanced disease and had fewer side effects. In the 1990s, even more effective and less toxic treatments for early-stage lymphoma were devised by reducing the dose and area of the body treated with radiation therapy in combination with briefchemotherapy such as ABVD. The German Hodgkin Study Group introduced an intensive seven-drugchemotherapy program, BEACOPP, to address thefact that approximately 30 percent of advancedHodgkin's lymphoma was not cured with ABVD. Although associated with more severe early toxicity andsterility, a higher cure rate and improved survival were achieved with BEACOPP in a randomized clinicaltrial (Horning '08). Although orally available methotrexate is prescribed for non-Hodgkin's lymphoma, there does not seem to be any FDA approved alternative to IV chemotherapy. The development of the drug rituximab as a therapy for B-cell lymphoma (a type of cancer affecting cells of the immune system) provides an excellent illustration of how great improvements in patient care were made through the discovery of a therapy that destroys cancer cells without harming other cells in the body. The discovery of rituximab, an antibody that recognizes CD20, a target shared by malignant lymphoma cells from almost all patients, but also found on normal, immune B cells. Rituximab proved to be effective in treating B-cell lymphoma, and the elimination of normal B cells was surprisingly not harmful. Because rituximab does not affect other normal cells in the body, it can be combined with other therapies. Today, rituximab is part of the regular treatment for almost all patients with B-cell lymphoma, and it has prolonged the lives of many of them. Rituximab can also treat many non-cancerous diseases caused by overactive B cells of the immune system. Rituximab has been used to treat rheumatoid arthritis, multiple sclerosis, and a growing list of non-cancerous conditions (Levy, Malony & Miller '08). There were 48,610 new cases and 23,720 deaths from leukemia estimated in the United States in 2013. The leukemias are malignant neoplasms of the hematopoietic stem cells characterized by diffuse replacement of the bone marrow by neoplastic cells. These cells may also infiltrate the liver, spleen, lymph nodes and other tissues throughout the body. Although the presence of excessive numbers of abnormal cells in the peripheral blood is the most dramatic manifestation of leukemia, it should be remembered that the leukemias are primary disorders of the bone marrow although some patients with a diffusely infiltrated bone marrow may present with leukopenia. Traditionally, leukemias are classified on the basis of the cell type involved and the state of maturity of the leukemic cells. Thus acute leukemias are characterized by the presence of very immature cells (called blasts) and by a rapidly fatal course in untreated patients. On the other hand, chronic leukemias are associated, at least initially, with well-differentiated (mature) leukocytes and with a relatively indolent course. Two major variants of acute and chronic leukemias are recognized: lymphocytic and myelocytic (myelogenous). Thus, a simple classification would have four patterns of leukemia: acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), acute myelocytic (myeloblastic) leukemia (AML), and chronic myelocytic leukemia (CML). Acute leukemias are associated with replacement of normal marrow elements by a sea of proliferating blast cells that do not seem to undergo normal maturation. Consequently, there is a loss of mature myeloid elements such as red cells, granulocytes, and platelets, and hence clinical features of acute leukemias are dominated by anemia, infections and hemorrhages. In chronic leukemia the grouping together of chronic lymphocytic and myelogenous leukemias is problematic. Neither of these disorders is rapidly fatal, but the clinical and morphological features that seem to unite the acute leukemias are lacking. In chronic myelogenous leukemia (CML), polycythemia vera, essential thrombocytopenia, and myeloid metaplasia are related disorders that represent clonal, neoplastic proliferations of the multipotent myeloid stem cells. The term chronic myeloproliferative disorders, best describes these neoplasms of the myeloid stem cell (Saunders 94: 648, 649). Differential Diagnosis of Leukemias and Lymphomas Type of LeukemiaDiagnosisCommentsAcute LeukemiasAnemia almost always present. White cell count elevated as high as 100,000 cells per L but in 50% is less than 10,000 cells per L. Immature white cells, including blast forms, make up 60 to 100% of all blood and marrow cells. Platelet count usually depressed to depressed to less than 100,000 per L Presents within 3 months of onset of fatigue due to anemia, fever reflecting an infection due to absence of mature leukocytes, bleeding (petechiae, ecchymoses, epistaxis gum bleeding secondary to thrombocytopenia; bone pain and tenderness, lymphadenopathy, splenomegaly and hepatomegaly; Central nervous system manifestations, such as headache, vomiting and nerve palsies resulting from meningeal spread.Acute lymphoblastic leukemia (ALL)90% of patients have numerical or structural changes to chromosomes of the leukemia cells hyperdiploidy >50 chromosomes is a good indicator, pseudoploidy of 46 structurally rearranged chromosomes, or translocations come with a poor prognosis for which allogenic bone marrow transplantation offers hope.2500 new cases per year. Primarily disease of children and young adults. 80% of childhood leukemias. Twice as common in whites as in nonwhites and more frequent in boys than in girls. Testicular involvement is common. More than 90% remission and two-thirds cure rate with modern chemotherapy. 90% of patients have chromosomal changesAcute myeloblastic leukemia (AML)Diagnosed if bone marrow contains more than 30% myeloblasts. Chromosomal abnormalities in 90% of patients. 50 to 70% of cases karyotypic changes can be detected by standard cytogenetic techniques. AML divided into eight categories depending on the degree of maturation (1) minimally differentiated AML, (2) AML without differentiation, (3) AML with maturation, (4) Acute promyelocytic leukemia, (5) acute myelomonocytic leukemia, (6) acute monocytic leukemia, (7) acute erytroleukemia, (8) acute megakaryocytic leukemiaAffects adults from ages 15 to 39 years. 20% of childhood leukemias. Diverse origin transformation of multipotent (trilineage) myeloid stem cells as evidenced by common cytogenetic abnormalities in granulocytic and erythroid precursors, though myeloblasts dominate the blood and bone marrow. Or common granulatocyte monocyte precursor involvement gives rise to myelomonocytic disease. Difficult to treat, 60% achieve remission but only 15 to 30% remain free for five years. 50 to 60% of those who undergo allogeneic bone marrow transplantation at first remission appeared cured.Myelodysplastic syndromesGroup of clonal stem cell disorders with maturation defects resulting in ineffective hematopoiesis and an increased risk of transformation to acute myeloblastic leukemias. Bone marrow is partly or wholly replaced by the clonal progeny of a mutant pluripotent stem cell that retains the capacity to differentiate into red cells, granulocytes and platelets, but in a manner that is both ineffective and disordered resulting in bone marrow that is usually hypercellular or normocellular, but the peripheral blood shows pancytopenia. The abnormal stem cell clone is unstable and prone to acute leukemia.Pre-leukemic condition affecting older people between 60 and 70 years of age. Patients present with weakness, infections and hemorrhages, all due to pancytopenia. Approximately half of the patients are asymptomatic, and the disease is discovered incidentally to blood tests. Ten to forty percent progress to frank AML. Median survival varies from 9 to 29 months. Chronic myeloid leukemia (CML)Neoplastic cloned pluripotent stem cell affecting virtually all hematopoietic lineages. Distinctive cytogenetic and molecular abnormality. >90% Ph chromosome reciprocal translocation t(9;22)(q34;q11). 10-20 fold increase in the mass of granulocytic precursor cells with smaller number of normal progenitor cells in the marrow. Usually elevated leukocyte count commonly exceeding 100,000 cell per mm3 circulating cells predominantly neutrophis and metamyelocytes, but basophils and eosinophils are also prominent. A small number of myeloblasts (<10%) can be found in peripheral blood. Up to 50% have thrombocytosis early in the course of disease. Almost total lack of alkaline phosphatase in granulocytes. The diagnostic feature is the presence of Ph chromosome and bcr-c-abl rearrangements. 15 to 20% of all cases of leukemia. Primarily affects adults between the ages of 25 and 60 years, with the peak incidence in the fourth and fifth decades of life. Initial symptoms are anemia or hypermetabolism due to increased cell turnover and include easy fatigability, weakness, weight loss and anorexia. Slow progression, without treatment a median survival of 3 years can be expected. After a variable period averaging 3 years, about 50% of patients have a leukemic blast crisis. In 70% the blasts have the features of myeloblasts, whereas the remaining 30% contain the enzyme TdT and express B-lineage antigens. Treatment is unsatisfactory. Although it is possible to induce remissions with chemotherapy, the median survival of 3 to 4 years is unaltered. Bone marrow transplantation is the only curative treatment. After the development of blast crisis all forms of treatment become virtually ineffective.Chronic lymphocytic leukemia (CLL)Lymphoid malignancy of B cells, T cells rare <5%. 50% of patients will CLL have abnormal karyotypes, Trisomy 2 is most common, in one-third of patients, with a poor prognosis. Total leukocyte count may be increased slightly or can reach 200,000 per mm3. Smudge cells with crushed nuclei of lymphocytes are common in peripheral blood smears. 25% of all leukemias in the US and Europe. Typically occurs in persons over 50, median 60 years, males twice as often as females. Uncommon in Japan and other Asian countries. Often asymptomatic, easy fatigability, loss of weight and anorexia. Generalized lymphadenopathy and hepatosphenomegaly are present in 50 to 60% of cases. Median survival is 4 to 6 years and blast crisis are uncommon.Hairy cell leukemiaFine hairlike projections on leukemic cells. Tartrate resistant acid phosphatase (TRAP) in neoplastic B cells. Pancytopenia, resulting from marrow failure and splenic sequestration, is seen in more than half the cases. Leukocytosis present in only 25% of patients. Hairy cells can be identified in the peripheral blood smear in most cases. Hairy cell leukemia occurs mainly in older males and its manifestations result largely form infiltration of bone marrowy, liver and spleen. Splenomegaly is more common than hepatomegaly. Lymphadenopathy is rare. Splenectomy is of benefit in two-thirds of patients. With old treatment median survival was less than 5 years, however, treatment with interferon- and newer chemotherapeutic agents has led to lasting remissions and possibly cures.Polycythemia veraProliferation of erythroid, granulocytic and megakaryocytic elements, all derived from clonal expansion of a pluripotent stem cell. Absolute increase in red cell mass due to domination of erythroid precursors. Associated with virtually undetectable levels of serum erythropoietin. Hemoglobin concentration ranges from 14 to 28 gm/dl with hematocrit values of 60% or more. The white cell count is elevated, ranging between 12,000 and 50,000 cells per mm3. The major anatomic changes stem from the increase in blood volume and viscosity brought about by the erythrocytosis. Plethoric congestion of all tissues and organs. The bone marrow is hypercellular. Hematopoiesisn expands markedly to replace fatty marrow. As the disease progresses the marrow becomes fibrotic (myelofibrosis) or may be replaced by blasts (leukemic transformation). The liver is enlarged and frequently contains foci of myeloid metaplasia. The spleen is also slightly enlarged, up to 250 to 300 gm. Appears insidiously in late middle age ~60 years. Blood is deoxygenated, patient has headache, dizziness, gastrointestinal symptoms, hematemesis, and melena common, 30% develop thrombotic complications affecting the brain and heart. Hemorrhages occur in a third of patients. Life threatening hemorrhages occur in 5 to 10% of cases. In patients who receive no treatment, death from vascular episodes occurs within months, however if that red cell mass can be maintained at nearly normal levels by phlebotomies, median survival of 10 years can be achieved. Myeloid metaplasia with myelofibrosisProliferation of neoplastic myeloid stem cells occurs principally in the spleen (myeloid metaplasia) and in the fully developed syndrome the bone marrow is hypercellular and fibrotic (myelofibrosis). Spleen is sometimes as large as 4000gm. Moderate to severe normochromic norocytic anemia. Red cells show all manner of variation in size and shape, but characteristic are teardrop-shaped erythrocytes (poikilocytes). The white cell count may be normal , reduced or elevated to 80,000 to 100,000 cells per mm3 basophils are usually prominent. Platelet count is normal or elevated at time of diagnosis but thrombocytopenia supervenes. Biopsy of the marrow to detect the early deposition of reticulin or the more advanced fibrosis is essential for diagnosis. Uncommon in individuals younger than 60 years. Usually begins with progressive anemia or marked splenic enlargement, producing a dragging sensation in the left upper quadrant. Fatigue, weight loss and night sweats from increased metabolism from expanded mass of myeloid cells. Hyperuricemia and secondary gout may complicate the picture. Median survival time varies from 1 to 5 years. Threats to life are recurrent infections, thrombotic episodes or bleeding related to platelet abnormalities and in 5 to 20% of cases, transformation to acute myeloid leukemia.Source: Saunders 94: 648-662 Historically, patients with CML lived no more than three to five years, during which time the disease would quickly transform from a chronic leukemia to an aggressive and fatal acute leukemia. In 1960, Peter Nowell and David Hungerford, working in Philadelphia, described a shortened chromosome in the blood and bone marrow of patients with CML. This was the first consistent chromosomal abnormality associated with a human cancer. Then, in 1973, Janet Rowley showed that this abnormal chromosome, now called the Philadelphia chromosome, came about because of an exchange of genetic material between two chromosomes. In the 1980s, it was demonstrated that the consequence of this chromosome exchange was the production of an abnormal gene calledBCR-ABL fueling the excess growth of white blood cells in CML. With the target identified, a drug discovery program was started, aimed at developing a drug to shut down the activity ofBCR-ABL. The compound that became known as imatinib (Gleevec) was developed in 1992, and studies showed that this compound killed CML cells without harming normal cells. In 1998, the drug was tested in patients with CML who had exhausted standard treatment options and whose life expectancy was limited. Within six months of starting the clinical trials of imatinib, all of the patients had their blood counts return to normal. Remarkably, this once-a-day pill had minimal side effects. These unprecedented results were confirmed in much larger clinical trials, and imatinib was approved by the U.S. Food and Drug Administration (FDA) in 2001, less than three years from the start of the clinical trials. With longer follow-up, this once routinely fatal leukemia now has a five-year survival rate of 95 percent. Newer drugs (dasatinib and nilotinib) have been developed that can shut down most of the mutated forms ofBCR-ABL, and have significant activity in patients with resistance to imatinib; these drugs are also FDA-approved (Druker '08). The spleen is secondarily involved in a wide variety of system disorders. As the largest unit of monomuclear phagocyte system, the spleen is involved in all systemic inflammations and generalied heatopoietic disorders and many metabolic disturbances. When the spleen is involved in systemic disease, splenic enlargement usually develops, and therefore splenomegaly is a major manifestation of disorders of this organ. When suffidiencly enlarged, the spleen may cause a dragging sensation in the left upper quadrant and through pressure on the stomach, cause discomfort after eating. It storage function may lead to the sequestration of significant numbers of blood elements, giving rise to a syndrome known as hypersplenism, which is characterizd by the triad of (1) splenomegaly, (2) a reduction of one or more of the cellular elements of the blood eading to anemia, leukopenia, thrombocytopenia, or any combination of these, in associatin with hyperplasia of the marrow precursors of the deficient cell types and (3) correction of the blood cytopenia(s) by splenectomy (Saunders 94: 669, 670). Enlargement of the spleen, sometimes also called acute splenic tumor, occurs in any blood-borne infection. The spleen is enlarged up to 200 to 400 gm. The splenic substance may be so soft as to flow out form the cut surface. Microscopically the major change is acute congestion of the red pulp, which may encroach on and sometimes efface the lymphoid follicles. At times there is acute necrosis of the centers of the splenic follicles. Congestive splenomegaly occurs when chronic congestion of the splenic vein or extrahepatic portal vein causes enlargement of the spleen, referred to as congestive splenomegaly, most commonly caused by the various forms of cirrhosis of the liver but particularly alcoholic cirrhoses. The venous congestion ultimately leads to portal or splenic vein hypertension. Thrombosis of the splenic vein may be initiated by the pressure of tumors in the neighboring organs. Systemic or central venous, congestion is encountered in cardiac decompensation involving the right side of the heart, as may occur in tricuspid or pulmonic valvular disease or chronic cor-pulmonale or following left-sided heart failure causing only moderate enlargement of the spleen, that rarely exceeds 500 gm in weight. Long-standing congestive splenomegaly produces enlargement of the spleen from 1000 5000 gm. The impairment of blood fow results in excessive destruction (hypersplenism). Focal hemorrhags give ris to Gandy-Gamna nodules fibrosis containing deposits of iron and calcium salts encrusted with connective tissue and elastic fibers. Splenic infarcts are comparatively common lesions caused by occlusion of the major splenic artery or any of its branches, alsmoalways due to emboli in the heart. The infarcts may be small or large pale wedge-shaped emboli, usually of the bland, anemic type. Septic infarcts are found in infective endocarditis of the valves of the left side of the heart. Neoplastic involvement of the spleen is rare except in tumors of the lymphohematopoietic system and the following types of benign tumors may aris in the spleen: fibromas, osteomas, chondromas, lymphangiomas, and hemangiomas. Congenital anomalies may involve rarely a complete absence of the spleen usually with other abnormalities such as situs inversus and cardiac malformations. Hypoplasia is more common and accessory spleens (spleniculi) are common and have been encountered singly or multiply. In some heatologic disorders such as hereditary spherocytosis, thrombocytopenic purpura and hypersplenism, splenectomy is a standard method of treatment but if a large accessory spleen is overlooked, the benefit of removal of the definitive spleen may be lost. Rupture of the spleen is usually caused by crushing injury or severe blow but rarely spontaneously ruptures in the absence of physical trauma most often in infectious monoceosis, malaria, typhoid fever, leukemia and the other types of acute splenitis. Rupture is usually followed by extensive, sometimes massive, intraperiotoneal hemorrhage. The condition usually must be treated by prompt surgical removal of the spleen to prevent death from loss of blood and shock (Saunders 94: 670, 671). 11. Vascular Neoplasms Primary tumors of the heart are rare but metastatic tumors to the heart occur in about 5% of patients dying from cancer. The most common primary tumors, in descending order of frequency are myxomas, fibromas, lipomas, papillary fibroelastomas, rhabdomyomas, angiosarcomas and other sarcomas. The five most common all are benign and account collectively for 80 to 90% of primary tumors of the heart. Myxomas are the most common primary tumor of the heart in adults. About 90% are located in the atria. Surgical removal is usually curative, although rarely the neoplasm recurs months to years later. Lipomas are most often located in the left ventricle, right atrium or atrial septum and are not necessarily neoplastic. In the atrial septum, the depositions are called lipomatous hypertrophy. Papillary fibroelastomas cluster as hair-like projections up to 1 cm in diameter, covering up to several centimeters of the endocardial surface. Rhabdomyomas are the most frequent primary tumor of the heart in infants and children. Cardiac angiosarcomas and other sarcomas are not distinctive from their counterparts in other locations. Occasionally cardiac complications represent the dominant feature of the presentation of a noncardiac malignant tumor. Chemotherapy and radiation also manifest their own district cardiovascular side effects and toxicities (Schoen 94; 569-571). In patients with carcinoid tumors, cardiac involvement, is one of the sequelae of the carcinoid syndrome. The syndrome is characterized by distinctive episodic flushing of the skin and cramps, nausea, vomiting and diarrhea in almost all patients; bronchoconstrictive episodes resembling asthma in about one-third of patients, and cardiac lesions in about one-half. The carcinoid syndrome is encountered in about 1% of patients who have carcinoid tumors (argentaffinomas) whatever the primary site and in 10% of those with gastrointestinal carcinoid tumors with hepatic metastes (Schoen 94: 555). Peripheral artery disease refers to changes in the aorta and its branches, the arteries. Aortic aneurysms can form along any part of this main blood vessel, or one of its branches. Sometimes the force of blood under high pressure will rip the lining of the aorta, this is called aortic dissection, or a dissecting aneurysm if it occurs in one of the enlarged areas. A number of changes can occur in the arteries, the veins and the optic nerve that connect to the eye, and the retina, where vision is detected on the back surface of the eyeball. Treatment for severe diabetic eye complications is more successful when blood pressure is normal (Wilson & Childre 06: 9, 40). Varicose veins and phlebothrombosis/thrombophlebitis together account for at least 90% of clinical venous disease. Varicose veins are abnormally dilated, tortuous veins produced by prolonged, increased intraluminal pressure. The superficial veins of the leg are the preponderant site of involvement, however, portal hypertension, usually due to cirrhosis of the liver, leads to varices in the esophageal and hemorrhoidal veins. It is estimated that 10 to 20% of the general population eventually develop varicose veins in the lower legs. The condition is much more common over age 50, in obese persons, and in women, a reflection of the elevated venous pressure in the lower legs caused by pregnancy. Occupations that require long periods of standing and long automobile or airplane rides frequently lead to marked venous stasis and pedal edema, even in normal individuals. Varicose dilation of veins renders the valves incompetent and leads to venous stasis, congestion edema, and thrombosis. Despite thrombosis of superficial varicose veins, embolism is very rare. Distention of the veins is often painful, but most patients have no symptoms until marked venous stasis and edema develop. Some of the most disabling sequelae are the development of persistent edema in the extremity and trophic changes in the skin that lead to stasis dermatitis and ulcerations. Because of the impaired circulation the tissues of the affected part are extremely vulnerable to injury. Wounds and infections heal slowly or tend to become chronic varicose ulcers. Because venous thrombosis inevitably leads to inflammatory changes within the vein wall, thrombophlebitis and phlebothrombosis are two designations for a single entity. Cardiac failure, neoplasia, pregnancy, obesity, the postoperative state, and prolonged bed rest or immobilization predispose to venous thrombosis. The deep leg veins account for more than 90% of cases of thrombophlebitis (Schoen 94: 504, 505, 506). Vascular neoplasms are divided into benign, intermediate and malignant based on two major anatomic characteristics (1) the degree of which the neoplasm is composed of well-formed vascular channels and (2) the extent and regularity of the endothelial cell proliferation. In general benign neoplasms are made up largely of well-formed vessels with well-differentiated endothelial cell proliferation, in contrast, malignant tumors are solidly cellular and anaplastic, with scant number of only poorly developed vascular channels. Benign tumors are several types of hemangioma, including capillary, cavernous, epithelioid, granuloma pyogenicum and deep soft tissue hematoma; Glomus tumor, and vascular ectasias. Intermediate tumors are hemangioendothelioma and epithelioid hemangioendothelioma. Malignant tumors are angiosarcoma, hemangiopericytoma and Kaposis sarcoma (Schoen 94: 506). Angiogenesis is the formation of new blood vessels. This process involves the migration, growth, and differentiation of HYPERLINK "http://www.cancer.gov/Common/PopUps/popDefinition.aspx?id=CDR0000044203&version=Patient&language=English" endothelial cells, which line the inside wall of blood vessels. The process of angiogenesis is controlled by chemical signals in the body. These signals can stimulate both the repair of damaged blood vessels and the formation of new blood vessels. Other chemical signals, called angiogenesis inhibitors, interfere with blood vessel formation. Normally, the stimulating and inhibiting effects of these chemical signals are balanced so that blood vessels form only when and where they are needed. Bevacizumab was the first angiogenesis inhibitor that was shown to slow tumor growth and, more important, to extend the lives of patients with some cancers. The FDA has approved other drugs that have antiangiogenic activity, including sorafenib (Nexavar), sunitinib (Sutent), pazopanib (Votrient), and everolimus (Afinitor). Sorafenib is approved for hepatocellular carcinoma and kidney cancer, sunitinib and everolimus for both kidney cancer and neuroendocrine tumors, and pazopanib for kidney cancer. Angiogenesis inhibitors are unique cancer-fighting agents because they tend to inhibit the growth of blood vessels rather than tumor cells. In some cancers, angiogenesis inhibitors are most effective when combined with additional therapies, especially chemotherapy. Hemangiomas are extremely common tumors, particularly in infancy and childhood, constituting 7% of all benign tumors. Capillary hemangiomas are composed of blood vessels that resemble cappilaries, narrow, thin-walled, and lined by relatively thin endothelium, usually occurring in the skin, subcutaneous tissues and mucous membranes of the oral cavities and lips, they may also occur in the internal viscera, such as the liver, spleen, and kidneys. Varying in size from a few millimeters up to several centimeters in diameter, they are bright red to blue, level with the surface of the skin or slightly elevated, with intact covering epithelium. The strawberry type of capillary hemangioma (juvenile hemangiomas) of the skin of newborns grows rapidly in the first few months, begins to fade when the child is one to three years old, and regresses by age five in 80% of cases. Cavernous hemangiomas are distinguished by the formation of large cavernous vascular channels. Often occurring in childhood, they have a predilection for the skin of the head and neck and mucosal surfaces of the body but are also found in many viscera, particularly the liver, spleen, pancreas and occasionally the brain. The usual cavernous hemangioma is a red-blue, soft, spongy mass 1 to 2 cm in diameter. In most situations the tumors are of little significance but can be a cosmetic disturbance, and when present in the brain, and potential source of increased intracranial pressure or hemorrhage (Schoen 94: 507). Granuloma Pyogenicum are of uncertain neoplastic nature. These masses appear as exophytic red nodules on the skin and gingival or oral mucosa and are often ulcerated. One-third of lesions develop after trauma, growing rapidly to reach a maximum size of 1 to 2 cm within a few weeks. Pregnancy tumor (granuloma gravidarum) is a granuloma pyogenicum occurring in the gingiva of 1 to 5% of pregnant women that regresses after delivery. Glomus tumor (Glomangioma) is a benign but exquisitely painful tumor that arises from the modified smooth muscle cells of the glomus body, a neuromyoarterial receptor that is sensitive to variations in temperature and regulates arteriolar flow. Glomus bodies may be located anywhere in the skin but are most commonly found in the distal portion of the digits, especially under the fingernails. Lesions are usually under 1 cm in diameter, and many are less than 3 mm. When present in the skin, they are slightly elevated, round, red-blue, firm, exquisitely painful modules (Schoeb 984: 507, 509). Vascular extasias (Telangiectases) designates a group of abnormally prominent capillaries, venules, and arterioles that creates a small focal red lesion, usually in the skin or mucous membranes, and are more representative of congenital anomalies than true neoplasms. Nevus flammeus, is a ten-dollar term for the ordinary birthmark. Most commonly on the head and neck, they range in color from light pink to deep purple and are ordinarily flat. The vast majority ultimately fade and regress. A special form of nevus flammeus, the so-called port-wine stain, may grow proportionately with a child, thicken the skin surface and become unsightly. Port wine stains in the distribution of the trigeminal nerve may be associated with the Sturge-Weber syndrome (encephalotrigeminal angiomatosis). Spider telangiectasis consists of a focal minute network of subcutaneous small arteries or arterioles arranged in a radial fashion about a central core. It is usually found on the upper pasts of the body, particularly the face, neck and upper chest, and is most common in pregnant women or in patients with liver disease, particularly cirrhosis of the liver, or with high levels of estrogen. Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu Disease) is characterized by multiple small aneurysmal telangiectases distributed over the skin and mucous membranes, present from birth as a dominant trait, affecting both sexes equally, about 20% of cases lack a family history. The small (less than 5 mm) lesions are found directly beneath the skin or mucosal surfaces of the oral cavity, lips, alimentary tract, respiratory and urinary tract as well as in the liver, brain and spleen. Nosebleeds and bleeding into the intestinal, urinary or respiratory tract are common clinical manifestations. The hemorrhagic tendency becomes more pronounced with age and sever hemorrhage may necessitate transfusions, patients with this condition have a normal life expectancy. Bacilllary angiomatosis is a potentially fatal infectious disease that causes a distinct non-neoplastic proliferation of small blood vessels, that appear as one to numerous red papules and nodules or rounded subcutaneous masses, in the skin, lymph nodes, and visceral organs of patients with human immunodeficiency virus (HIV) infection and other states of immunocompromise, it is treated with doxycycline (Schoen 94: 509). Hemangioendothelioma is used to denote a true neoplasm of vascular origin composed predominantly of masses of endothelial cells growing in and about vascular lumina. The hemangioendotheliioa represents an intermediate grade between the well-differentiated hemangiomas and the frankly anaplastic, totally cellular angiosarcomas. Most frequently seen in the skin but may affect the spleen and liver. Epithelioid hemangioendothelioma is a unique vascular tumor occurring around medium-sized and large veins in the soft tissue of adults. Occuring in the lung as a so-called intravascular bronchoalveolar tumor, such a tumor can be misdiagnosed as metastatic carcinoma. Clinical behavior is variable, most are cured by excision, but up to 40% recur, and 20% eventually metastasize (Schoen 94: 509, 510). Angiosarcoma (Hemangiosarcoma) is a malignant neoplasm of vascular origin. It may occur in both sexes and at all ages, anywhere in the body, but most often in the skin, soft tissue, breast and liver. Beginning small, most angiosarcomas become large, fleshy masses of pale gray-white, soft tissue. Clinically, angiosarcomas, have all the usual features of malignancy, with local invasion and distal metastatic spread. Some patients survive only weeks to months, whereas others may live for many years. Angiosarcomas are usually treated with paclitaxel (Taxol), docetaxel (Docefrez, Taxotere), sorafenib (Nexavar), or bevacizumab (Avastin). Hemangiopericytoma, a rare neoplasm, may occur anywhere in the body, but most commonly on the lower extremitites and in the retroperitoneum. Electron microscropic studies have clearly traced the origin of these tumors to pericytes. Most of these neoplasms are small, but rarely they achieve a diameter of 8 cm. They consist of numerous capillary channels surrounded by and enclosed within nests and masses of spindle-shaped cells, which occasionally can be ovoid or even round. The tumors may recur, and as many as 50% metastasize to lungs, bone and liver. Regional lymph nodes are sometimes affected (Schoen 94: 510, 511). Resection is the standard treatment in most, although regrowth and metastases are common even after resection. Lymphangiomas are the lymphatic analog of the hemangiomas of blood vessels. Simple (Capillary) Lymphangioma are masses composed of small lymphatic channels, tend to occur subcutaneously in the head and neck region and in the axilla. Rarely, they are found in the trunk, within internal organs, or in the connective tissue in and about the abdominal or thoracic cavities. On endothelium lined lymph spaces they are slightly elevated or sometimes pedunculated lesions, 1 to 2 cm in diameter, differentiated from the capillary channels only by the absence of blood cells. Cavernous lymphangioma (Cystic hygroma) are benign lymphatic tumors composed of cavernous lymphatic spaces and therefore are analogous to the cavernous hemangioma. Almost invariably occurring in children on the neck or axilla and only rarely retroperiotoneally, they occasionally achieve considerable size, up to 15 cm in diameter. The margins of the tumor are not discrete and these lesions are not encapsulated making their removal difficult. When bits of tumor are left in surgical resections, recurrence may be expected. Lymphangiosarcoma is a rare tumor that develops after prolonged lymphatic obstruction with lymphedema. Most cases occur in the edematous arms of patients treated by radical mastectomy for carcinoma of the breast. The nodules are frequently multiple, on average, they appear about 10 years after the mastectomy and have a poor prognosis. They may also develop after prolonged lymphedema in the lower legs (Schoen 94: 512). Amputation of the affected limb is prescribed. Chemotherapeutic drugs such aspaclitaxel, doxorubicin,ifosfamide, andgemcitabineexhibit antitumor activity. Recently, there has been interest in evaluating the effectiveness of anti-angiogenic drugs in the treatment of lymphangiosarcoma. Early evidence suggests that treatment with one such drug, Bevacizumab, may be effective in treating lymphangiosarcoma.Investigation of bevacizumab in combination with other chemotherapy agents is underway. Long considered an obscure tumor Kaposis sarcoma frequently occurs in patients with acquired immunodeficiency syndrome (AIDS). Four forms of the disease are recognized. (1) the classic, or European form, first described by Kaposi in 1862, was endemic to older men of Eastern European (especially Ashkenazic Jews). This form consists of red to purple skin plaques or nodules primarily in the lower extremities, slowly increasing in size and number and spreading to more proximal sites. Rarely do they involve visceral organs or cause the death of the patients. African Kaposis is clinically similar to the European form, but occurs in children and younger men in equatorial Africa. It has a very high prevalence in these regions, representing up to 10% of all tumors. In young children, the disease is often associated with generalized involvement of lymph nodes, resembling lymphoma. (3) transplant associated Kaposis sarcoma occurs in organ transplant recipients who receive high doses of immunosuppressive therapy. Lesions are either localized to the skin or widely metastatic but often regress when immunosuppressive therapy is discontinued. (4) AIDS-associated Kaposis sarcoma is found in approximately one-third of AIDS patients, and it is more common in male homosexuals than in other risk groups. The tumors respond to cytotoxic chemotherapy and to therapy with alpha-interferon. Most patients eventually succumb to the infectious complications of AIDS rather than directly from the consequences of Kaposis sarcoma. About one-third of these patients with Kaposis sarcoma, however, subsequently develop a second malignancy, usually lymphoma, leukemia or myeloma (Schoen 94: 511). Interferon-alfa was the first drug specifically approved for the treatment of Kaposi's. It is of particular interest because of its antiproliferative, antiviral (anti-HIV), antiangiogenic, and immune-modulating properties. Etoposide (VP-16) has been evaluated as both an oral and an intravenous treatment for KS. As an oral agent, VP-16 has been evaluated primarily in patients who have undergone prior treatment with multiple cytotoxic agents.When VP-16 is given intravenously (150 mg/m2on days 1 to 3 every 4 weeks), high response rates (78%) have been reported in patients without prior treatment and with good prognosis (no history of opportunistic infection and no constitutional symptoms). The primary toxicity of this agent is myelosuppression, which may necessitate the use of colony-stimulating factors, particularly in patients with advanced disease receiving other myelosuppressive agents. Additionally, alopecia frequently occurs in association with etoposide therapy, and is a consideration for patients who are receiving treatment of their KS for primarily cosmetic purposes. In patients with KS of poor prognosis, bleomycin given intramuscularly (5 mg/day for 3 days) or as a 4-day continuous infusion (6 mg/m2/day) produced a 48% partial response rate. Results of a small, single-institution study in which bleomycin was given as a 72-hour infusion (20 mg/m2/day) to 17 patients indicated a partial response rate of 65%. Bleomycin toxicity appears to be acceptable, with neutropenia an infrequent complication. Doxorubicin (also known by its trade name Adriamycin) is a component of the most widely used combination regimen for HIV-associated KS. In one trial, however, weekly treatment with doxorubicin (25 mg/m2) in patients with AIDS-related KS achieved a partial response rate of only 10%. The primary toxicity of weekly doxorubicin is myelosuppression, even with the relatively low doses prescribed for KS treatment. Alternating vincristine and vinblastine weekly achieves a response rate of 33%. Toxicity includes vincristine-induced neurotoxicity (which limits its usefulness as a single agent) and vinblastine-induced myelosuppression. Paclitaxel A partial response was reported in 13 of 20 patients (65%), with 5 of 6 patients with known pulmonary KS responding, as well as 6 previously treated patients with nonpulmonary KS achieving a partial response. In a second trial, of the 30 evaluable patients, 16 (53%) achieved a partial response. The time to response was short (median of three cycles of treatment). Dramatic improvement in symptomatic lymphedema was noted in 25 of 26 patients. Therapy was well tolerated.Vinorelbine, a semisynthetic vinca alkaloid with a favorable therapeutic index compared to other vinca alkaloids, was evaluated in previously treated patients with progressive AIDS-related KS. Thirty-five evaluable patients were treated with vinorelbine 30 mg/m2 every 2 weeks. Clinical complete and partial remissions were achieved in 43% of patients, with a median progression-free survival of 151 days. The agent was well tolerated, with neutropenia the most frequent dose-limiting toxicity. Two liposomal agents are currently approved for the treatment of KS: liposome-encapsulated daunorubicin (DaunoXome) and liposome-encapsulated doxorubicin (Doxil). Both agents are highly active against KS and have less toxicity than the nonliposomal anthracyclines. Myelosuppression, however, remains the dose-limiting toxicity. 12. Congenital Defects Congenital heart disease is a general term used to describe abnormalities of the heart or great vessels that are present from birth. Most such disorders arise from faulty embryogenesis, during gestational weeks 3 through 8, when major cardiovascular structures undergo development. Most are associated with live births. Some may produce manifestations soon thereafter but others do not become evident until adulthood (e.g. aorti coarctation or atrial septal defect (ASD). Congenital anomalies of blood vessels may predispose the myocardium to infarction or may cause sudden death. Among these diverse vascular anomalies, two have particular importance: developmental or berry aneurysms (involving the cerebral vessels) and arteriovenous fistulas or aneurysms. Congenital heart disease is the most common type of heart disease among children. The incidence is higher in premature infants and in stillborns. Interestingly, monozygotic twins, despite having identical genes, have only a 10% concordance for ventricular septal defects. Nevertheless, chromosomal abnormalities compose about 5% of cases. Fewer than 1% are attributed to environmental influences. The increased risk in subsequent children is small (probably below 5%). The varied structural anomalies in hearts with congenital defects fall primarily into two major categories: shunts or obstructions. A shunt is an abnormal communication between changers or blood vessels (or both). The adult congenital heart disease patient population includes those who have never had cardiac surgery, those who have had reparative cardiac surgery and require no further operation, those who have had incomplete or palliative surgery and those who are inoperable, apart from organ transplantation. More than 85% of the estimated 25,000 infants born annually with congenital malformations of the heart are likely to reach adulthood. Many patients with congenital heart disease have an increased risk of endocarditis, those with cuanotic congenticla heart disease may have specific difficulties owing to hyperviscosity, abnormal hemostasis and abnormal renal function and urate metabolism. With certain congential cardiac malformations, childbearing imposes a formidable threat to maternal and fetal survival (Schoen 94: 579). Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu Disease) is characterized by multiple small aneurysmal telangiectases distributed over the skin and mucous membranes, present from birth as a dominant trait, affecting both sexes equally, about 20% of cases lack a family history. The small (less than 5 mm) lesions are found directly beneath the skin or mucosal surfaces of the oral cavity, lips, alimentary tract, respiratory and urinary tract as well as in the liver, brain and spleen. Nosebleeds and bleeding into the intestinal, urinary or respiratory tract are common clinical manifestations. The hemorrhagic tendency becomes more pronounced with age and severe hemorrhage may necessitate transfusions, patients with this condition have a normal life expectancy (Schoen 94: 509). In approximately 1 to 2% of the population, the aortic valve is congenitally bicuspid. Bicuspid aortic valves are generally neither stenotic nor symptomatic at birth or throughout early life, but they are predisposed to progressive calcification. The raphe that composes the incomplete commissure is frequently a major site of calcific deposits. With or without calcification, bicuspid aortic valves may also become incompetent or be complicated by infective endocarditis. As the stenosis worsens, angina or syncope, and risk of sudden death, may appear. The onset of symptoms such as angina, syncope of congestive heart failure, in aortic stenosis carries a poor prognosis if not treated by surgery (death in more than 50% within 3 years). Patients with aortic stenosis are often drastically improved by surgical aortic valve repair or replacement. Doppler echocardiography, which measures the flow velocities a well as structure, can be used repetitively to examine the progression of disease with time (Schoen 94: 545). Coarction of aorta is a frequent obstructive structural anomaly. Males are affected three to four times more often than females, although females with Turners syndrome frequently have coarction. Murmurs are often present throughout systole and sometimes a thrill is present. With uncomplicated coarctation, surgical resection and end-to-end anastomosis or replacement of the affected aortic segment by a prosthetic graft yields excellent results. Postoperative persistent hypertension is a complication in some patients. Untreated, the mean duration of life if about 40 years, and death are usually caused by CHF, intracranial hemorrhage, infective aortitis at the point of narrowing and rupture or dissection of the precoarctation aorta. Pulmonary stenosis or atresia with intact ventricular septum is a relatively frequent malformation of the pulmonary valve. With atresia, ther is no communicatoion between right ventricle and lungs, and so flow bypasses the right ventricle through an AD, entering the lungs through a PDA. Pulmonary stenosis may be mild to severe. Mild stenosis may be asymptomatic and compatible with long life. Valvular stenosis is easily corrected with surgery or in some bases by ballon valvuloplasty. When these lesions are associated with right ventricular hypertrophy, the surgical options are more complex and risky. Aortic stenosis and atresia may result from acquired calcific disease or congenital anomaly or a combination of both. The most common congenital anomaly is a biscuspid aortic valve, that is of little significance early in life, but predisposed to calcification in adulthood. Aortic stenosis is an isolated lesion in 80% of cases. A prominent systolic murmur is usually detectable. In general congenital stenosis are well tolerated unless very severe. Mild stenosis can be managed conservatively with antibiotic prophylaxis and avoidance of strenuous activity, but the threat of sudden death with exercise always looms. Surgical correction is usually eventually indicated, for both mild and severe stenosis (Schoen 94: 578, 579). Ventricular septal defect is a congenital abnormality that allows the free communication between right and left ventricles, usually in association with other structural defects particularly tetralogy, transposition and trucus, but also PDA ASD and aortic coarctation. About 30% occur as isolated anomalies. Depending on the size of the defect it may produce difficulties from birth, or, with smaller lesions, may not be recognized until later or may even spontaneously close. Small defects (less than 0.5 cm in diameter) are known as Rogers disease, most are muscular and 50% close spontaneously, and the remainder are generally well tolerated for years. They induce a loud murmur however, heart throughout systole. Surgical closure is generally not attempted during infancy, in hope of spontaneous closure. Correction, however, is indicated in older children with large defect, before pulmonary hypertension and obstructive pulmonary vascular disease develops and renders the lesion inoperable. Wolff-Parkinson-White (WPW) syndrome is a condition in which there is an extra connection between the atrium and ventricle (accessory pathway) (Cohen 10: 62). The four features of Fallots tetralogy, the most common form of cyanotic congenital heart disease are (1) VSD, (2) obstruction of the right ventricular outflow tract (subpulmonary stenosis), (3) an aorta that overrides the VSD and (4) right ventricular hypertrophy. Even untreated, patients with tetralogy often survive into adult life, about 10% were alive at 20 years and 3% at 40 years. The prognosis depends on the severity of subpulmonary stenosis and most infants are cyanotic from brith. Complete surgical repair is possible for classic tetralogy but is more complicated for patients with pulmonary atresia and dilated bronchial arteries. Transposition of Great Arteries implies ventriculoarterial discordance, such that the aorta arises from the right ventricle, and the pulmonary artery emanates from the left ventricle. The result is separation of the systemic and pulmonary circulations, a condition incompatible with postnatal life, unless a shunt exists for adequate mixing of blood. This malformation, particularly common in offspring of diabetic mothers, causes cyanosis from birth. Without surgery most patients die within the first months of life with only a few making it to young adulthood. Truncus arteriosus arises from a developmental failure of separation of the embryologic truncus arteriosus into the aorta and pulmonary artery. This results in a single great artery that receives blood from both ventricles. Truncus arteriosus is associated with a large number of concomitant defects, including right aortic arch (30%). There is early systemic cyanosis as well as increased pulmonary blood flow. Surgical correction is attempted at an early age, often with gratifying results. Tricuspiud atresia describes complete occlusion of the tricuspid valve orifice which causes the mitral valve to be larger than normal and underdevelopment (hypoplasia) of the right ventricle. Cyanosis is present virtually from birth, there is a high mortality in the first weeks or months of life. Palliative or reparative surgery is usually possible. Total anomalous pulmonary venous connection (TAPVC) describes a condition in which no pulmonary veins directly joint the left atrium, resulting embryologically when the common pulmonary vein fails to develop or becomes atretic, causing primitive systemic venous channels from the lungs to remain patent. The left atrium is hypoplastic but the left ventricle is usually normal in size. Cyanosis may be present owing to a large right-to-left shunt (Schoen 94: 571-577). Congenital heart defects that produce right-to-left shunts which causes a dusky blueness of the skin and mucous membranes (cyanosis) from poorly oxygenated blood entering systemic circulation, and clubbing of the fingersare known as cyanotic congenital heart disease (e.g. tetralogy of Fallot, transportation of the great arteries (TGA), persistent truncous arteriosus, tricuspid atresia and total anomalous pulmonary venous connection (TAPVC). Left-to-right shunts are not usually associated with cyanosis but can result in progressive pulmonary hypertension and right ventricular overload with hypertrophy. The shunt can reverse creating what is called late cyanotic congenital heart disease or Eisenmengers syndrome. Atrial septal defect (ASD) represents an abnormal opening in the atrial septum that allows free communication of blood between the right and left atria. A nonfunctional oblique slit known as a patent foramen ovale persists in about one-third of individuals, but permits little or no flow because of the flap valve. Pulmonary blood flow may be two to three times normal. An isolated large ASD usually does not become symptomatic in a patient before 30 years of age, whereas a small ASD is virtually always asymptomatic. A murmur is often present. Irreversible pulmonary hypertension develops in fewer than 10%. The objective of surgical closure of an ASD are the reversal of the hemodynamic abnormalities and the prevention of complications, including heart failure, paradoxic embolization and irreversible pulmonary vascular disease. Mortality is low and postoperative survival is comparable to that of a normal population. Patent ductus arteriosus (PDS) results when the ductus arteriosus, a normal aortopulmonary vacular channel during intrauterine life, remains open after birth. There is generally agreement that a PDA should be closed up as early in life as is feasible by surgery, or more commonly pharmacologic closure using indomethacin to suppress vasodilatory prostaglandin E synthesis. Preservation of ductal patency (by administering prostaglandin E) assumes great importance in the survival of infants with various forms of congenital heart disease with obstructed pulmonary or systemic blood flow. Atrioventricular (AV) septal defects result from abnormal development of the embryologic AV canal, in which the superior and inferior endocardial cushions fail to fuse adequately resulting in incomplete closure of the AV septum and inadequate formation of the septal tricuspid and anterior mitral leaflets. The two most common combinations are partial AV sepatal defect and complete AV septal defect, essentially a hole in the center of the heart that allows all four cardiac chambers to freely communicate, inducing volume hypertrophy of each. More than one-third of all patients with the complete AV septal defect have Down syndrome. Surgical repair may be possible. Common associated gene subtypes for inherited rhythm disorders DisorderGene subtypesArrhythmogenic right ventricular dysplasia (fat deposits in right ventricular wall)PKP2, DSP, GSG2Hypertrophic cardiomyopathy (thickened heart muscleMYH7, MYBPC3Long QT syndrome (has specific ECG patterns)KCNQ1 (long QT1); KCNH2 (long QT2); SCN5A (long QT3)Brugada syndrome (has specific ECG pattern)SCN5ASource: Table 35.1 Cohen 10: pg. 143 Hereditary spherocytosis (HS) is an inherited disorder (autosomal recessive) characterized by an instrinsic defect in the red cell membrane that renders erythrocytes spheroidal, less deformable and vulnerable to splenic sequestration and destruction. The prevalence of HS is highest in people of northern European extraction, in whom rates of 1 in 5000 have been reported. Although a deficiency of any one of the membrane skeletal proteins could adversely affect the red cells, a deficiency of spectrin seems to be the most common abnormality in patients with all forms of HS. Moderate splenic enlargement is characteristic of HS (500 to 1000 mg), in few other hemolytic anemias is the spleen enlarged as much or as often. The clinical features are anemia, splenomegaly and jaundice. The severity of the disease varies. A hemolytic crisis may develop, a sudden onset of a wave of massive hemolysis accompanied by fever, abdominal pain, increasing jaundice, low blood pressure and even shock. Alternatively, an aplastic crisis (triggered usually by parvovirus infection of the marrow red cell precursors) may appear. Transfusions may be necessary to support the patient, but eventually both these crises remit in most instances. Gallstones may also produce symptoms so diagnosis is usually based on family history and evidence of spherocytosis. The cardinal role of the spleen in the premature demise of the spherocytes is proved by the invariably beneficial effect of splenectomy. The spherocytes persist, but the anemia is corrected (Saunders 94: 589-591). Sickle cell disease is the prototype of hereditary hemoglobinopathies, characterized by the production of structurally abnormal hemoglobin, HbS. If an individual is homozygous for the sickle mutation, almost all hemoglobin in the erythrocyte is HbS. In the heterozygote, only about 40% is HbS, the remainder being normal hemoglobins. Where malaria is endemic, as many as 30% of black Africans are heterozygous. This protection may be related to the slight protection against falciparum malaria imparted by HbS. On deoxygenation the changes that occur in the HbS molecules convert hemoglobin from a freely flowing liquid to a vicious gel, leading ultimately to distortion of the red cells, which acquire a sickle or holly-leaf shape. Sickled cells lose potassium and water and at the same time gain calcium, which normally is rigorously excluded. The formation of HbS has two major consequences (1) a chronic hemolytic anemia, and (2) occlusion of small blood vessels, resulting in ischemic tissue damage. Irreversibly sickled cells (ISC) have a very rigid non-deformable cell membrane and have difficulty negotiating the splenic sinusoids. They become sequestered in the spleen, where they are destroyed by the mononuclear phagocyte system. Some intravascular hemolysis may also occur due to the increased mechanical fragility of the sickle cells. The average red cell survival correlates with the percentage of ISC in circulation and is shortened to approximately 20 days. In children, the continued scarring caused by this disease often causes a progressive shrinkage of the spleen so that by adolescence or early adulthood only a small nubbin of fibrous tissue may be left, this is called autosplenectomy, which predisposes to septicemia and meningitis by Streptococcus pneumoniae and Haemophilus influenzae, the most common causes of death in children with sickle cell anemia. Chronic hemolysis in a fairly severe anemia exhibits hematocrit values ranging between 18 and 30%. Vaso-occlusive crises, also called painful crises, represent episodes of hypoxic injury and infarction with extreme pain in abdomen, chest or joints, and may produce a seizure or stroke. Aplastic crisis represents a temporary cessation of bone marrow activity, usually triggered by parvovirus infection of erythroid progenitor cells causing reticulocytes to disappear from the peripheral blood and there is sudden and rapid worsening of anemia. A sequestration crisis may appear in children with splenomegaly caused by massive sequestration of deformed red cells and sometimes shock. Despite improvement in therapy sickle cell anemia shortens longevity and many patients die within the first 3 years owing to overwhelming infections, and those who cross these hurdles may live up to the fourth or fifth decade (Saunders 94: 592-596). The thalassemia syndromes are a heterogeneous group of mendelian disorders characterized by a lack of or decreased synthesis of either the alpha or the beta-globin chain of hemoglobin A (22).   thalassemia is characterized by deficient synthesis, or total lack, of the beta chain, whereas   thalassemia is characterized by deficient synthesis of the alpha chain. The hematologic consequences of diminished synthesis of one globin chain derive not only from the low intracellular hemoglobin (hypochromia) but also from the relative excess of the other chain.  thalassemia syndromes can be classified into two categories (1) 0- thalassemia associated with total absence of beta-globin chains in the homozygous state and (2) +-thalassemia with a reduced (but detectable) beta-globin synthesis in the homozygous state. Sequencing reveals approximately 100 different mutations responsible for these two disorders. Cell membrane damage, caused by unbound  chain aggregation, leads to a loss of K+, excessive absorption of dietary iron, and impaired DNA synthesis. The net effect is destruction of the red cell precursors within the bone marrow, 70 to 85% of marrow normoblasts are destroyed in severely affected patients. In general, individuals who are homozygous for the   thalassemia genes (0 or +) have a very severe transfusion dependent anemia and are said to have   thalassemia major. Thalassemia major is most common in Mediterranean countries and parts of Africa and Southeast Asia. The anemia is very severe and first manifests 6 to 9 months after birth. In untransfused patients Hb levels range between 3 and 6 gm/dl. The spleen may increase up to 1500 gm. Unless supported by transfusion, children suffer from growth retardation and die at an early age from anemia. In those who survive the face is overlarge and somewhat distorted with malocclusion. Cardiac disease resulting from progressive iron overload and secondary hemochromatosis is an important cause of death even in patients who can otherwise be supported by transfusion. To reduce iron overload most patients receive iron chelators. Many patients survive into the third decade. Bone marryow transplantation from an HLA-identical sibling is the only therapy that offers a cure. The presence of one normal gene in the heterozygotes usually leads to enough normal beta-globin chain synthesis so that the affected individuals are usually asymptomatic with only a mild anemia, referred to as   thalassemia minor or   thalassemia trait, or for intermediate cases   thalassemia intermedia, predominantly in the same ethnic groups. Because the non-alpha chains in general form more soluble and less toxic aggregates than those derived from alpha chains, the hemolytic anemia and ineffective erythropoiesis tend to be less severe in   thalassemia. The most common cause of reduced alpha-chain synthesis seems to be the deletion of alpha-globin genes.   thalassemia is classified on the basis of the number and position of the alpha-globin genes deleted, which determine the clinical syndrome. The silent carrier state is characterized by the deletion of a single alpha-globin gene and barely detectable reduction in alpha-globin chain synthesis. These individuals are completely asymptomatic and do not have anemia. -thalassemia trait is characterized by deletion of two alpha-globin genes and although they have minimal or no anemia and no abnormal physical signs, the position of the deleted genes makes a big difference to the likelihood of severe forms of the disease such as HbH disease or hydrops fetalis. Hemoglobin H disesase is associate with deletion of three of the four alpha-globin genes. HbH is seen mostly in Asians and rarely in Africans. Patients have a moderately severe anemia. Hydrops fetalis is the most severe form of   thalassemia, resulting from the deletion of all four alpha-globin genes. Severe tissue anoxia associated with the total failure to deliver oxygen to the tissues, invariably leads to intrauterine fetal death (Saunders 94: 596-601). Qualitative defects of platelet function may be congenital or acquired. Congenital disorders are rare and can be classified into three groups on the basis of the predominant functional abnormality (1) defects of adhesion, (2) defects of aggregation and (3) disorders of platelet secretion (release reaction). Defective adhesion is best illustrated by the autosomal recessive Bernard Soulier syndrome in which there is an inherited deficiency of platelet membrane glycoprotein complex (GpIb/IX) that is a receptor for von Willebrands factor which is essential in normal platelet adhesion to collagen. Defective platelet aggregation is exemplified by the autosomal recessive trait thrombasthenia in which platelet fail to aggregate with ADP, collagen, epinephrine, or thrombin, owing to a deficiency of GpIIb/IIIa, the fibrinogen receptor. Disorders of platelet secretion are characterized by normal initial aggregation with collagen or ADP, but the subsequent responses, such as secretion of prostaglandins and release of granulebound ADP, are impaired causing storage pool disease. There are two clinically significant acquired defects of platelet function (1) related to aspirin and other NSAIDs, which may significantly prolong bleeding time and lead to bruising, with ingestion of as little as 1g in 10% of normal healthy subjects and (2) uremia (Saunders 94: 619, 620). Hemophilia A and von Willebrands disease, are two of the most common inherited disorders of bleeding, both caused by qualitative or quantitative defects involving the factor VIII-vWF complex. Plasma factor VIII-vWF is a complex made up of two separate proteins. Synthesized separately through noncovalent bonds, factor VIII is linked to a much larger protein called von Willebrands factor (vWF) which forms approximately 99% of the complex, which circulates in the plasma to promote clotting and the platelet vessel wall interactions necessary to ensure hemostatis. Von Willebrands factor binds to several other proteins involved in hemostasis, most importantly subendothelial collagens, but also heparin and platelet membrane glycoproteins (GpIb and IIb/IIIa). The half-life of factor VIII in the circulation is 12 hours if vWF is present but only 2.4 hours if the latter is lacking. vWF can be assayed with a ristocetin aggregation test. With an estimated frequency of 1% von Willbrands disease (vW) is one of the most common inherited disorders of bleeding in humans. It manifests as sponataneous bleeding from mucous membranes, excessive bleeding from wounds, menorrhagia and a prolonged bleeding time in the presence of a normal platelet count. More than 20 variants have been described, most are autosomal dominant. Types I and III vWD are associated with a reduced quantity of circulating vWF. Type I, an autosomal dominant disorder, accounts for approximately 70% of these cases and is relatively mild. Type III, an autosomal recessive disorder is associated with extremely low levels of vWF and correspondingly clinical manifestations are severe, but is much less common. Type II vWD involves a qualitative defect in vWF, that is inherited as an autosomal dominant disorder, where the vWF that is formed is abnormal, and intermediate multimers, the most active forms of vWF are missing from plasma. Type II vWD accounts for 10 to 15% of all cases and is associated with mild to moderate disease. Patients with von Willebrands disease have a compound defect involving platelet function and the coagulation pathway. However, except in the most severely affected (e.g. homozygous) patients, effects of factor VIII deficiency such as bleeding into the joints, which characterizes hemophilia, are uncommon (Saunders 94: 621, 622). Hemophilia A is the most common hereditary disease with serious bleeding caused by a reduction in the amount or activity of factor VIII. Hemophilia A is inherited as an X-linked recessive trait, and thus occurs in males and in homozygous females. However, excessive bleeding has been described in heterozygous females. Approximately 30% of patients have no family history presumably because the disease is caused by new mutations. Those with less than 1% of normal activity develop severe disease, levels between 2 to 5% of normal are associated with moderate disease and patients with 6 to 50% of activity develop mild disease. Typically patients wit hemophilia A have normal bleeding time and platelet counts, with prolonged partial thromboplastin time. Factor VIII assays are required for diagnosis. Treatment of hemophilia A involves infusion of factor VIII, currently derived from human plasma. Replacement therapy however carries the risk of transmission of viral diseases. Until the mid-1980s, before routine screening of blood for HIV antibodies, thousands of hemophiliacs received factor VIII concentrates containing HIV and many developed AIDS. Although blood bank standards have improved the only safe factor VIII will be a recombinant factor VIII derived from cloned factor VIII gene. Hemophilia B, also known as Christmas disease, involves a severe factor IX deficiency that is clinically indistinguishable from hemophilia A, the partial thromboplastin time is prolonged and bleeding time is normal. It is also inherited as an X-linked recessive trait and may occur asymptomatically or with associated hemorrhage. In about 14% of these patients, factor IX is present but nonfunctional. Identification of Christmas disease, named after the first patient) is possible only by assay of the factor levels (Saunders 94: 622, 623). About 10% of all people are born with potentially significant malformations of the urinary system. Renal dysplasias and hypoplasias account for 20% of chornic renal failure in children. Congenital renal disease can be hereditary but is most often the result of an acquired developmental defect that arises during gestation. Genetic abnormalities may also cause enzymatic or metabolic defets in tubular transport, such as syctinuria and renal tubular acidosis. All except horseshoe kidney are uncommon. Horseshoe kidney is caused by fusion of the upper or lower poles of the kidneys produces a horsehoe-shaped structure that is found in 1 in 500 to 1,000 autopsies. Ninety percent tof such kidneys are fused atht hlower pole and 10% are fused ath the upper pole. Agenesis of the kidney can be bilateral, which is incompatible with life, usually encountered in stillborn infants, and is often associated with other congential disorders and leads to early death. Unilatera agenesis is compatible with normal life if no other abnormalities exist. The opposite kidney is usually enlarged as a result of compensatory hypertrophy. Some patients eventualy develop progressive glomerular sclerosis in the remaining kidney. Hypoplasia refers to a failure o fhte kidneys to develop to a normal size. This anomaly may occur bilaterally, resulting in renal failure in early childhood, but it is more commonly encountered as a unilateral defect. Most cases probably represent acquired scarring but a truly hypoplastic kidney shows no scars and has a reduced numer of renal lobes and pyramids, usually six or fewer. In one form of hypoplastic kidney, oligomeganephronia, the kidney is small with fewer nephrons that are markedly hypertrophied. Ectopic kidneys lie either just above the pelvic brim or within the pelvis. They are usualy normal or slightly small in size but otherwise not remarkable, because of their abnormal position, kinking or tortuosity of the ureters may cause some obstruction to urinary flow, which predisposes to bacterial infection. Multicystic renal dysplasia is characterized by the persistence in the kidney of abnormal structures-cartilage, undifferentiated mesenchyme and immature collecting ductures, and by abnormal lobar organization. Most cases are associated with ureteropelvic obstruction, ureteral agenesis or atresis and other anomalies of the lower urinary tract. Dysplasia, enlargement of the kidney, can be unilateral or bilateral and is almost always cystic. When unilateral surgical nephrectomy is performed, when bilateral renal failure may ultimately result (Alper '10: 954-956). Cystic diseases of the kidney may be hereditary, developmental or acquired disorders. Besides Multicystic renal dysplasia, explained above, polycystic kidney disease is a hereditary disorder. Polycystic kidney disease can be autosomal-dominant (adult) polycystic disease (ADPKD) or autosomal-recessive (childhood) polycystic disease (ARPKD). ADPKD is characacterized by multiple expanding cysts of both kidneys that ultimately destroy the renal parenchyma and cause renal failure. It is a common condition affecting roughly 1 of every 400 to 1000 live births and accounting for 5-10% of cases of chronic renal failure requiring transplantation or dialysis. The likelihood of developing renal failure with a PKD1 mutation is less than 5% by 40 years of age, rising to more than 35% by 50, more than 70% at 60 and m ore than 95% by 70. With a PKD2 mutation the odds of renal failure are less than 5% by 50, 15% at 60, and about 45% at 70. Progression is accelereated in blacks (largely correlated with the sickle cell trait), in males, and in the presence of hypertension. Individuals with PKD tend to have extrarnal congenital anomalies and about 40% have one to several cysts in the liver (polycystic liver disease) that are usually asymptomatic. Cysts are derived from biliary epithelium. Cysts occur much less frequently in the spleen, pancreas, and lungs. Intracranial berry aneurysms arise in the circle of Willis, and subarachnoid hemorrhages from these account for death in about 4-10% of inviduals. Mitral valve prolapse and other cardiac valvular anomalies occur in 20-25% of patients, but most are asymptomatic. Patients may survive for many yars with azotemia slowly progressing to uremia. Ultimately, about 40% of adult patients die of coronary or hypertensive heart disease, 25% of infection, 15% of a ruptured berry aneurysm or hypertensive intracerebral hemorrhage, and the rest of other causes. ARPKD is genetically distinct. Patients who survive infancy may develop a peculiar type of congential hepatic fibrosis. In older children the hepatic disease is the predominant clinical concern. Such patients may develop portal hypertension with splenomegaly (Alper '10: 956- 959). Alport Syndrome is a hereditary nephritis that is manifest by hematuria with progression to chronic renal failure, accompanies by nerve deafness and various eye disorders, including lens dislocation, posterior cataracts and corneal dystrophy. The disease is inherited as an X-linked trait in 85% of cases with males expressing the full syndrome and females as carriers limited to hematuria although autosomal recessive and autosomal dominant pedigrees exist. Symptoms appear at ages 5 to 20 years, and the onset of overt renal failure is between the ages of 20 and 50 years in men. Thin basement membrane lesion (Benign Familial Hematuria) is a fairly common hereditary entity manifested clinically by familial asymptomatic hematuria and diffuse thinning of the GBM to between 150 and 250 nm (compared with 300-400 nm in normal adults) renal function is normal and prognosis is excellent but most patients are heterozygous for the defective gene and may be carriers, homozygotes or compound heterozygotes may progress to renal failure (Alpers '10: 929-933). Downs syndrome, mongolism, is the result of an extra number, trisomy of 21 chromosome, that causes mental retardation and hypotonia as well as systemic problems with congenital heart defects and gastrointestinal anomalies that shorten life-expectancy. About one of every 691 babies born in the United States each year is born with Down syndrome, about 6,000 annually. At maternal age 20 to 24, the probability is one in 1562; at age 35 to 39 the probability is one in 214, and above age 45 the probability is one in 19. Down syndrome is the most common chromosome abnormality in humans.It is typically associated with a delay in cognitiveability (mental retardation, or MR) andphysical growth, and a particular set of facial characteristics.The averageIQof young adults with Down syndrome is around 50, whereas young adults without the condition typically have an IQ of 100.(MR has historically been defined as an IQ below 70.). Following improvements to medical care, particularly with heart problems, evident at birth in 50 percent, the life expectancy among persons with Down syndrome has increased from 12 years in 1912, to 60 years and the oldest on record is 87 (Wiederhort 88: 302). To prevent heart disease it is important to eat a healthy diet, without salt, fat and sugar and exercise regularly (Cohen 10: 153). Lysosomal storage diseases are a family of over 30 disorders classified according to the nature of the primary stored material and include mucopolysaccharidoses, lipid storage diseases, mucolipidoses, glycoprotein storage diseases and others. Lysosomes are are cytoplasmic organelles containing acid hydrolases that degrade macromolecules to their basic builing blocks: peptides, amino acids, monosaccharides, nucleic acids and fatty acids. Defects of myelin degradation cause white matter disease; defective glycolipid degradation causes organomegaly; and defects in the degradation of mucoplysaccharides, which are ubiquitous, cause abnormalities in numerous tissues. The disorders are progressive, and most affected individuals appear normal at birth and develop manifestations after months or years. Many of the disorders are fatal in childhood or adolescence, although there is extensive phenotypic variability (McGovern '98: 2169). Of the three common autosomal trisomies found in live-born babies, only trisomy 21 is compatible with survival past infancy. The phenotype produced by an extra chromosome 21, formerly known as mongolism but now called the Down syndrome or Trisomy 21 syndrome, is characteristic and easily diagnosed. Cardiac malformations lead to death in infancy in one-third of individuals, However, subjects who survive infancy often reach adulthood, and many reach old age (German '98: 401). Special Olympians who sustain a competitive athletic work-out routine tend to look like very healthy normal people who might be ready to learn on a vegan diet after exercising from eight to noon, like an atherosclerotic amyloidal elder. II. Treatment 1. Toxicology Mathieu J.B. Orfila (1787-1853) is known as the father of toxicology and is credited with establishing many of the basic principles of toxicology and is probably the first person to have conducted experiments on the effects of poisons, using dogs and other animals for his research (Newton '07). Formulated in 1973 and modified in 1986 and 1993 the contemporary view of the pathogenesis of atherosclerosis is called the response to injury hypothesis. The injury postulated is a form of endothelial dysfunction without necessary denudation, which increases permeability to plasma constituents, including lipids, and permits blood monocytes and eventually platelets to adhere to endothelium. Monocytes adhere and subsequently enter the intima, transform into macrophages and accumulate lipid to become foam cells, contributing to the evolution of the lesion. Single or short lived injurious events can be followed by restoration of endothelial function and regression of the lesion. Repeated or chronic injury, however, results in the development of an atheromatous plaque. Endothelial injury has been induced in experimental animals by mechanical denudation, hemodynamic forces (AV fistula), immune complex deposition, irradiation, and chemicals to cause intimal smooth muscle proliferation and in the presence of high-lipid diets, typical atheromas and ischemia (Schoen 94: 480). American scientists, at medical campuses, tend to induce ischemia in laboratory animals without disclosing the name of the prohibited toxin in the journal articles it takes to get a full keg of mental retardation (Down's syndrome is best treated as congenital hyperlipidemia, with vegan diet and Special Olympic level athletics), like equally accident prone European scientists who cite their source. Besides being a sedentary activity computers, televisions and microwaves emit a small amount of radiation which has been regulated by the FDA Office of Medical Devices and Radiological Health to be harmless. CD-ROM drives on computers emit a lot more radiation about 1 mSv and can be hi-jacked and sabotaged to emit even more radiation, about 10 mSv and hour, enough to trigger the 100 milliSievert (mSv) threshold of cardio-sensitivity to radiation sickness, by the deadline, 1 Sv of radiation or greater is enough to induce vomiting, and neoplastic infection of irradiated necrosis becomes likely, although tumors are very rare in the heart. Radioactive ore can be cardiosensitive to the touch and radioactive waste or long exposure to any cardio-reactive material or over-exposure to radiation at levels emitted by old-fashioned x-ray machines and some newer diagnostic tests and radiation treatment are definitely cardio-toxic and can be sensed as angina pectoris from necrotic cardiovascular tissue and exposure limited before reaching carcinogenic levels of tissue damage (Sanders '11). Cardio-toxic insult, caused by specific bacteria, radioactive or chemical compounds, can cause sudden cardiac death if exposure is not ceased before reaching a lethal dose, but is more likely to be administered to cause constant pain and heightened risk of death fueling demand for expensive medical treatment and surgery. Hygiene, new wardrobes, scrubs, beds, carpets, fabrics, friends and houses are in order but camping gear may be necessary to dodge the draft and be pain free. Besides the risk of sudden death detection can be complicated by lasting roughening, hardening, of the arteries due to lesions and scars, which lipids stick to, forming painful atheromatous plaques, prone to infection, that can cause myocardial infarction if the occlusion of the coronary artery nears or reaches stenosis, which causes a spreading necrosis of ischemic myocardial and vascular tissue, known as a heart attack, or heart attack scar, prone to infection, all of which lead to a long lasting, lifetime, painful and life-threatening allergy to all animal products known as hyperlipidemia. Over 10,000 different poisons are known, but only a small number of these substances are likely to be involved in some kind of criminal activity with which a forensic toxicologist has to deal. Examples of those poisons are arsenic, strychnine, atropine and cyanide. Poisons that cause angina pectoris in sublethal doses are known cardiac glycosides. Over 400 cardiac glycosides have been identified. Poisons are often divided into two general categories; inorganic substances and organic substances. Some examples of inorganic poisons are the compounds of metals and semimetals such as antimony, arsenic, barium, cadmium, copper and iron. Some common organic poisons are the carbamate pesticides, digoxin and digitoxin, the organophosphorus pesticides, nicotine and strychnine. The major poisonous principles found among plants are organic compounds, such as alkaloids, diterpenes, cardiac and cyanogenic glycosides, notri-containing compounds, oxalates, resins, and certain proteins and/or amino acids. Alkaloids are a heterogeneous group of thousands of different compounds. Distribution of most alkaloids in higher plants is highest in Apocynaceae, Berberidaceae, Fabaceae, Papaveraceae, Panunculaceae, Rubiaceae, and Solanaceae whereas Lamiaceae, Rosaceae, and Gymnosperms are almost alkaloid-free. Glycosides yield one or more sugars (glylcone) and one or more other compounds (aglycones) on hydrolysis. Toxicity is commonly associated with aglycone moiety of these compounds. The cardioactive glycosides are characterized by their specific action on the cardiac muscle. The aglycones are steroidal (ElvinLewis 77: 13, 14). The IPCSINTOX database published by the International Programme on Chemical Safety of the United Nations Environment Programme lists 113 different poisons with methods for testing that are, in most cases, unique to a specific poison. Only a few tests can provide unequivocal evidence of the presence of a specific chemical compound in a test sample. The most popular method now used for confirming the presence of a specific compound in a sample being tested uses a combination of two tests familiar to many high school chemistry students: gas chromatography (GC) and mass spectrometry (MS). The two tests are carried out in tandem to identify compounds present in a sample (Newton '07: 89, 90). Chromatography is a method for separating a mixture into its component parts. When a mixture of substances is passed over a fixed base the individual substance in that mixture have varying tendencies to adhere to that base. After the mixture has passed over the bas, the components of which it is made are deposited at different positions on the base. The base can then be analyzed to determine what each of the components of the mixture is. In gas chromatography, the substance to be analyzed is first vaporized and mixed with an inert gas. The two gases most commonly used in this process are nitrogen and helium. The carrier gas and the sample to be tested are then passed through a gas column. A thin layer of some material is deposited on the inside of the column. As the carrier gas and dissolved sample pass through the glass tube, the components of the sample are attracted in varying degrees to the material in the thin layer. Those most attracted to the thin layer will be deposited near the top of the tube, while those less strongly attracted will be carried farther down the column before they are deposited on the inside of the tube. As the carrier gas flows out the bottom of the tube and exits, a sensing device detects the individual components of the mixture. The detector then converts the information to an electrical signal that can be registered by the recorder as a graph showing the concentration of various substances detected over a period of time. The recording, known as a chromatogram, provides a visual record of the number and type of components present in the original sample. The tester identifies the components obtained in any given experiment by comparing the chromatogram with a library of chromatograms for many different substances. Gas chromatography is sensitive, it is capable of detecting material at nanogram (10-9g) levels. Chromatograms for two or more substances may be so similar that it is impossible to tell which of the substances is present in any given case. When gas cromatography is paired with mass spectrometry, however, this disadvantage is overcome. The mass spectrograph, first invented in 1919, is based on the principle that the path taken by a charged particle moving through a magnetic field is dependent on the electrical charge (e) and the mass (m) of that particle. As the components obtained from gas chromatography enter the spectrometer, they are bombarded by electrons, a process that results in the loss of a single electron fro each of the molecules present in the mixture. The molecules then become positively charged ions and can be represntd by the expression e/m where e is the same for all molecules and m is unique for every molecule of the type likely to be encountered in this analysis. Each type of molecule will follow slightly different path depending on its own value of e/m. A detector placed at the back of the spectrometer detects the specific path taken by each type of molecule that enters the instrument (Newton '07: 89-97). Many different genera of the Apocynaceae family have compounds having digitalislike action on the heart and circulation. Cardioactive glycosides are not restricted to the Apocynaceae, in fact, the most widely used cardiac glycosides used in medicine today are found int eh disparate genus Digitalis of the Scrophulariaceae. It is logical that the cardioactive glycosides of the Lilliaceae arose independently of those found in the Aponcynaceae and Scrophulariaceae. As many as 400 cardiac glycosides have been characterized, most from the Apocynaceae (Acokanthera, Apocynum, Nerium, Strophanthus, Tanghinia, thevetia), Aslepiadaceae (Asclepias, Calotropis), Liliaceae (Bowiea, Convallaria, Urginea), Moraceae (Antiaris), Ranunculaceae (Adonis, Helleborus), and Scrophulariaceae (Digitalis, Scrophularia). Helleborus foetidus, H. niger (Christmas rose) and H. viridis all contain cardiac glycosides that cause violent purging, delirium, convulsions and death from respiratory failure. The main cardiac stimulant is hellebrin. Moraceae (Mulberry) Antiaris toxicaria (upas tree) latex containing two cardioactive glycosides antiarin x and z, is extremely toxic and is used in tropical Asia as a principal poison for arrows and darts. It was used as an instrument of execution in Java in 1776 to punish 13 concubines of the king who were convicted of infidelity. All died within five minutes of being pierced with a poisoned awl, in great agony. Sesbania spp. (coffeebean, rattlebox, sesbane) seeds contain saponins that result in diarrhea, rapid pulse, respiratory failure, and even death. Flowers are also poisonous (ElvinLewis 77: 13, 14, 18, 31, 45). Phylogenetic Group 11 Lobaniaceae (Logania) produce Strychnos nux-vomica (strychnine tree) and S. ignatii (poison nut) of tropical Asia, the dried seeds yield the indole alkaloids strychnine and brucine, which are the main toxic constituents. All parts of the palnts including the flowers contain strychnine, which is extremely toxic and fatal to man at doses from 60 to 90 mg. Strophantus spp. seed extracts, containing the cardiotonic agent strophanthin are used in modern medicine when immediate relief from heart failure is needed. Tanghinia venenifera (Tanghin) of Madagascar seeds are notoriously poisonous, they contain tanghin, a cardiac glycoside characterized by digitalislike activity. The seeds have a long history as an ordeal poson for judgments of all kinds of crimes from murder, conspiracy and witch doctor, to stealing or for settling a debt. Forced to drink a draft or be killed by a soldiers spear, the accused was judged innocent by the ruling regime if he wallowed in a gulp and promptly vomited, but if afraid, he would sip slowly and die almost immediately. Guilt, of course, was predetermined, and since death was related to the strength of the extract, the judge could decide well in advance which way he wanted the trial to go. Such ordeals became infamous and the French, who colonized the island destroyed all the tanghin trees they could find. Thevetia peruviana (yellow oleander) contains the cardiac glycosides cerbrin, neriifolin, and thevetin, which produce symptoms similar to those of fatal digitalis poisoning. All parts of the plant are dangerous, and most fatalities are the result of misuse of decoctions in folk medicine. Urechites spp. (yellow nightshade) seed pods eaten in quantity will cause heart failure (Elvin-Lewis '77). Asclepiadeaceae (milkweed) Asclepias spp. (milkweeds) are dangerous to cattle, the cardiac glycosides known to be present in almost all species of the genus result in severe poisoning not only to livestock but to man. Calotropic procera (giant milkweed) latex, containing the cardiac glycoside calotropin, is extremely potent and is used on arrows in Africa. Minute amounts are said to produce death. It has also been used for murders and suicides in tropical America. Scrophulariaceae (Snapdragon) Digitalis purpurea (foxglove) are a source of cardiac glycosides used in controlled does for treatment of heart disease, poisoning can result from overdose of medication or when children eat the seeds or leaves, or such the flowers. Symptoms include vomiting and purging, severe headache, irregular heartbeat and pulse, convulsion and death, which occurs suddenly. Solanaceae (Potato) green shoots are highly toxic. Phylogenetic Group 15 Liliaceae (Lily): Ornithogalum umbellatum (star of Bethlehem) contains cardiac glycosides, which can cause nausea and gastroenteritis. Veratrum spp (false hellebore) contains many alkaloids, with major effects on the heart and vessels. Blood pressue is lowered, arterioles are dilated, and a general cardiac depressant effect is caused by these alkaloids. Most cases of poisoning have been through misuse of medical preparations (Elvin-Lewis 77: 52-57, 60-62). Cardiac and hyptertensive drugs are the second leading cause of fatal drug overdose (Bronstein '12) and are often abused (Moore '98). There is no denying that antihypertensive drugs developed in the 1950s from the Ayurvedic schizophrenia remedy Rauwolfia serpentine and the diuretic hydrochlorothiazide (HCTZ) have brought malignant hypertension, a formerly fatal disease of the kidney causing hypertrophy of the left ventricle, under control. The ABC of adrenergenic blockers developed in the 1970s, although they are competitive with Rauwolfia for the treatment of high blood pressure and dominate academic literature, seem to be misprescribed as medicine for the life threatening conditions of arrhythmia and congestive heart failure. The one year survival rate for people with congestive heart failure treated with adrenergenic drugs was worse than untreated people (Heger et al '04). It must be made clear that the fact that a drug is an essential medicine for treating essential hypertension of the kidneys does not make it an essential medicine for the treatment of heart failure, arrhythmia, angina or endocarditis and in fact all hypertension medicines tend to cause brachycardia and other cardio-toxic side-effects, although they might help with some acute cases of atrial flutter, they should not be taken regularly by anyone without high blood pressure, and don't even treat the underlying kidney infection or post-infectious malabsorption due to Bactrim consumption. For congestive heart failure the only prescription medicines indicated are (1) nitrates and nitrites can provide relief in 5 minutes in some patients and (2) Digitalis spp. preparations, sold as Digitoxin (Crystodigin), Digoxin (Lanoxin), not exactly the organic toxins digoxin and digitoxin, that work by increasing the force with which the heart pushes blood to compensate for low ejection fraction in congestive heart failure, but is not highly recommended by cardiologists and discontinued by 20% of patients, nor considered an essential medicine in the literature and the FDA requires labels state, "Digitalis alone or with other drugs has been used in the treatment of obesity. This use of digoxin or other digitalis glycosides is unwarranted. Moreover, since they may cause potentially fatal arrhythmias or other adverse effects, the use of these drugs in the treatment of obesity is dangerous"  HYPERLINK "http://edocket.access.gpo.gov/cfr_2011/aprqtr/21cfr201.317.htm" 21CFR201.317. Statin drugs have been found to prolong life and are highly useful in treating the accumulation of atheromatous plaque that cause the vast majority of congestive heart failure, infection, arrhythmia and heart disease. Hawthorne is, in fact, the supreme herb for the heart, and seems to be the only specific medicine for the treatment of the heart and all manners of heart disease such as lowering cholesterol, moderating high and low blood pressure, arrhythmia, and anti-rheumatic cartileganous nutrition, and is a delicious heart tonic, as an herbal tea infusion of leaves, flowers and berries, or tincture, without any known side-effects or contraindications (Elvin-Lewis '77)(Gladstar '12) but a vegan diet (athletic physical exercise routine and non-exposure to cardio-toxins) is the only truly essential medicine for curing heart disease in the absence of infection. Antibiotics are prescribed by cardiologists as a prophylaxis to treat the Strep, Staph and fecal coliform that often infect the heart and kidneys and antibiotic resistance is a major factor in the pathogensis of kidney disease and a complete lack of antibiotics is a serious problem for the uninsured with rheumatic heart disease. Strep, the most common bacteria to infect the heart and lungs responds best to penicillin, however some people are allergic and can develop rashes and life-threatening anapholactic shock and many synthetic penicillins are toxic to the kidneys, which can cause hypertension. Doxycycline, the "once a day antibiotic" is uniquely effective against Staph, although it permanently yellows the teeth of children under 9, and works for Strep and many skin infections of the heart including acne vularis and methicillin resistan stapholococcus aureus (MRSA). Metronidazole (Flagyl ER) is uniquely effective to treat infections of the gastrointestinal tract, bone and joint infections, including Bactroides fragiles and Peptocstreptococci that can infect the heart, and does not cause antibiotic associated colitis, nor does it tend to cause malabsorption or vitamin B12 deficiency, like every other antibiotic. Antibiotic resistance is a serious issue in regards to the kidneys because Escherichia coli is not only highly pathogenic and antibiotic resistant, but it is the most common cause of kidney infection, and the medicine that claims to treat E. coli Bactrim (trimethoprim-sulfamethotrexate) invariably causes chronic post-infectious malabsorption problems that are as likely a cause of the auto-immune kidney disease underlying hypertension and renal insufficiency as an untreated streptococcus infection. Metronidazole (Flagyl ER) is therefore recommended as a substitute for Bactrim for the treatment of E. coli and all abdominal and lower extremity infections of bacterial or protozoal origin, but is not useful for viruses or fungi. There has been a 40% decline in the prescription of antibotics from 1990 to 2000 (Huffnagle '07) and as the result of the incessant trial of new antibiotics in journals common issues of antibiotic resistance explained above go unresolved. Patients are now expected to purchase their own prescription antibiotics and antifungals online without prescription for their medicine cabinet and are highly advised to take a probiotic supplement containing at least 25 billion organisms within two hours of taking an antibiotic, NSAID or antifungal chemotherapeutic agent and for two weeks after completing the course to ensure a healthy diversity of gut flora that comprise 30% of healthy fecal matter and protect against proliferations of bad bacteria and vitamin B12 deficiency, and are needed for a already thin vegan to prevent chronic diarrhea and dental cavities (Sanders '12). Everybody who has suffered a myocardial infarction should have some penicillin, doxycycline and metronidazole in their medicine cabinet in case the dead or scarred cardiovascular tissue becomes infected. Furthermore, Sporanox (itraconazole) is a highly effective antifungal for the treatment of all major pathogenic fungi, such as Aspergillis, Histoplasmosis, Cryptospoiridium and Candida, that infect the human body and hypothetically, through their large cellular size and morphologic enzymes, cause almost all antibiotic resistant rheumatoid arthritis, cancerous growths and leukemias after intial toxic injury, such as defloration of competitive bacterial species that would naturally keep the fungal population in check by the use of antibiotics, and a microscopic stress fracture, or allograft presented the opportunity. There are also some chemotherapeutic agents, effective against bacteria, viruses, fungi and mutant human cancer cells, the latter upon which their effectiveness is gauged, that are so safe and effective they are available for oral consumption, namely, Methotrexate for cancers of the head and neck, Gleevac for leukemia, myeloma and bone cancer, and Cisplatin for soft tissue tumors. Buyer beware $1 athlete's foot crme (clotrimazole) can cure a cripple but the antifungal foot powder (prescribed to elders) spray (Toftate) causes diffuse crippling pain. An increasing number of drugs are known to be nephrotoxic. First reported after the use of sulfonamides, acute tubulointerstitial nephritis and renal papillary necrosis most frequently occurs with synthetic penicillins (methicillin, ampicillin) other synthetic antibiotics (rifampin), diuretics (thiazides), allopurinol, cimetidine, aristolochic acid found in some herbal remedies, NSAIDs, analgesics mixtures including phenacetin, aspirin, caffeine, acetaminophen and codeine. Selective COX-2 inhibitors, while sparing the gastrointestinal tract, affect the kidneys. Acute uric acid nephropathy can be caused by the precipitation of uric acid crystals in the renal tubes particularly in individuals with leukemias and lymphomas who are undergoing chemotherapy whereas the drugs induce death of tumor cels and uric acid is produced as relased nucleic acids are broken down. Gouty nephropathy is often precipitated by the consumption of moonshine whiskey contaminated with lead. Papillary necrosis is readily induced experimentally by a mixture of aspirin and phenacetin, usually combined with water depletion. The disease begins about 15 days (2-40) after exposure to the drug and characterized by fever, eosinophilia, a rash in 25% of patients and renal abnormalities in the form of hematuria, mild proteinuria and lukocyturia (often including eosinophils). A rising serum creatinine level or acute renal failure with oliguria develops in about 50% of cases, particularly older patients. Withdrawal from the offending drug is followed by recovery, although it may take several month, and irreversible damage occurs occasionally in older subjects. While drugs are the leading cause of acute interstitial nephritis in 30-40% of patients no offending drug or mechanism can be found. Urinary tract infections complicate 50% of cases (Alper '10: 944-946). 2. Diagnostic Tests A cardiologist is a doctor who specializes in the care of patients who have (or are suspected of having) heart disease. A general cardiologist specializes in a wide range of heart-related problems. In addition to medical school training, cardiologists have three years of internal medicine preparation and at least three years in cardiology. A cardiac imaging cardiologist specializes in noninvasive imaging studies that help diagnose structural and functional abnormalities of the heart. Studies include echocardiography, computer tomography angiography (CT angiography) with contrast dye, cardiac magnetic resonance imaging (cardiac MRI) and nuclear cardiology. An interventional cardiologist specializes in diagnosis and treatment of heart-related problems by inserting catheters into blood vessels and then injecting contrast due into the catheters to visualize abnormalities. One of the invasive procedures these specialists perform is a percutaneous coronary intervention (PCI) in which coronary artery blockages are opened via a balloon (angioplasty) and one or more stents (small metal mesh tubes) are placed to keep the vessels open. A cardiac rehabilitation cardiologist is a general cardiologist who helps patients recover from heart surgery and other heart interventions using a graduated and monitored exercise program. These doctors often educate patients and coach them on healthy diet, exercise, and lifestyle modifications. A heart failure specialist is a cardiologist who specializes in the treatment of congestive heart failure and helps patients maintain an optima diet and lifestyle. These specialists also prescribe and monitor patients medications and strive to provide optimal medical therapy. A cardiothoracic surgeon performs open-heart surgery to bypass blocked arteries and to treat valvular heart disease. The cardiac surgeon may also perform procedures to treat heart rhythm abnormalities and has the advantage of directly visualizing the heart. Cardiothoracic surgery encompasses entirely different surgical training than is required in general cardiology and its subspecialties (Cohen 10: 9). Blood pressure is usually measured by inflating a cuff that is connected to a column of mercury, or to a mechanical device that simulates a column of mercury. A stethoscope is placed over the brachial artery at the elbow; the cuff is wrapped around the upper-arm and inflated until the artery is compressed so firmly that blood cant get through, and then the cuff is deflated. Listening through the stethoscope over the artery reveals a tapping sound when the pressure of the blood in the artery is enough to push blood through, and the tapping sound goes away when the artery stays open between beats. Because the pressure wave is generated by the contraction of the heart (systole) the top pressure is called systolic pressure, when the artery stays open between beats, which corresponds to the relaxation phase of the heart (diastole), this is called diastolic pressure. Both readings are important. An ideal blood pressure would be below 120/80 (Spence 06: 78). The kidneys play an important role in blood pressure regulation by at least three mechanisms (1) renin-angiotensin system (2) sodium homeostasis and (3) renal vasodepressor substances, which should be confirmed by laboratory assay in cases of hypertension which are not immediately brought under control. Environmental factors implicated in the causation of hypertension include stress, obesity, smoking, inactivity, and heavy consumption of salt, found in bread and cheese and meat. Hypertension is associated with two forms of small blood vessel disease: hyaline ateriolosclerosis and hyperplastic arteriolosclerosis (Schoen 94: 485, 486, 488). Categories for Blood Pressure Levels in Adults (in mmHg, millimeters of mercury) CategorySystolic (top number)Diastolic (bottom number)NormalLess than 120Less than 80Prehypertension1201398089High blood pressureStage 11401599099Stage 2160 or higher100Credit: Sanders 08 By counting the number of pulsations over a fifteen-second interval and multiplying that number by four, the heart rate can be calculated in beats per minute. A normal heart rate is between 60 and 100 beats per minute. A slower than normal rhythm in which the heart rate is below 60 beats per minute indicates sinus bradycardia. If the rhythm exceeds 100 beats per minute, a sinus tachycardia would be present. Heart rates slower than 60 beats per minute can be normal if you dont have symptoms such as fatigue, shortness of breath, light-headedness or dizziness. Rapid heart rates (greater than 100 beats per minute) may be normal or abnormal, depending on circumstances. Conditions that weaken the heart muscle may cause rapid heart rhythms, called tachycardias, with rates greater than 100 beats per minute and possibly much faster. The faster the heart rate, the great the chance that delivery of oxygen and other nutrients to the brain and other organs will be impaired. With very fast beats (over 200 a minute) the person will likely become light-headed and dizzy and even pass out. The heart may also beat too slowly (called bradycardia) with heart rates below 60 beat per minute. Reversible causes of bradycardia are nonessential medicines such as beta blockers, calcium channel blockers, digitalis, antiarrhythmic drugs such as sotalol and amiodarone, Lyme disease, hypothyroidism, electrolyte abnormality and drug toxicity. Sinus bradycardia is commonly caused by second-degree heart block, Mobitz type I (block typically occurs in the AV node), second-degree heart block, Mobitz type II (block typically occurs in the His bundle or below), third-degree heart block or complete heart block, Asystole. An irregular heart rate might indicate early beats, called premature contractions (coming from either the atria or the ventricles) or may be an indicator of a rhythm problem called atrial fibrillation, in which the atria beats at rates greater than 400 beats per minute (Cohen 10: 12, 61, 13, 22, 23, 14). Electrocardiogram (ECG) Reading  Credit: IVLine May 2010 A single electrocardiogram (ECG) recording of a heartbeat shows the electrical sequence of the heart. The electrical signal may be broken into different waves. The P wave represents atrial electrical activity; the QRS complex represents ventricular electrical activity; and the QT interval (from the beginning of the Q wave to the end of the T wave) represents the ventricles returning to a resting state. Sometimes a test is performed through the esophagus (called a transesophageal echocardiogram) where it is particularly useful in looking for the presence of blood clots in the left atrium. Blood clots may form in the left atrial appendage (a site that is not well visualized by standard echocardiogram) (Cohen 10: 60, 68). An electrocardiogram, or ECG, is an electrical recording from the limbs and the surface of the chest that shows the pattern of electrical activity in the heart. The ECG can detect rhythm disturbances such as atrial fibrillation, may detect the presence of an old myocardial infarction, and in some circumstances, particularly when repeated daily for several days, can detect a recent heart attack (myocardial infarction). The accuracy of this diagnosis by ECG is greatly aided by measuring enzymes or other markers from the heart released into the bloodstream when the heart muscle breaks down, such as CK (creatine phosphokinase) and troponin. An electrocardiogram requires sticking electrodes to the limbs and the chest, and then making a recording. It is completely safe and painless (except for the pulling of chest hair when the electrodes are removed) (Spence 06: 43). Cholesterol, triglycerides, saturated fats, trans-fatty acids, homocysteine and other harmful substances from food. Because fat is not soluble in water, and blood is mostly water, fat from food goes from the intestine to the liver in lymphatic fluid, and is then taken out of the blood by cells in the liver. It travels in the bloodstream in packages made up of an outer layer of protein, with fat in the center. These proteins are called lipoproteins (proteins that transport lipids) (Spence 06: 80). It is estimated that 65 million American adults with high blood cholesterol need to make the therapeutic lifestyle changes (TLC) needed to lower their cholesterol and, with it, their risk for heart disease.To understand high blood cholesterol, it is important to know more about cholesterol. Cholesterol is a waxy, fat-like substance that is found in all cells of the body. Your body needs some cholesterol to work the right way. Your body makes all the cholesterol it needs.Cholesterol is also found in some of the foods you eat. Your body uses cholesterol to make hormones, vitamin D, and substances that help you digest foods. Blood is watery, and cholesterol is fatty. Just like oil and water, the two do not mix. To travel in the bloodstream, cholesterol is carried in small packages called lipoproteins. The small packages are made of fat (lipid) on the inside and proteins on the outside. Two kinds of lipoproteins carry cholesterol throughout your body. It is important to have healthy levels of both: Low-density lipoprotein (LDL) cholesterol is sometimes called bad cholesterol. High LDL cholesterol leads to a buildup of cholesterol in arteries. The higher the LDL level in your blood, the greater chance you have of getting heart disease. High-density lipoprotein (HDL) cholesterol is sometimes called good cholesterol. HDL carries cholesterol from other parts of your body back to your liver. The liver removes the cholesterol from your body. The higher your HDL cholesterol level, the lower your chance of getting heart disease (Sanders 08: 25). Lipid Profile LDL Cholesterol LevelCategoryLess than 100 mg/dLOptimal100 to 129 mg/dLNear or above optimal130 to 159 mg/dLBorderline high160 to 189 mg/dLHigh190 mg/dL and aboveVery highTriglyceride LevelCategoryLess than 150 mg/dLNormal150199 mg/dLBorderline high200499 mg/dLHigh500 mg/dL and aboveVery highCredit: American Heart Association The American Heart Association endorses the National Cholesterol Education Program (NCEP) guidelines for detection of high cholesterol. The Third Report of the Expert panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III or ATP III) was released in 2001. It recommends that everyone age 20 and older have a fasting "lipoprotein profile" every five years. This test is done after a 9-12-hour fast without food, liquids or pills. If total cholesterol is 200 mg/dL or more, or HDL cholesterol is less than 40 mg/dL (for men) and less than 50 mg/dL (for women), a lipoprotein profile should be done to determine LDL cholesterol, triglyceride, homocysteine and C-reactive protein (CRP) levels (Sanders 08: 26). Triglyceride is the most common type of fat in the body. Many people who have heart disease or diabetes have high triglyceride levels. Normal triglyceride levels vary by age and sex. A high triglyceride level seems to speed up atherosclerosis, the buildup of fatty deposits in artery walls and atherosclerosis increases the risk for heart attack and stroke. Other potentially cartiotoxic lipoproteins can be detected, but are not necessary to confirm a diagnosis of hyperlipidemia. C-reactive protein (CRP) has been known for many years as a non-specific test for inflammation that led to the discovery in the 21st century of the use of CRP as a marker of arteriosclerosis risk. Homocysteine is major cause of arteriosclerosis and some process intimately involved in the methionine/homocysteine metabolic interplay but other factors are likely to be involved (Graveline 04: 72, 59). Folate is known to reduce homocysteine levels. Niacin reduces cholesterol. Statin drugs are effective at reducing cholesterol by 20-30% which reduces the death rate from ischemic heart disease and stroke by 30-50%, but the reasons for discontinuing the medicine unfortuneately does not include recovery, known to happen with Hawthorne, the supreme herb for the heart, and most necessarily a vegan diet until no longer overweight when a vegetarian diet, including aged cheese (does not contain lactose after two months) and probiotic yoghurt, will be needed daily to prevent vitamin B12 and phosphorus deficiencies in the absence animal products such as biologically metabolized triglycerides. Acomplete blood count (CBC)test gives your doctor important information about the types and numbers of cells in your blood, especially the red blood cells and their percentage (hematocrit) or protein content (hemoglobin), white blood cells, and platelets. The results of a CBC may diagnose conditions like anemia, infection, and other related disorders such as cancers of the blood. Theplatelet countand plasma clotting tests (prothombin time, partial thromboplastin time, and thrombin time) may be used to evaluate bleeding and clotting disorders. Complete blood count (CBC) is dome by automated cell counters that measure the hemoglobin, red blood cell count, red blood cell volume distribution, platelet count, and white blood cell count. Blood appears red because of the large number of red blood cells, which get their color from the hemoglobin. The percentage of whole blood volume that is made up of red blood cells is called the hematocrit and is a common measure of red blood cell levels, the mean cell volume (MCV) (based on volume distribution), mean cell hemoglobin (MCH) (hemoglobin divided by RBC count), mean cell hemoglobin concentration (MCHC) (hemoglobin divided by hematocrit) and the red cell distribution width (RDW). The red cell indices and RDW are used together with a direct inspection of the Wright-stained blood smear to evaluate red blood cell morphology (Hillman 98: 334-336). To count the specific white blood cells a CBC with Differential is ordered. Complete Blood Count (CBC), Coagulation Tests and White Blood Cell (WBC) Differential TestNormal RangeCommentsComplete Blood Count (CBC)Red Blood Cell (RBC) countM 4.7-6.2 million/cu mm F 4.2-5.4 million/cu mmLow anemia, hemorrhage High chronic anoxiaHemoglobin (Hgb)M14-18 g/dl F12-16Same as aboveHematocrit (Hct)M42-52% F37-47%Same as aboveMean corpuscular volume (MCV)80-95 cu/u High - RBC macrocytic Low RBC microcoticMean corpuscular hemoglobin concentration (MCHC)32-36 g/dl (32-36%)Low Hypochromic cellIron (Fe)60-190 g/dlLow-iron deficiency anemiaTotal iron binding capacity (TIBC)250-420 g/dlSame as aboveSerum haptoglobin100-150 mgLow-Hemolysis liver disease High-Inflammatory diseaseHemoglobin electrophoresisHgb A1 95-98% Hgb A2 2-3% Hgb F 0.8-2% Hgb S 0% Hgb C 0%Variations indicate hemoglobinopathies, High Hgb F thalassemia found in Central asians. Hgb S-sickle cell anemia and Hgb C mild hemolytic anemia found in American blacks Direct Coombs' and Indirect CoombsNegativeTo detect antibodies against RBC in transplant rejectionReticulocyte counts0.5%-2% of total RBCLow-inaquate RBC production High-Polycythemia veraWhite Blood Cell (WBC) count5000-10,000/cu mmHigh-infection Low-Bone marrow failurePlatelet count150,000-400,000/cu mmLow-Bone marrow failure, hypersplenism, accelerated consumption High-Hemorrhage, polycythemia vera, malignanciesCoagulation TestsProthrombin test (PT)11-12.5 seconds (85-100%)High-Deficiency of factors V and VIIProthrombin time test (PTT)30-40 secondsHigh-Deficiency of factors II, V, VIII, IX, XI, XIIPlatelet count150,000-400,000/cu mmLow-Bone marrow failure, hypersplenism, accelerated consumption High-Hemorrhage, polycythemia vera, malignanciesBleeding time1-9 minutesHigh Thrombocytopenia, marrow infiltration, inadequate platelet functionEublobin lysis time90 minutes-6 hoursLow-FibrinolysisFibrin degradation products (FDP) test < 10g/mlHigh DIC, fibrinolysisWhite Blood Cell (WBC) DifferentialWhite Blood Cell (WBC) count5000-10,000/cu mmHigh-infection Low-Bone marrow failureNeutrophils50-70High-Inflammation, Invasive tumorsEosinophils2-4High-Allergic states, Drug reactions, Parasitic Infections, Some skin disease and neoplasmsBasophils0.5High-Asthma, some Carcinogens, Inflammatory bowel disease, Chronic inflammationMacrophages5-7High-Chronic infections, Liver disease, NeutropeniaLymphocytes20-35High-some CarcinomasPlasma Cells?Multiple myelomaSource: Griffin '86: Table 1.1 pg. 5-6; Table 2-3 pg. 32 The iron level with Total Iron Binding Capacity (Fe and TIBC) test detect certain kinds of anemia, such as iron deficiency after blood loss. Serum Haptoglobin Test detect intravascular destruction of RBCs associated with hemolytic anemia. Hemoglobin electrophoresis enable one to detect abnormal forms of Hgb (hemaglobinopathies). Direct and indirect Coombs tests detect the presence of antibodies to RBC found in tissue and fetal rejection. A reticulocyte count (Retic count) is a test for determing bone marrow function in which immature RBC as a percentage of total RBC production. Theplatelet countand plasma clotting tests (prothombin time, partial thromboplastin time, and thrombin time) may be used to evaluate bleeding and clotting disorders. To count the percentage of total white blood cell volume occupied by specific white blood cells a CBC with Differential is ordered. The white blood cell (WBC) differential is a measure of the total number of white blood cells and the percentages of the five types of WBC descriptive of infection, stress and bone marrow failure (Griffin '84: 3-16). An echocardiogram, also called an echo or a cardiac ultrasound, uses sound waves to create images of the heart. This test can reveal your hearts ejection fraction (EF), the presence of leaky or tight (stenotic) valves, weak heart muscles (cardiomyopathies), thick heart muscles (hypertrophy), blood clots or masses in your heart, or fluid in the sac around the heart (the pericardium). The echocardiogram is also useful in showing the presence and location of a heart attack. An ultrasound examination called an echocardiogram echo, for short, reveals the action of the heart valves, as well as the pattern of contraction of the heart muscle and areas that are not contracting, including aneurysms. Valves at the outlet of each chamber of the heart prevent the blood from going backward in the system. Sometimes problems with the valves can lead to stickiness on their surface, and to a buildup of clot or a clump of clotting protein and inflammatory cells, which may be infected. Sound beams are directed into the heart, and a computer analyzes the return echoes and converts them into images. The test is completely safe and harmless, it is essentially the same kind of imaging used to check out babies in the uterus. Occasionally the test may require putting a tube into the esophagus in a procedure called transeosophageal echocardiogram (TEE) (Spence 06: 43, 44). Since 1990 it has been possible via ultrasound to see the plaque in the artery wall and in 1992 it became possible to use the software to measure the size of plaques which is useful over time to gauge the effectiveness of treatment. If all the plaques are measured, and the total area of plaque is added up, this gives information about both risk and response to therapy. Individuals with a lot of plaque have a higher risk of stroke, death and heart attack: those in the top quartile of plaque have a five-year risk that is 3.4 times higher than those in the bottom quartile, even after adjusting for all the traditional risk factors. Furthermore, those whose plaques increase in the first year despite treatment of the traditional risk factors have twice the risk of those with stable plaque or regression. For those individuals, physicians need to try harder. Tests can investigate newer risk factors such as homocysteine (an amino acid that increases clotting and irritates the lining of blood vessels), lipoprotein (a) borderline hypothyroidism, borderline B12 and so on. The latest development in the field of arterial plaque ultrasound is the ability to measure plaque volume in three dimensions (3-D) (Spence 06: 55). A test called a computer tomography (CT) angiogram may be useful in demonstrating heart function and visualizing arteries in the heart. A CT angiogram is also helpful in diagnosing coronary artery disease because it is a direct method of looking at the coronary arteries. The cardiac magnetic resonance imaging (MRI) is used to take pictures of the heart to diagnose coronary artery disease, assess damage caused by a previous heart attack, and diagnose heart failure as well as valve problems. The cardiac MRI is particularly useful at looking for an inherited condition called arrhythmogenic right ventricular dysplasia (in which fat deposits are seen within the wall of the right ventricle) who should be considered candidates for implantable cardioverter defibrillator (ICD) (Cohen 10: 71-72). The definitive way to determine whether there is a problem with blockage of the coronary arteries is to do a radiological (X-ray) examination of the arteries, a procedure called angiography. This begins with putting a needle into the artery at the top of one leg. A thin plastic tube called a catheter is threaded through the needle and advanced up through the bloodstream until it reaches the top of the aorta, just where it leaves the heart. The catheter is maneuvered into the opening of each coronary artery, the first branches off the aorta, just above the aortic valve and an injection of X-ray contrast material, or dye, is injected through the catheter to show up the artery and its branches. The feeling of heat that once accompanied each injection is much diminished with the development of newer dyes (nonionic contrast material) which are slightly safer than the older dyes and cost about ten times more. An angiogram does carry a small risk including a reaction to the X-ray dye as well as a serious complication from an injury to one of the arteries about a 1: 1,000 risk of dying or needing an operation immediately to reopen a coronary artery blocked because the dye injection caused a peeling off or dissection of the artery lining (Spence 06: 46, 47). In a stress test, one exercises on a treadmill while the ECG is monitored. Walking or running speed is progressively increased along with the grade (or slope) as the doctor continuously analyzes blood pressure as well as the ECG. T-wave alternans (TWA) is a test that can be performed in a doctors office. The patient is attached by electrodes to computerized equipment and undergo a stress test. An intravenous line is inserted and continuous ECG monitoring is performed. The computer analyzes the heart rhythm for a scientific phenomenon called microvolt T-wave alternans (TWA). TWA helps to determine the risk for ventricular tachycardia. It is not useful if the patient is in atrial fibrillation (Cohen 10: 77). The doctor may perform a nuclear stress test in which a nuclear agent (radioisotope) is injected into your vein and images of your heart are acquired to identify whether areas in the heart muscle are receiving enough blood. Stress tests are useful for sedentary patients before they begin an exercise regimen, to evaluate whether exercise is safe for them. For all stress tests and invasive procedures the patient must have nothing by mouth (NPO) for at least 6 hours prior to the procedure. In addition, the doctor may ask the patient to stop taking blood thinners, such as warfarin (Coumadin) and antiplatelet medications, such as acetylsalicylic acid (aspirin) and clopidogrel (Plavix), before a procedure (Cohen 10: 63, 64, 65). A nuclear medicine scan assesses how well blood is flowing to the heart muscle (myocardium) and is most useful for diagnosing coronary artery disease individuals whose routine treadmill stress test is inconclusive. Many people with coronary artery disease have a history of chest pain brought on by exertion and relieved by rest; others may exhibit no symptoms, and about 40 percent of myocardial infarction are silent a heart attack without any chest pain or other symptoms. The nuclear medicine scan involves injecting a small dose of a radioactive tracer into a vein while the individuals heart is speeded up either by some kind of exercise such as rotating a pedal system with the arms, or by injection of a drug such as dipyridamole. An array of detectors similar to small Geiger counters detect the arrival and disappearance of the radioactive tracer in various regions of the heart muscle and thus image and measure the blood flow to the heart. If one of the coronary arteries is blocked or narrowed, the part of the myocardium that would normally get its blood supply from that artery fails to light up on the scan; in some cases this scan can also detect the abnormal movement of an aneurysm. Although radioactivity sounds scary, one or even several scans pose no danger. The gamma radiation involved is the same kind we get every day from sunlight; the dose is about the equivalent of going to Denver for a week of skiing, or crossing the Atlantic once in an airliner (radiation levels are higher at higher altitudes) (Spence 06: 45, 46). The procedure for coronary angiography involves inserting a needle into a large artery, usually in the leg; a thin plastic catheter is advanced through the bloodstream to where the brain arteries branch off the aorta and the catheter is advanced into the origin of the artery. Contrast material dye is injected into the artery, and a picture is made of the artery and its branches. With new computerized scanners, measurements can be taken from the screen, and the images are stored in a computer for analysis and prints some representative images, often on film that looks like X-ray film. The risks of coronary angiography include reactions to the dye and injury to the arteries by the needle or the catheter. The risk of dying form a bad reaction to the dye is approximately 1: 40,000. There is some risk of damage to the kidneys and of heart failure, which is lessened by the reduced dose of dye when digital imaging methods are used. Because the contrast material is denser than blood, it puts a strain on the heart similar to that caused by injecting a stronger than normal solution of salt. Kidney damage may be caused by the dye. The risk of angioplasty is warranted if the reason is to plan carotid surgery (endarterectomy), to look for inflammation of the arteries (vasculitis), or to look for and treat the cause of a hemorrhage, such as an aneurysm or arteriovenous malformation. There are essentially no serious medical risks from CT scanning, MRI or ultrasound (Spence 06: 56, 57, 58, 59). An invasive procedure called a cardiac catheterization is performed in a specialized catheterization laboratory (cath lab) under x-ray visualization (cinefluoroscopy) by placing catheters (tubes) through sheaths into the blood vessels (artery and/or vein) and threading the catheters into the heart. Patients are generally given sedation before or during the procedure so they feel more comfortable. Contrast dye is administered to visualize structures, and pressures are recorded to determine heart and valve function. The doctor must be informed if the patient has a contrast dye allergy or a shellfish allergy (Cohen 10: 73). The electrophysiology study (EP study) is a crucial procedure for identifying heart rhythm problems. During the EP study catheters are guided through blood vessels into the heart using an x-ray technique called fluoroscopy imaging. The catheters are placed through the veins, arteries, or both up into the chambers of the heart. The doctor is able to pace (stimulate) the heart at a faster rate than normal and take readings of the signals. Electrical signals are recorded directly from the heart. This test can reveal if a pacemaker or a defibrillator is needed (Cohen 10: 78). 3. Surgery Heart surgery is used to correct heart problems. The operative risk rate in a good center is around 5 percent or less. Although there has been a trend toward operatin on sicker and more elderly patients results continue to improve with overall mortality rates for otherwise healthy individuals of less than 3% (Heger et al '04: 263). Risk of dying during bypass surgery 4.6 11.9 percent. Risk of permanent brain damage from bypass surgery 15-44 percent. Recipients of bypass surgery for whom it prolongs life 2 percent. Risk of death during angioplasty 0.4 2.8 percent. Risk of major complications developing during angioplasty 10 percent. Studies that have found that angioplasty prolongs life or prevents heart attacks but serious mechanical complications can result from trying to threat a tube through an artery. Patients undergo bypass and angioplasty operations primarily to relieve angina and improve blood flow to the heart. Yet there is however a 25 to 50 percent likelihood that within six months their blood vessels will again be blocked, and their chest pain will recur, assuming they continue to eat a meat-based diet (Robbins 01: 23). Opening up blocked arteries via either surgery on the carotid (neck) artery or stenting (inserting a metal expanding sleeve into a narrowed artery to hold it open) reduces stroke risk substantially: in persons in whom the carotid artery is narrowed by 70 percent or more and who have had warning symptoms of stroke, surgically removing the inner layer of the artery with the plaque that is blocking the artery (endarterectomy) reduces stroke or death by two-thirds over two years. (For patients with a narrow carotid artery who have not yet had warning symptoms of a stroke, surgery is only for those at high risk of stroke, as evidence by the particles breaking off the plaque (microemboli) that can be detected by ultrasound of the brain arteries (transcranial Doppler). Patients need to follow their diet, quit smoking and take medication (Spence 06: x, 72). Heart surgery can be done to: correct a congenital heart defect, repair abnormal or damaged arteries and structures in the heart; repair or replace valves that control blood flow through the heart; Implant medical devices that regulate heart rhythms or blood flow; or replace a damaged heart with a healthy heart from a donor (heart transplant). Traditional open heart surgery, is done by opening the chest wall to operate on the heart. Almost always, the chest is opened by cutting through a patient's breastbone. Once the heart is exposed, the patient is connected to a heart-lung bypass machine. The machine takes over the pumping action of the heart. This allows surgeons to operate on a still heart.Heart surgery is done to correct problems with the heart. More than half a million heart surgeries are done each year in the United States for a variety of heart problems. For very ill people with severe heart problems, heart surgery can reduce symptoms, improve quality of life, and increase lifespan (Sanders 08: 20). Ferdinand Sauerbruch (1875-1951) was a German surgeon who introduced a new era into the surgery of the pleural cavity. As a result of the differential pressure procedure he invented it became possible to open the thorax in a low-pressure chamber, without the lung collapsing and respiration ceasing. Today the differential pressure procedure has been replaced by endotracheal narcosis and artificial bronchial respiration. Through the creation of the heart-lung machine, the most difficult heart operations, such as the artificial replacement of the heart-valve, have become possible, today thousands of people are walking around with artificial heart-valves made of Silastik, synthetic material that is not rejected by the living organism. Electrical pacemaker machines are set into the pleural cavity to govern the constant stimulation or regulation of the disturbed activity of the heart (Venzmer 71: 341, 342). At the end of 1967 Professor Christian Barnard, a surgeon in Cape Town, South Africa, succeeded in transplanting the heart of an accident casualty into a patient whose own heart was on the point of failing. In 1968 other heart transplants were undertaken with varying success in the U.S.A. Japan and in Europe. Once the immunity barrier is conquered and the rejection reaction arrested, a whole new era of medicine dawned (Venzmer 71: 341, 342, 345, 346). Approximately 20,000 operations of the heart and circulation in patients with congenital heart disease are performed each year in the United States. Nearly 80% of the first-year survivors live to reach adulthood. The trend in cardiac surgery for congenital heart disease has gone from palliative to staged anatomic correction to single-stage total repair (Heger et al '04). The most common type of heart surgery for adults iscoronary artery bypass grafting(CABG). More than 500,000 operations were completed in 2000 (Heger et al '04: 263). Bypasses are done using grafts of either autologous reversed saphenous vein or internal mammary artery (usually the left internal mammary artery is used owing to the proximity to the heart). The long-term patency of saphenous vein grafts is 60% or less at 10 years, owing to pathologic changes, including thrombosis (usually occurs early), intimal thickening (which usually occurs several months to several years postoperatively) and atherosclerosis in the graft, sometimes with superimposed plaque rupture, thrombi or aneurysms (usually more than 2 to 3 years). In contrast the internal mammary artery has a greater than 90% patency at 10 years (Schoen 94: 515). The clinical performance of a vascular graft depends primarily on its type and location. Large-diameter (>10 cm) Dacron grafts in current use function well in high-flow, low resistance locations such as the aorta. In contrast, small-diameter fabric vascular grafts (<6 to 8 mm in diameter) perform less well. The most widely used small vessel replacements are autologous saphenous vein (the patients own vein, dissected free, reversed in direction, and transplanted to a different site) and expanded-polytetrafluoroethylene (ePTFE), essentially a spongy Teflon fabric. Failure of small-diameter vascular postheses (<6 mm diameter) is most frequently due to thrombotic occlusion or intimal fibrous hyperplasia, either generalized (in vein grafts) or anastomotic (in synthetic grafts). The ability to endothelialize cardiovascular prostheses is limited in humans and full endothelialization of clinical grafts is unusual. Luminal coverage develops relatively slowly and incompletely, formation of neointima (a surface covered by endothelial cells, is generally restricted to a 10 to 15 mm zone near the anastomosis and the remainder of the graft surface constitutes a pseudointima (thrombus or cells other than endothelial cells) (Schoen 94: 514). It has been recognized for many years that the left internal mammary is the optimum coronary artery bypass conduit, with a patency rate of more than 90% at 10-year follow-up. During CABG, surgeons use healthy arteries or veins taken from another part of the body to bypass (that is, go around) blocked arteries. CABG relieves chest pain and reduces the risk ofheart attack. Minimally invasive techniques allow surgeons to perform single and sometimes multiple coronary bypass operations through small anterior thoractotomy incisions instead of the traditional median sternotomy. The left internal mammary artery is anastomosed to the left anterior descending artery with the heart beating, thus avoiding the risks of cardiopulmonary bypass and cardiac arrest. There is however concern regarding the long term patency of minimally invasive procedures (Heger et al '04: 263). Surgery for patients with end-stage congestive heart failure currently is limited to heart transplantation, frequently after a period of left ventricular assistance with a mechanical device. Transplant surgery makes use of the super-cooled foreign organs of people who have died in accidents, is complicated by the defense mechanism of the organism against foreign albumen. The number of heart transplants performed in the United States each year is limited to approximately 2,000 (2,500 worldwide) because of the shortage of donor organs. Patients older than age 60 have been shown to have similar early mortality ad length of hospitalization as younger gropus. Five year survival ranges from 71% in older patients to 82% in younger patients. The major current limitation to the long-term success of cardiac transplantation is late, progressive diffuse stenosing intimal proliferation of the coronary arteries (graft arteriosclerosis), which is a problem because denervated hearts feel no chest pain, and congestive heart failure or sudden death is the usual outcome. Hypercholesteremia affects 60-80% of recipients and may contribute to coronary vasculopathy. Statins reduce the level of cholesterol and appear to have the added advantage of decreasing the incidence of cardiac rejection. The outlook is good with a 1-year survival of 70 to 80% and 5 year survival of more than 60% Transplant atherosclerosis is responsible for many later deaths (Heger et al '04: 264). Three major factors contribute to the widespread success of cardiac transplantation; (1) better selection of candidates, (2) improved maintenance immunosuppression (including the use of cyclosporine A, along with steroids and azathioprine) and (3) early histopathologic diagnosis of acute allograft rejection by sequential endomyocardial biopsy. When myocardial injury is not extensive, the rejection episode is usually successfully reversed by increased immunosuppressive therapy. Advanced rejection may be irreversible and fatal often as the result of infection and development of malignancies, particularly lymphomas (generaly related to fungus or the Epstein-Bar virus in the presence of profound chonic therapeutic immunosuppression) (Schoen 94: 580). In catheter ablation a long thin medical device called an ablation catheter is inserted by hand through a blood vessel and then is guided into the heart using x-ray or mapping equipment to find and treat abnormal rhythms. The success rate of catheter ablation is 90 percent or greater for superventricular tachycardia, such as atrial flutter, atrial tachycardia, AV node, AV node reentrant tachycardia, Wolff-Parkinson-White syndrome, 50 to 85 percent for atrial fibrillation, 50 to 75 percent for ventricular tachycardia from coronary artery disease and 90 percent or greater for focal ventricular tachycardia (Cohen 10: 87, 89). Although the risks vary depending on the case, cardiac catheterization in a stable patient at a catheterization laboratory carries a less than 1% probability of morbidity, with major complications such as stroke, myocardial infarction, major bleeding, less than 0.5% and overall mortality less than 0.2% (Heger et al '04: 93. The solution for dysrhythmia is often an implanted battery-powered pacemaker which will jolt the heart to keep it in line. An implantable cardioverter defibrillator (ICD) is connected to at least one wire, which is typically inserted through a blood vessel into the heart. A doctor may prescribe an ICD if there might be a high risk for sudden cardiac death without one. An ICD helps to treat lethal arrhythmias such as ventricular tachycardia and ventricular fibrillation (Cohen 10: 16, 28). When the heart rate is too slow, a person may develop symptoms and may need to have a pacemaker surgically implanted to correct the problem. Disease inside or outside the specialized cardiac conduction tissue can also result in fast heart rhythm problems that might require treatment with medications, catheter ablation (a procedure that identifies the heart rhythm abnormality and destroys specific tissue to cure the rhythm problem) or an implantable device such as a defibrillator (Cohen 10). A pacemaker pulse generator is used to treat slow heart rhythms. One, two or three leads may be attached to the device depending on the number of heart chambers that are required to receive pacing therapy. ICDs were developed in the early 1980s and are very similar to pacemakers. ICDs help regulate both fast rhythms (tachycardias) and slow rhythms (bradycardias). Simply put, ICDs monitor the heart rate, and if it is greater than a predetermined (or programmed) value, the ICD may deliver therapy to treat the arrhythmia. Ventricular tachycardia or ventricular fibrillation may be treated by the delivery of a shock (defibrillation) or rapid pacing (also called antitachycardia pacing). This ability to deliver a shock to the heart to terminate tachycardias is one important difference between and ICD and a simple pacemaker. Implantable cardiac monitors are useful in identifying very rare or infrequent abnormal cardiac rhythms that may result in light-headedness, dizziness, or loss of consciousness. The term pacemaker dependent is used when a patient is completely dependent on the pacing function from the device and has little or no underlying heart rhythm. (Cohen 10: 106, 109, 117, 126). In the United States, medical devices are regulated by the Food and Drug Administration (FDA). The FDA issues three classifications of recall. The most serious is class I recall, in which the device problem may severely impair the safety of the patient and has the potential for severe injury, including death. A class II recall might also have a risk for injury or death, but these outcomes are much less likely to occur. A class III recall is for a problem that is not likely to harm the patient, though there is a very remote chance of injury (Cohen 10: 127). Replacement of damaged cardiac valves with prostheses has become a common and often lifesaving mode of therapy. Artificial valves fall primarily into two categories mechanical prostheses using different types of occluders, such as old style caged balls, tilting disks, or hinged flaps and tissue valves usually bioprostheses consisting of chemically treated animal tissue, especially porcine aortic valve tissue, which has been preserved in a dilute glutaraldehyde solution and subsequently mounted on a prosthetic fram (called a stent) or cryopreserved aortic homografts offer durability in younger patients without the need for anticoagulation. The Medronic-Hall valve is a pivoting disk mechanical prosthesis that is extremely low profile. The St. Jude and Carbomedics valves are hinged, bileaflet valves that are popular among cardiac surgeons becaue of the excellent hemodynamics and ease of implantation. Cryopreserved aortic homografts from deceased human organ donors offer durability in younger patients without the need for anticoagulation. They require special techniques for procurement, storage and implantation and are particularly applicable for patients with native or prosthetic valve endocarditis and the patience to wait for a donor. The Ross procedure is particualry effective in young patietns with aortic valve disease. This technique einvolves replacing the patient's diseasesaortic valve with his or her own pumonic valve and reimplanting the coronary arteries. The pulmonary valve is then replaced with a pulmonary homograft. The Ross procedure offers superior longevity over bioprostheses in younger patients, as well as the advantage of not requiring anticoagulation. Bioprotheses continue to the valve replacement of choice in older patients, especially those older than age 70. Three popular bioprotheses are available in the United States: The Hancock and Carpentier-Edwards valves, which are both porcine bioprostheses, and the Bacter pericardial vavle, which is constructed from bovine pericardium. Bioprostheses are not composed of living tissue; they are a combination chemically treated biologic tissues and artificial materials. In general, these valves have a low incidence of thromboembolisms, especialy in the aortic position. Many patients can go without anticoagulation, but anticoagulation still is advisable for patients with atrial fibrillation, atrial clots, or previous thromboembolism. The primary concern of bioprosthetic valves is valve durability. They are susceptible to primary vavle failure as a result of calcification and structural deterioration, which tends to be accelerated in patients under the age of 40 (Heger et al '04). Approximately 60% of substitute valve recipients have a serious prosthesis-related problem within 10 years postoperatively. The most frequent valve-related complications include (1) thromboembolism (local occlusion of the prosthesis by thrombus or distant thromboemboli), (2) partial dehiscence (separation) of the suture line anchoring the valve leading to a paravalvular leak, (3) infective endocarditis, (4) durability problems caused by structural deterioration, and (5) intrinsic (design-related) obstruction to forward flow. Thromboembolic complications constitute the major problem with mechanical valves. This necessitates long-term anticoagulation. Hemorrhagic side-effects, such as stroke or gastrointestinal bleeding, may arise. Infective endocarditis is an infrequent but serious potential complication developing in about 6% of patients within 5 years of valve replacement. Bioprosthetic valves may develop vegetations that directly involve the prosthetic valvular cusps and can embolize. The major contaminating organisms are staphylococcal skin contaminants (e.g. S. aureus, S. epidermidis) early (less than 1 month) postoperatively and streptococci later. Within 10 years postoperatively, at least 30% of tissue valves require replacement for calcification, often with tearing. Other complications, such as hemolysis induced by high blood shear, mechanical obstruction to flow by mechanical valves and dysfunction due to ingrowth of fibrous tissue, may be serious (Schoen 94: 556, 557). Surgical approaches the pareserve the mitral apparatus result in substantial improvement in left ventricular function compared to replacement procedures in which the subvalvular apparatus is disrupted. Ideal patients for mitral valve repair are those with concalcified valves and mitral regurgitation. Valve repair can include partial resectin of leaflets, lengthening, shortening, transposition, or replacement of chorda tenineae, and placement of valvuloplasty rings to decrease the dize oth e mitral annulus. In 1996 minimally invasive valve surgery began with new technology using smaller incisions, transeosophageal echocardiography (TEE) to assess the competency of the operating room repair, newer perfusion techniques and is as safe or safer than convention open sternotomy cases (Heger et al '04: 265, 266). An endarterectomy is an operation in which a surgeon removes the inner lining of an artery, along with the plaque attached to it. In the case of blockage in the carotid artery, the surgeon makes an incision along the length of the neck, exposing the artery, and clamps the artery above and below the area that needs to be cleaned out. The artery is then opened lengthwise, and the inner lining and plaque are removed. The artery is then sewn closed, the clamps removed and the skin sutured. Some teams routinely put in a shunt. Some medical centers are better than others and it is wise to have a carotid endarterectomy performed in a center where such operations are routine, with a complication rate, established by audit, of 3 percent or less. This surgery should be done by experts with lots of practice, and if a surgeon claims a complication rate of zero, you should assume the complication rate has not been audited and find another surgeon. Until 1991, nobody knew whether this operation produced better results than medical therapy, even though the surgery had been done in about a million individuals. In general surgeons believed that the operation was beneficial, and neurologists had some doubts. In 1991 a major study found that for individuals with severe narrowing of the carotid arteries and symptoms, the benefit of endarterectomy was so clear that the study was stopped after two years, when only 691 individuals had been enrolled. In persons with narrowing of 70 percent or more, stroke and death were reduced from 26 percent to 9 percent over two years; in other words with surgery, they were nearly three times better off. The actual risk at the tie of surgery was a 1 percent risk of death and a 1 percent risk of a severe stroke, with a 4 percent risk of lesser complications. Another clinical trial in Europe produced similar results. In persons with less severe narrowing of the arteries, the benefit of surgery is much less. It is now clear that there is no benefit from surgery in individuals with narrowing less than 50 percent, with narrowing between 50 percent and 70 percent, the benefits depend on other risk factors such as ulceration of the artery, the specific symptoms (ocular vs. hemispheric) sex and associated conditions such as diabetes. The number of patients who need to be treated with surgery (carotid endarterectomy) to prevent 1 stroke in 2 years is estimated for symptomatic narrowing of the carotid artery >70% at 1 patient in 6, for symptomatic moderate narrowing 50-70% 1 patient in 15 and asymptomatic narrowing >60% 1 patient in 67 (Spence 06: 60, 61, 62, 63). At one time, aortic dissection was almost invariably fatal, but the prognosis has markedly improved. The development of surgical procedures involving the aortic wall and the early institution of intensive antihypertensive therapy permit salvage of 65 to 75 percent of patients (Schoen 94: 500, 504). Treatment recommendations for aortic aneurysms are based on the size of the aneurysm. Small aneurysms found early can be treated with "watchful waiting." If the diameter of the aorta is small-less than 3 centimeters (cm)-and there are no symptoms, "watchful waiting" and a followup screening in 5 to 10 years may be all that is needed, as determined by the doctor.If the aorta is between 3 and 4 cm in diameter, the patient should return to the doctor every year for an ultrasound to see if the aneurysm has grown.If the aneurysm is between 4 and 4.5 cm, testing should be repeated every 6 months.If the aorta is larger than 5 cm (2 inches around or about the size of a lemon) or growing more than 1 cm per year, surgery should be considered as soon as possible.Two main types of surgery to repair aortic aneurysms are open abdominal or open chest repair and endovascular repair. The traditional and most common type of surgery for aortic aneurysms is open abdominal or open chest repair. It involves a major incision in the abdomen or chest. General anesthesia is needed with this procedure. The aneurysm is removed and the section of aorta is replaced with an artificial graft made of material such as Dacron or Teflon. The surgery takes 3 to 6 hours, and the patient remains in the hospital for 5 to 8 days. It often takes a month to recover from open abdominal or open chest surgery and return to full activity. Open abdominal and chest surgeries have been performed for 50 years. More than 90 percent of patients make a full recovery. The risk of rupture for a small abdominal aortic aneurysm (less than 4 cm) is about 2%, aneurysms larger than 5 cm are the most dangerous, with a risk 5 to 10% per year. Timely surgery is key, operative mortality for untreated aneurysms is approximately 5% whereas emergency surgery after rupture carries a mortality rate of more than 50% (Schoen '94: 500). Coronary angioplasty is a medical procedure in which a balloon is used to open a blockage in a coronary (heart) artery narrowed by atherosclerosis. This procedure improves blood flow to the heart.Angioplasty is done on more than 1 million people a year in the United States. Serious complications don't occur often, but can happen no matter how careful your doctor is, or how well he or she does the procedure (Sanders 08). For arteries that are causing trouble because they are too narrow a stiff-walled balloon on the tip of a catheter can be used to dilate the artery, a procedure called angioplasty. This method is most useful where the problem is due to reduced blood flow in the heart, leg arteries or kidney arteries. In the brain, however, because there are so many backup arteries, the problems from blocked arteries are mainly due not to reduced blood flow but to emboli, that is chunks of artery wall or of plaque. For that reason angioplasty is not very useful at preventing strokes. The process of balloon dilatation of an atherosclerotic vessel characteristically causes plaque fracture, often with accompanying localized hemorrhagic dissection of the adjacent arterial wall. The plaque splits at is weakest point, which is not necessarily the area most severely obstructed. Uncommonly, abrupt reclosure follows the angioplasty. Nevertheless, most patients improve symptomatically following angioplasty, thereby avoiding the need for aortocoronary bypass graft surgery at that time. The long term success of angioplasty is limited by the development of proliferative restenosis that occurs in approximately 30 to 40% of patients within the first 4 to 6 months following angioplasty (Schoen 94: 513, 514). Percutaneous transluminal coronary angioplasty (PTCA) has changed extensively since it was developed in 1977. Initially, PCTA was limited to sinlge-vessel lesions in patietns with coronary artery disease (CAD) who were symptomatic and undergoing medical therapy. Later this evolved into a much broader spectrum of pateitns undergoing this nonsurgical technique, including those with muyltivessel CAD, patietns with previous CABG surgery and steonosis of the native or graft vessels, patietns with acute myocardial infarction who present early in the course to a propertly equipped facility, patietns with total occlusion, and certain high-risk surgical cases (elderly patietns with renal failure, systemic diseae, and some with severe left ventricular dysfunction). In experience hands, PTCA is a low-risk procedure with 1% or less mortality and approximately 5% morbidity, including myocardial infarction, infection, bleeding and the need for emergency CABG becaue of dissection or acute closure. The success rate for experienced operators is 90% per vessel dilated. The major pitfall is that restenosis which occurs in 30 to 50% of cases and to a variable degree in virtually all lesions. Acute gain is difference in lumen diameter before and immediately after intervention and is the result of arterial expansion or plaque removal. Late loss is the difference in lumen diameter after intervention and at follow-up; late loss is the result of intimal hyperplasia, elastic recoil and vascular remodeling. Restenosis presents as recurrent angina not myocardial infarction or sudden death because the restenotic lesions are less prone to rupture and acutely thrombose. Stenting has had an enormous impact in lowering restenosis rates, accounting for a 30 to 50% decrease. Stenting prevents elastic recoil and constrictive remodeling and are used in more than 80% of interventions (Heger et al '04: 93, 94). Placementof an Endovascular Stent Graft  Credit: American Heart Association In coronary and other arteries that do not stay open after a simple angioplasty to dilate them, it is necessary sometimes to place a metal frame or stent, like a self-expanding sleeve over the balloon used in angioplasty. When the balloon is inflated, the stent opens up and holds itself in place against the artery wall, so that it stays there when the balloon is deflated. Because a stent in essence covers the artery wall with a mesh preventing chunks from embolizing a stent in the carotid artery or possibly the aorta is likely to be useful for preventing strokes. Aortic stents would have to be huge and could likely be put in place with an operation that involves entering the aorta with a large catheter that could be passed through a needle. At present, stents available are not perfect for the carotid arteries: they can kink when you turn your neck. So far, several clinical trials have shown that angioplasty of the carotid arteries carries a much higher risk than carotid endarterectomy (cleaning out the interior artery wall) (Spence 06: 71). To place an endovascular stent graft in an aortic aneurysm a catheter is inserted into an artery in the groin (upper thigh). It is then threaded up to the abdominal aorta, and the stent graft is released from the catheter. The stent graft allows blood to flow through the aneurysm. To perform endovascular repair, the doctor first inserts a catheter into an artery in the groin (upper thigh) and threads it up to the area of the aneurysm. Then, watching on x ray, the surgeon threads the graft (also called a stent graft) into the aorta to the aneurysm. The graft is then expanded inside the aorta and fastened in place to form a stable channel for blood flow. The graft reinforces the weakened section of the aorta to prevent the aneurysm from rupturing. Endovascular repair surgery reduces recovery time to a few days and greatly reduces time in the hospital. The procedure has been used since 1999. Not all aortic aneurysms can be repaired with this procedure. The exact location or size of the aneurysm may prevent the stent graft from being safely or reliably positioned inside the aneurysm (Sanders 08). In 1868, two investigators from Prussia and Italy were the first to report that bone marrow generates blood cells in mammals. This observation was the starting point of intense efforts to replace malfunctioning marrow through the transplantation of blood-forming (hematopoietic) cells in humans. However, it took an entire century to develop reliable techniques to identify suitable donors, design potent antibiotics, and establish essential supportive care methods to successfully perform clinical hematopoietic cell transplantation (HCT) procedures. This important accomplishment would not have been possible without understanding issues related to graft rejection and the prevention of graft-versus-host disease (GVHD), a serious reaction caused by the donors immune cells attacking the recipients vital organs. In 1968, three patients in the United States and the Netherlands suffering from severe combined immunodeficiency syndromes, in which the ability of the bodys immune system to fight infections is compromised, were successfully transplanted and cured by HCT. Since then, the number of HCT procedures has risen to 50,000-60,000 per year, and the cumulative number of patients treated worldwide has now reached 800,000. The majority of HCT recipients are patients with leukemia, lymphoma, myeloma, myelodysplasia, bone marrow failure conditions, severe red blood cell disorders such as sickle cell disease or thalassemia, and certain solid tumors (Blume '08). Hematopoietic cell transplant (HCT) can be obtained from suitably matched related or unrelated volunteer donors (allogeneic HCT) or from the patients own tissues (autologous HCT). Sources of hematopoietic cells include the bone marrow, blood, or umbilical cord blood. International unrelated volunteer donor banks containing information on approximately 12 millionvolunteers are interconnected by worldwide computer systems. Approximately 3,500 HCT procedures from unrelated donors are now performed annually, and almost 40 percent of such transplants involve a donor who is from a different country from the recipient. Inparallel, umbilical cord blood banks are rapidly growing in size and usage. To date, some 10,000 HCT procedures with umbilical cord blood grafts have been performed. The choices of which type of HCT (allogeneic or autologous) and the source of the graft (bone marrow, blood, or cord blood) depend mainly on the patients underlying disease and whether it is in remission. Before transplant, the patient is treated with high-dose chemotherapy, with or without radiation therapy, to eradicate the cancerous cells (prior to both autologous and allogeneic HCT), and to suppress the patients immune system to prevent it from attacking the donor hematopoietic cells (prior to allogeneic HCT). Morerecently, it has been established that less intensive pre-transplant treatment also allows successful transplantation, but with less severe side effects. Such reduced intensity transplants prevent later relapses by maintaining the bodys ability to launch an immuneattack by the new marrow against the cancer. This graft-versus-malignancy effect is a critical element for cure through allogeneic HCT. Reduced-intensity regimens have also made it possible to extend HCT to older patients (up to 75 years) and younger patients with health problems that make them ineligible for high-intensity regimens. Significant post-transplant problems can result from toxic effects related to the preparatory treatments, GVHD, infections, and relapse of the underlying disease. Continued research is leading to further improvements and better survival results. The long-term outcome of HCT procedures depends on whether or not the patient is in remission. While 50-80 percent ofleukemia patients can be cured by allogeneic HCT if performed during first remission, the expectation for success is markedly reduced for those whose HCT is carried out in more advanced stages of their disease. Likewise, the long-term results of autologous HCT are strongly influenced by the amount of cancer in the patients body at the time of transplantation, with relapse being the leading cause for treatment failure (Blume '08). Parathyroid gland surgery is performed if some calcium stones are caused by overactive parathyroid glands, which are located on the four corners of your thyroid gland, just below your Adam's apple. When these glands produce too much parathyroid hormone (hyperparathyroidism), calcium levels can become too high and kidney stones may form as a result. Hyperparathyroidism sometimes occurs when a small, benign tumor forms in one of the parathyroid glands or another condition leads these glands to produce more parathyroid hormone. Removing the growth from the gland stops the formation of kidney stones. Or a doctor may recommend treatment of the condition that's causing your parathyroid gland to overproduce the hormone. Surgery is the most common treatment for primary hyperparathyroidism and provides a cure in at least 90 percent of all cases. A surgeon will remove only those glands that are enlarged or have a tumor (adenoma). If all four glands are affected, a surgeon will likely remove only three glands and perhaps a portion of the fourth leaving some functioning parathyroid tissue. Surgery may be done as an outpatient procedure. The indication for kidney transplantation isend-stage renal disease(ESRD), regardless of the primary cause. This is defined as a glomerular filtration rate <15ml/min/1.73 sq.m. Common diseases leading to ESRD includemalignant hypertension,infections,diabetes mellitus, andfocal segmental glomerulosclerosis; genetic causes includepolycystic kidney disease, a number of inborn errors of metabolism, and autoimmune conditions such as HYPERLINK "http://en.wikipedia.org/wiki/Systemic_lupus_erythematosus" \o "Systemic lupus erythematosus" lupus. Diabetes is the most common cause of kidney transplantation, accounting for approximately 25% of those in theUS. The majority of renal transplant recipients are on dialysis (peritoneal dialysis or hemofiltration) at the time of transplantation. However, individuals with chronic renal failure who have a living donor available may undergo pre-emptive transplantation before dialysis is needed. There is good evidence that kidney donation is not associated with long-term harm to the donor.In some cases of male living donors a hydrocele may occur in the scrotum related to the side of the nephrectomy. Traditionally, the donor procedure has been through a single incision of 47 inches (1018cm), but live donation is being increasingly performed bylaparoscopic surgery. This reduces pain and accelerates recovery for the donor. Operative time and complications decreased significantly after a surgeon performed 150 cases. Live donor kidney grafts have higher long-term success rates than those from deceased donors.Since the increase in the use of laparoscopic surgery, the number of live donors has increased. Any advance which leads to a decrease in pain and scarring and swifter recovery has the potential to boost donor numbers. In January 2009, the firstall-robotickidney transplant was performed atSaint Barnabas Medical Centerthrough a two-inch incision. In the following six months, the same team performed eight more robotic-assisted transplants. In 2004 the FDA approved the Cedars-Sinai High Dose IVIG therapy which reduces the need for the living donor to be the sameblood type(ABO compatible) or even atissue match. The therapy reduced the incidence of the recipient's immune system rejecting the donated kidney in highly sensitized patients. In 2009 at theJohns Hopkins Medical Center, a healthy kidney was removed through the donor's vagina. Vaginal donations promise to speed recovery and reduce scarring. Since medication to prevent rejection is so effective, donors do not need to be genetically similar to their recipient. Most donated kidneys come from deceased donors; however, the utilization of living donors in the United States is on the rise. In 2006, 47% of donated kidneys were from living donors.This varies by country: for example, only 3% of kidneys transplanted during 2006 in Spain came from living donors. 4. Medicine Hawthorne (Crataegus laevigata) is considered the herb supreme for the heart (Elvin-Lewis 77: 194)(Gladstar '12). The berries are tasty and often enjoyed in syrups, jams and jellies. They also make good medicine, as do the flower and leaf. The berries, leaves and flowers are rich in bioflavonoids, vitamin C, antioxidants, choline, acetylcholine, quercitin, triterpenoids, cretegin, rutin and procanidins, which feed and tone the heart. Hawthorne works in part by dilating the arteries and veins, enabling blood to flow more freely and releasing cardiovascular constrictions and blockages. It strengthens the heart muscle while helping to normalize and regulate blood pressure. It also helps maintain healthy cholesterol levels. Hawthorne is outstanding both to prevent heart problems and to treat high or low blood pressure, heart disease, edema, angina and heart arrhythmia. Hawthorn doesnt store in the body and isnt accumulative in action, its important to take on a regular basis if using as a heart tonic. Hawthorne also helps to stabilize collagen and support the health and repair of ligaments, tendons and muscles. Hawthorne strengthens capillaries, useful for bruises. Combine with lemon balm, the milky tops of oats and St. Johns wort for a wonderful tea that helps alleviate grief. Powder dried Hawthorne berries with cinnamon, ginger and cardamom powder and sprinkle on boiled or steamed vegetables to boost flavor and treat heartache. The trees are hardy and can live 200 years. Some species are short and scraggly, some grow as thick hedgerows in the Irish, English and Italian countryside, all have thorns. Hawthorne does well in full-sun or partial shade at the edge of a forest or wooded area. It prefers rich, alkaline soil. Several varieties can be found at nurseries but hawthorne self-sows readily, and its easy to dig up the young saplings usually found in abundance beneath the mother tree to transplant to a new location (Gladstar '12). The miraculous affects of Digitalis against congestive heart failure and of Rauvolfia against hypertension were among the great medical advances of the eighteenth and twentieth centuries. Both substances had long histories of use in domestic medicine before their rediscovery by researchers and incorporation into orthodox medical practice. Adverse reactions are found in about 20% of hospitalized patients receiving Digitalis preparations (Elvin-Lewis 77: 184, 186). The FDA required warning for Digitalis and related cardiotonic drugs for human use in oral dosage forms, states "Digitalis alone or with other drugs has been used in the treatment of obesity. This use of digoxin or other digitalis glycosides is unwarranted. Moreover, since they may cause potentially fatal arrhythmias or other adverse effects, the use of these drugs in the treatment of obesity is dangerous"  HYPERLINK "http://edocket.access.gpo.gov/cfr_2011/aprqtr/21cfr201.317.htm" 21CFR201.317 to which could be appended, "Hawthorne is the supreme herb for the heart". With Digitalis as the competition the ABC of adrenergenic blockers developed since the 1970s have been abused in the treatment of congestive heart failure and because these drugs have monopolized the literature pertaining to hypertension and cardiovascular drugs it seems fitting to first prescribe Rauvolfia alkaloids, hydrochlorothiazide (HCTZ) or felodipine to minimize paranoia regarding the appropriate treatment of malignant hypertension for which medicine is essential. Are the blood pressure moderating effects of Hawthorne adequate? Hawthorne in bloom  Credit: Sanders '12 Angina pectoris pain occurs when myocardial oxygen consumption exceeds the capacity of the coronary system to deliver oxygen. Papaverine, from Papaver somniferum and aminophylline from Camellia sinensis (black and green tea) also relax smooth muscles and used in the treatment of angina pectoris (Elvin-Lewis 77: 178). It is probably a good idea to drink tea (Camellia sinensi) instead of coffie. Coronary vasodilators act directly but non-selectively on smooth muscles to produce relaxation without paralyzing the muscle. Nitrates and nitrites are effective. Although they have been shown to improve exercise tolerance and the quality of life of patients with coronary artery disease enabling a full recovery in many cases, there is no evidence that nitrates improve mortality as a result of ischemic heart disease. The usual maintenance dose of isosorbide dinitrate is 30 mg for the immediate-release preparation and 40 mg for the extended-release preparation. All nitrates cause rapid development of tolerance, but a dosing interval at 7 am, noon, 5 pm and a drug free overnight interval can larely reverse the tolerance that develops during the day. Transdermal nitroglycerin preparations, are being replaced with extended-release oral preparations. Unfortunately, although some patients are able to exercise and make a recovery nitrates and nitrites do not show the statistical improvement in longevity and resistance to heart attacks exhibited by statins and anti-platelet drugs such as Aspirin (Heger et al '04: 278). Prescription cardiac drugs, other than statins which reduce the risk of dying from heart attack by 30% and stroke by 50%, but including antihypertensive drugs which are rattled off as heart medicine by every nursing school graduate (note the ACE inhibitor, Angiotensin Receptor Blocker (ARB), Alpha, Beta and Calcium channel blocker in light of 18USC(113A,B, & C), are consistently the second leading cause of fatal drug overdose reported by the annual report of the National Association of Poison Control Centers (Bronstein '10-11). Drugs called anticoagulants, such as warfarin (Coumadin, and other names), which reduce the production of clotting proteins, will reduce stroke risk by about half over one year in patients with atrial fibrillation (rapid, irregular heart contractions), and in other cases where clots are forming in the heart or veins and embolizing to the brain. Other drugs that reduce clotting by interfering with blood platelets, antiplatelet agents such as Aspirin, (acetylsalicylic acid (ASA)), Plavix (clopidogrel) or combination of ASA/dipyridamole (marketed as Aggrenox) will reduce ischemic stroke risk by about 25-30 percent in three to four years, but these will prevent only strokes due to embolization of platelet aggregates, and would very likely be fatal in a hemmorhagic stroke usually caused by high blood pressure. When administered within three hours of a stroke tissue plasminogen activator (tPA) reduces the chances of permanent disability by 30% (Spence '05: X). Heparin, a natural anticoagulant in blood, is commercially available from animal sources, especially beef lung. Hemorrhage due to overdose of anticoagulants may be controlled quickly by the administration of vitamin K, found in green leafy vegetables (Elvin-Lewis 77: 192). The AMA Code of Medical Ethics states The right of self-decision can be effectively exercised only if the patient possesses enough information to enable an intelligent choice (Graveline 04: vi) 81 mg aspirin is not enough, heart patients need to leave the emergency room with a prescription for scrubs, four hours daily cardiovascular exercise, aspirin, Hawthorne herbal tea or tincture, statin cholesterol lowering drugs and vegan diet!!! The vegan diet, no animal products, is the appropriate response to angina pectoris. People with high blood pressure need to be salt free and this includes cheese and bread that is not labeled salt free. Atherosclerosis, the leading cause of death, is generally initiated by exposure to cardiac glycosides that cause hyperlipidemia whereby fats, particularly animal fats, stick to the artery wall, partially or fully occluding blood flow the myocardial muscle which induces ischemia, necrosis of damage cardiac muscle and vascular tissue, with a propensity for bacterial infection and a life-threatening allergy to all animal products and cardiac glycosides in the plant kingdom. The extent of arteriosclerosis is dependent on the availability of (animal) fats and to a lesser extent glucose (sugar), simple carbohydrates, and gluten (wheat protein) that is consumed. A daily vegetarian diet, including probiotic yoghurt, aged cheese and maybe egg, which constites a lacto-ovo-vegetarian, may be needed to avoid dependency on the medicinal constipating and dental benefits of meat. The heart however does not tolerate anything but organic fruit, vegetables and whole grains boiled in water. By not introducing any cholesterol or fat into the body levels of low density lipoproteins, bad cholesterol, and triglycerides, the most common form of fat cell, are lowered, and then through osmosis the blood will reabsorb fatty atheromatous plaques and necrotic heart muscle tissue, that will scar and be healed. No fat, sugar or salt. The heart is a higher treatment priority than diarrhea, other than cholera, but in the long run animal products are needed to prevent malabsorption and protect the teeth from cavities. 25-50 billion probiotic organism capsules, vitamin B12, vitamin D, calcium supplementation and phosphorus found in soy and mung beans are very useful, for sustaining a vegan diet. It may take a serious myocardial infarction causing angina pectoris up to seven weeks to heal in the absence of inactivity, infection, re-exposure to cardiac glycosides (beware of sugar, gluten, politics and alma mater), famine or any fat in the diet, at all. Body fat burns in tolerable exertion related doses. Starving is highly ill-advised, vegetables are low in calories so the active obese vegan will need to eat more pounds of food than usual to avoid being hungry but is still more likely to lose weight than any other fad diet. Exercise is critical. It is absolutely critical that sedentary work be limited and balanced with adequate four hour minimal healing walk or one hour run and one hour floor exercise daily. Gainful physical labor involving constant weight lifting for eight hours a day is typically the best exercise for the heart. In the study of medicine the balance between athletics and scholarship is as vital as rice and vegetables. Before 1950 the inflexible fate of those with high blood pressure was a stroke, heart failure, or kidney failure, but today, thanks to the use of Rauvolfia extracts, an Ayurvedic treatment for schizophrenia, a large percentage of cases of hypertension can be controlled. Reserpine and other Rauvolfia alkaloids act on the sympathetic nervous system by depleting almost all the neurotransmitter substance, norepinephrine, from sympathetic nerve tissue. This neural blocking results in relaxation of the vessels and output of the heart, with subsequent reduction in blood pressure. By chance patients being treated for malaria with Cinchona bark containing quinine and other alkaloids were found to be free of arrhythmias. Subsequent investigation proved that quinine, and more importantly quinidine, regulated atrial fibrillation and flutter. Quinidine may suppress abnormal rhythms in any chamber of the heart but in other studies can cause certain dangerous arrythmias. Allocryptopine from Fagara coca controls atrial arrhythms and is said to be more effective than quinidine (Elvin-Lewis '77: 5, 187, 190-191). The ABC of adrenergenic blockers developed since the 1970s have been abused in the treatment of congestive heart failure and because these drugs have monopolized the literature pertaining to hypertension and cardiovascular drugs it seems fitting to first prescribe Rauvolfia alkaloids to minimize paranoia regarding the appropriate treatment of malignant hypertension for which medicine is essential. A daily dose of 12.5 mg hydrochlorothiazide (HCTZ) is the commonest and cheapest drug for treating high blood pressure. Drugs in the class called dihydropyridines, the largest group, tend to be the best at lowering blood pressure. The best value is felodipine, and if it is causing too many side effects, amlodipine may be better (Spence '05). Digitalis purpurea, or foxglove had been used by illiterate farmers and housewives in England and on the Continent for centuries to treat congestive heart failure and arrhythmia. Digitalis slows the wildly beating ventricles to a normal level by blocking or delaying the conduction of the electric impulse through the atrioventricular node. By increasing the heart stoke, Digitalis increases the amount of blood being oxygenated by the lungs, as well as the blood in general circulation, by as much as 30% with each beat. Because of this improved action of the heart and circulation, the drug tends to improve renal secretion to relieve edema, and to aid the cardiac muscle to compensate for mechanical defects or structural lesions. More than 3 million heart patients in the United States routinely use the glycoside digoxin from D. lanata, and this is but one of six glycosides from Digitalis prescribed today. Digitalis whole leaf, digitoxin, digoxin, lanatoside C, acetyldigitoxin and deslanoside. Digitoxin and digoxin are not only listed toxic cardiac glycosides but are sold under those names. Since the effective dose may be as high as 70% of the toxic dose, administration must be done carefully on an individual basis. Various Digitalis glycosides, all taken orally, include D. purpurea whole powdered leaf, containing a large number of glycosides of which about 30 are identified besides the medicinally important digitoxin, gitaloxin, and gitoxin. The average concentration of these three glycosides in a leaf is 0.16%. Recently it has been recommended the use of whole leaf preparations over isolated glycosides. Cardiac glycosides bring only temporary relief and must be administered orally during the whole course of the disease. Adverse reactions are found in about 20% of hospitalized patients receiving Digitalis preparations (Elvin-Lewis 77: 184, 186). Other cardiac stimulants and tonics include Apocynum cannabinum (dogbane), Asarum canadense (American wild ginger), Asclepia spp (milkweeds), Crateagus tomoentosa (hawthorne), Euonymus atropurpureus (wahoo or burning bush), Heuchera spp. (alum root) Ilex opaca (American Holly), Ipomoea leptophylla (bush morning glory), Monarda spp. (horsemint), Veratrum californicum (hellebore), Veratrum viride (green hellebore), and Viola spp. (violet). Without foxglove, or other plants producing cardiotonic compounds, congestive heart failure and death would occur inevitably, and perhaps quickly. More than 3 million Americans take an extract of foxglove daily. But for some reason related to the limited effectiveness of the prescription for 81 mg Aspirin at avoiding unnecessary surgeries the hospital has neglected to prescribe the "supreme herb for the heart", the only medicine that treats the full constellation of congestive heart failure symptoms Hawthorne (Elvin-Lewis '77: 193, 194) and statin life extending drugs, as they have their kidneys. In 1950 Philip S. Hench and Edward C. Kendall were awarded the Nobel Prize for their development of cortisone. In 1955 American research scientists succeeded in dehydrating cortisone under the influence of micro-organisms. This resulted in the creation of cortisone derivatives which could be taken orally in tablet form as the corticosteroids prednisone, prednisolone and dexamethasome, considerably extended the range of application. The classic disease susceptible to cortisone treatment, chronic rheumatic endocarditis, has long stopped being the exclusive disease treated by the new preparations, they also act with considerable reliability on Addisons disease, gout, asthma, hay fever, and other conditions due to hypersensitivity, they are also used when extraordinary demands are placed on the body, such as the results of operations, graft versus host disease, accidents and the like, as well as in many other kinds of diseases (Venzmer 71: 343). Bacterial endocarditis results from actual colonization of the endocardium by infectious agents through the interstitial capillary bed beneath the endothelium and the blood within the endo-cardial lumen. Chronic angina pectoris that doesnt fully go away after a day or two, week, month or year, usually happens when dead heart muscle from a myocardial infarction (heart attack) becomes infected with pyogenic organisms most obviously Streptococcus pyogenes, in about 50% of cases of endocarditis, which causes strep throat and rheumatic fever in children and rheumatic heart disease in adults with necrotic heart attack damaged cardiac muscle that doesn't go away like most infections, attacks the valves, creates huge septic vegetations over the myocardium and burdens the vegetarian patient with a 25 percent chance of dying over 10 years, if untreated by antibiotics. Untreated or drug resistant infection is the main reason that the body doesn't heal and acute injury progresses to chronic disease in six months, generally. Some streptococcal illnesses of the heart may last up to 6 weeks without antibiotics and can be severe. Organisms most commonly recovered from such infections are Streptococcus sanguis, S. faecalis, and in heroin addicts, also Candida parapsilosis. It has been reported that 90% of plaques contain Chlamydia pneumoniae. Antibiotics may be necessary to treat bacterial endocarditis, usually caused by -hemolytic strains of pneumococcal bacteria, and the chronic heart patient will want to purchase them online. The bacteria can be found in most plaques and colonize  vegetations on atherosclerotic arteries and necrotic heart muscle that even with treatment is prone to re-infection. Penicillin is generally the most effective treatment for Streptococcus spp. but some people have a life threatening allergy to penicillin, and any antibiotic will work. Most of the bacterial species that infect the heart and kidneys are easily treated with a five day course of any twice a day broad-spectrum antibiotic. This is good because most physicians these days are very poor at treating antiobiotic resistance and have fallen out of love with the best medicine of the 20th entirely, despite the ease with which probiotics taken within two hours of antibiotics consumption and for two weeks after completing the course. Between 1990 and 2000 prescription of antibiotics declined 40% and uninsured people might not be only the patients with chronic rheumatic heart disease because they have not tried any antibiotics, or treated antibiotic resistant bacteria, virus and fungi, since they became infected. Doxycycline, the once a day antibiotic, that permanently yellows the teeth of children under 8, and metronidazole (Flagyl ER) are essential to solving the problem of antibiotic resistance. When pyogenic organisms such as Staphylococcus aureus and Bactroides fragiles are involved, acute bacterial endocarditis may result that does not respond to most antibiotic drugs. Bactroides fragilis, from as far away as the large intestine, can be involved, and there is definitely a connection between diet and the heart. Staphylococcus aureus, often transmitted by the meticulously washed hands of health care workers, tends to resistant to all antibiotics except doxycycline, and the lesions are painful and dangerous with 50% of acute endocarditis from Staph infection resulting in death, according to some health care professionals who don't necessarily know to prescribe doxycycline or use effective and strong chlorine bleach preparations for institutional cleaning and HibiClens for the hands, nonetheless Staph is particularly painful and causes large lesions that are readily colonized by Strep. The fecal coliform Bactroides fragiles and Peptostreptococcus, which may infect the heart, and Clostridium difficile which causes serious infectious diarrhea resist any antibiotic but metronidazole (Flagyl ER). To avoid idiopathic malabsortive disorders of the gut and kidneys it is probably more effective to treat E. coli, the most common cause of bladder and kidney infections, with metronidazole rather than Bactrim, which monopolizes the monograph for E. coli despite a long list of adverse drug reaction and nearly certain vitamin B12 deficiency, post-infectious auto-immune diarrhea and kidney disease due to malabsorption and antibiotic resistance of Clostridium difficile and the common streptococcus treated by all other antibiotics. Viruses and fungi are rare in the heart and many bacterial diseases are kind to the heart although they devastate other parts of the anatomy. Because Sporanox (itraconazole) is stongly contraindicated for the treatment of congestive heart failure due to interactions with Digitalis and hypertension drugs and fungal infections are not likely to compete with bacterial endocarditis, in the absence of profound immunosuppression with antibiotics. Candida albicans is the most common fungal pathogen to arise from antibiotic resistance, $1 athlete's foot cream (clotrimazole) applied topically to the affected area should be effective although an oral anti-Candidal remedy might be purchased over-the-counter to cure antibiotic associated diarrhea. Echovirus is an entero and respiratory infection that also attacks the heart cured only to Human Immune Globulin IV (Elvin-Lewis 77: 178, 28). Cardiovascular and Hypertensive Drugs Drug ClassGeneric (Trade) NameVasodilatorsNitrates and NitritesNitroglycerin, Isosorbide dinitrate, and Isosorbide mononitrateDigitalis drugsDigitoxin (Crystodigin), Digoxin (Lanoxin) Peripheral vasodilator Hydralazine (Apresoline), Terazosin (Hytrin)Antiplatelet agents Cyclo-oxygenase inhibitorAcetylsalicylic acid (ASA; Aspirin)ThienopyridinesClopidogrel (Plavix), Prasugrel (Effient), Ticlopidine (Ticlid), Phosphodiesterase inhibitorDipyridamole (Persantine)CombinationDipyridamole/ASA (Aggrenox)AnticoagulantWarfarin (Coumadin), Heparin (Heparin)Low-molecular weight heparinEnoxaparin (Lovenox), Dalteparin (Fragmin), Nadroparin (Fraxiparine), Danaparoid (Orgaran), Tinzaparin (Innohep), Fondaparinux (Arixtra)Lipid loweringStatins (cholesterol lowering)Atorvastatin (Lipitor), Fluvastatin (Lescol), Lovastatin (Mevacor), Rosuvastatin (Crestor), Pravastatin (Pravachol), Simvastatin (Zocor)Cholesterol absorption inhibitorEzetimibe (Ezetrol, Ezetia)FibratesGemfibrozil (Lopid), Bezafibrate (Bezalip), Fenofibrate (Lipidil)Bile-acid sequestrantCholestyrmaine (Questran), Colestipol (Colestid), Psyllium mucilloid (Metamucil)Niacin, slow-releaseNiacin SR (Ezetrol, Ezetia)Folate vitamin B9 (homocysteine lowering)Antihypertensives (to reduce blood pressure)Rauwolfia alkaloidsRauwolfia serpentine, Rauwolfemms, Reserpidine Oral (Serpasil, Serpalan, Harmonyl, Novoreserpine, Raudixin, Rauval, Rauverid, Reserfia, Serpalan, Serpasil, Wolfina), Deserpidine and Hydrochlorothiazide or Methyclothiazide (Demi-Regroton, Diupres, Diurigen with Reserpine, Diutensen-R, Dureticyl, Enduronyl, Enduronyl Forte, Hydropres, Oreticyl, Oreticyl Forte, Rauzide, Regroton)Diuretic (to reduce water retention)Hydrochlorothiazide (HCTZ) (Hydrodiuril, etc.), Amiloride (Midamor), Chlorothalidone (Hygroton), Furosemide (Lasix), Indapamide (Lozide), Spironolactone (Aldactone)Angiotensin receptor blocker (ARB)Candesartan (Atacand), Eposartan (Teveten), Irbesartan (Avapro), Telmisartan (Micardis), Valsartan (Diovan), Losartan (Cozar)ARB plus diureticCandesartan/HCTZ (Atacand Plus), Eposartan/HCTZ (Tevetan Plus), Irbesartan/HCTZ (Avalide), Telmisartan/HCTZ (Micardis Plus), Valsartan/HCTZ (Diovan Plus) Diuretic combinationAmiloride/HCTZ (Moduret), Atenolol/chlorothalidone (Tenoretic), Ethacrynic acid (Edecrine), Spironolactone/HCTZ (Aldactazide), Triamterene/HCTZ (Dyazide)ACE inhibitorCaptopril (Capoten), Cilazapril (Inhibace), Enalapril (Vasotec), Fosinopril (Monopril), Lisinopril (Zestril), Quinapril (Accupril), Ramipril (Altace), Trandolapril (Mavik) ACE inhibitor plus diureticEnalapril/HCTZ (Vasoretic), Lisinpril/HCTZ (Zestoretic), Perindopril/indapamide (Coversyl Plus), Quinapril/HCTZ (Accuretic)Alpha blocker (to block adrenaline receptors that constrict the arteries, called alpha receptors)Doxazosin (Cardura), Prazosin (Minipress)Beta blockerAcebutolol (Monitan), Atenolol (Tenormin), Metoprolol (Lopressor), Nadolol (Corgard), Pindolol (Visken), Propranolol (Inderal), Timolol (Blocadren) Beta blocker plus diureticAtenolol-chlorthalidone (Tenoretic), Pindolol/HCTZ (viskazide)Calcium channel blockers (to reduce blood pressure, heart pain and arrhythmias)Amlodipine (Norvasc), Felodipine (Plendil), Nifedipine (Adalat), Nicardipine (Cardene), Verapamil (Isoptin, Chronovera)Anti-arrhythmicQuinidine Glutonate, AllocryptopineWegener's granulomatosis and Polyarteritis nodosa (PAN)Corticosteroids (prednisone) and cyclophosphamide IVKawasawki DiseaseGamma globulin IV administered with aspirinSource: Spence '05: xvii xix Five main kinds of drug treatments exist for adverse lipid profiles: (1) bile-acid sequestrant resins such as cholestyramine and colestipol, which work by binding bile salts, which are made from cholesterol, in the bowel, so they are eliminated); (2) exetimibe, which reduces absorption of cholesterol; (3) niacin (a B vitamin); (4) fibrate drugs such as gemfibrozil, bezafibrate, and fenofibrate; and the (5) statin drugs, which inhibit cholesterol synthesis in the liver by inhibiting an enzyme, HMG CoA reductase often called HMG CoA Reductase Inhibitors, called statins such as: Lovastatin, simvastatin, pravastatin, fluvastatin, atorvastatin, and rosuvastatin. The easiest and cheapest cholesterol lowering treatment is Niacin B vitamin 100 mg, or half a 5000 mg tablet three times a day after meals, and then increase it about every third day until you are up to 500 mg three times a day. Some people take a gram (1,000 mg) or more three times a day, but 500 mg three times a day will achieve most of the benefit with less risk of gout and diabetes. For many individuals with osteoarthritis, best treated with ibuprofen, or painful backs and necks, acetylsalicylic acid (ASA, Aspirin) or acetaminophen (Tylenol) may be more effective than other NSAIDs. People with gout may find allopurinol a useful preventive and colchicine, a useful treatment, rather than relying on NSAIDs for prevention. Colchicine, which can be used even in kidney failure and heart failure, is an old remedy (Spence '05: 113, 115, 123, 124). Statin drugs, which reduce blood cholesterol levels by inhibiting a key enzyme involved in the biosynthesis of cholesterol, reduce heart attacks by 40 percent in six years, or better. They also reduce stroke in individuals with coronary disease by about 30 percent. The risk of a significant adverse reaction from a cholesterol-lowering drug is about 1:1,000 and that risk can be virtually eliminated by having a blood test to measure the blood levels of enzymes from the muscles and liver; if a problem shows up and you stop the drug, the problem will almost always clear up, unless the blood test was done too late A risk of 1: 1,000 is 0.1 percent; subtract that from 40 percent and you still have a net benefit of 39.99 percent in other words, the benefit outweigh the risk by about 400 to 1. The risk of a serious adverse effect from the drug is about one in a thousand, so the balance is strongly in favor of staying on the medication unless there is strong evidence that the medication is causing the symptoms. Most people tolerate statins very well; only about 1 in 15,000 will have significant liver problems which go away after stopping the drug. About 1-3 percent of people will have an increase in blood levels of liver enzymes, reflecting not liver damage, but a change in enzyme kinetics. Occasionally, diarrhea is a problem. In addition to large studies that show a decrease in coronary events with use of statins, a number of smaller studies show that these drugs result in improvement of the coronary arteries in some individuals and slow down the rate at which they get worse in virtually all individuals. Ultrasound studies of the carotid arteries also show regression of atherosclerosis with effective LD cholesterol reduction and increases in HDL. Lowering cholesterol makes plaques less likely to rupture and improves the function of the endothelium (the lining of the artery) (Spence '05: 112, 117). Cholesterol, discovered as a major constituent of gallstones, was identified in 1775 as the first known steroid. After decades of concentrating on cholesterol as the supposed culprit in arteriosclerosis the development of statin drugs was almost inevitable. Statin drugs Lipitor, Mevacor, Zocor, Pravachol, or the ill-fated Baycol, all use HMG-CoA reductase enzyme inhibitors to halt the cholesterol synthetic pathway. HMG-CoA reductase step is a natural control point for cholesterol synthesis since the reaction was not reversible and it was the slowest step of the entire cholesterol pathway. The Baycol trial held in Corpus Christi, Texas, studied the side effects of statin drugs ending in an injunction against the drug. Monascus purpureus, red yeast rice, is a natural HMG-CoA inhibitor that has been used to ferment rice into wine and as both a spice and preservative (Graveline 04: 39, 40, 43, 41). A 1994 study called the Scandinavian Simvastatin Survival Study (also called 4S) found that lowering cholesterol can prevent heart attacks and reduce death in men and women who already have heart disease and high cholesterol. For over 5 years, more than 4,400 patients with heart disease and total cholesterol levels of 213 mg/dL to 310 mg/dL were given either a cholesterol-lowering drug or a placebo (a dummy pill that looks exactly like the medication). The drug they were given is known as a statin, and it reduced total cholesterol levels by 25 percent and LDL-cholesterol levels by 35 percent. The study found that in those receiving statin, deaths from heart disease were reduced by 42 percent, the chance of having a nonfatal heart attack was reduced by 37 percent, and the need for bypass surgery or angioplasty was reduced by 37 percent. A very important finding is that deaths from causes other than cardiovascular disease were not increased, and so the 42 percent reduction in heart disease deaths resulted in a 30 percent drop in overall deaths from all causes (Sanders 08: 28). In 1996 the results of the Cholesterol and Recurrent Events (CARE) Study also showed the benefits of cholesterol lowering in heart disease patients. This study reported that even in patients with seemingly normal cholesterol levels (average of 209 mg/dL), cholesterol lowering with a statin drug lowered the risk of having another heart attack or dying by 24 percent.A study published in 1998, the Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) study, examined the effects of cholesterol lowering in people with CHD (those who had already experienced a heart attack or had been hospitalized for angina) and who had relatively average cholesterol levels. The LIPID study used a statin drug to lower cholesterol levels in the treatment group. All study participants were counseled about following a cholesterol-lowering diet. The LIPID results showed that a drop of 18 percent in total cholesterol and 25 percent in LDL-cholesterol produced a 24 percent decrease in deaths from CHD among the treatment group compared with the control group (Sanders 08: 28, 29). A recent study of statin drugs in British patients with established, severe arterial damage and were considered at high risk of heart disease. Although a third of these patients had cholesterol levels that were below the level recommended for statin treatment by US guidelines, they like others in the study, lowered their risk for heart attack and stroke by a third if they took Zocor, the statin used in the study. Present knowledge, however, suggests caution against the tendency for broader use of statin drugs (Graveline 04: 72, i) The Scandinavian simvastatin survival study, CARE (Choleseterol and Recurrent Events trial) ECEL, the WOSCOPS (West of Scotland Coronary Prevention trial) and the AFCAPS/TEXCAPS (Air Firce/Texas Coronary Atherosclerosis Prevention study) have failed to show significant statin benefit. Every report of stroke or heart attack risk reduction is effectively neutralized by corresponding increases in all cause mortality or cancer death risk. Recent large-scale prospective trials of statin therapy to lower plasma cholesterol have shown no benefit to all-cause mortality, and several studies show that statin therapy slightly increases the incidence of cancer mortality, offsetting the slight improvement in mortality from vascular disease. Defenders of Lipitor, Zocor, Pravachol, Mevacor and Lescol point out that statins reduce the risks of heart attacks, strokes and cardiovascular deaths. This is true, but helping people also means reducing the risks of serious side effects like chronic muscle pain, muscle injury, liver injury, kidney injury, psychological changes, cognitive impairments, global amnesia and cancer. After years of using statins without difficulty, 1 in 2,000 people develop nerve injuries that can be severe and permanent. With twenty million Americans taking statins, thats 10,000 people per year (Graveline 04: i, v). Statins should probably be discontinued in cases of cancer, dementia, and muscle which is the most common reason given for discontinuing statins. Although recovery is not given as a reason for discontinuing statin use, the $2 per pill price surely limits its use to acute hyperlipidemia following exposure to a cardiac glycoside or fatty meal. Statins are drugs that inhibit cholesterol synthesis in the liver by inhibiting the enzyme, HMG-CoA reductase. There most common side effect is aching and cramps in the muscles, caused by depletion of ubiquinone, also called co-enzyme Q10 (CoQ10). This happens because inhibiting the liver enzyme HMG-CoA reductase lowers not only the cholesterol levels but also the levels of all the metabolites along the pathway, including one that is used to make CoQ10. Biosynthesized in the mitochondria, the tiny powerhouse of the cell that is responsible for cellular respiration and energy ubiquinone functions as a vital and necessary electron carrier to our ultimate respiratory enzyme, cytochrome oxidase. Because of the extremely high energy demands of the heart, this organ is usually the first to feel statin associated CoQ10 depletion as cardiomyopathy and congestive heart failure. CoQ10 supplementation is highly recommended for all patients on statin drugs, as well as limiting doses or stopping statins (Graveline 04: 42). The mitochondria (the metabolic engines of the cells) in the muscles need CoQ10 to work properly, so its depletion can cause muscle cramps and aching. People who develop muscle problems with statins have a genetic predisposition because of metabolic abnormalities that affect the function of the mitochondria. Supplements of CoQ10 reduce muscle pain from statins taken about 60-120 mg twice daily. Another approach is to reduce the dose of statin and add ezetimibe, a drug that lowers cholesterol by blocking its absorption in the lining of the intestine. Ezetimibe doesnt affect the muscles, but it helps the statin work eight times better, so a much lower dose of statin will be effective (Spence '05: 153, 154). Homocysteine is an amino acid (protein building block) produced in the body that may increase blood clotting and irritate blood vessels, leading to blockages in the arteries. High levels homocystine (two homocysteine molecules attached) in the blood and excreted in the urine (homocystinuria) have been identified in seizures, premature strokes, abnormalities of the lens of the eye and development problems. Homocystinuria is due to an inherited deficiency in the enzyme that converts homocyteins to another amino acid, cystathionine. To its work, that enzyme needs vitamin B6 also called pyridoxine, as a cofactor. High blood levels of total homocystein (tHcy, which mens the total of three variants of homocysteine in the blood) affect about 20 percent of North Americans, and about half of individuals who have artery problems. Homocysteine creates problems by producing free radicals such as hydrogen peroxide and by damagaing the inner lining of the artery (the endothelium). Free radicals are chemically active compounds that, among other negative reactions, oxidize LDL cholesterol; homocysteine also consumes nitric oxide, the protective substance produced by the artery wall. High blood levels of homocysteine therefore increase the activatin of platelets and blood clotting, cause constriction of the arteries, and cause proliferation of smooth muscle cells in the artery wall called atherosclerosis, blockage in the arteries. Folic acid 2.5 mg daily will normalize blood levels of homocysteine in about half the cases; a combination of folic acid 1 mg, vitamin B6 10 mg, and vitamin B12 1 mg (1000 mcg) will normalize levels in more than 95 percent of cases. A high dose of B12 is needed. Blood levels of B12 should be above 300 pmol/L. In some cases it is necessary to add a fourth supplement called betaine, and vitamins are not as effective for individuals with kidney failure. Overnight daily dialysis is more effective at lowering homocysteine than routine dialysis three times a week, and sulfur containing compounds called thiols may be useful (Spence '05: 157, 158). Only about 25 percent of people with hypertension have it well controlled. Thiazine diuretics are the commonest and cheapest drug for treating high blood pressure is hydrochlorothizide, a drug that is particularly effective in the elderly and people with African ancestors, it acts first as a diuretic; after six weeks or so, iuts main effect is to relax the small artery branches, the arterioles. The main issue with this drug is determining the correct dose: for most indiviuals a dose of 12.5 mg daily I enough, and for others 12.5 mg every other day. H;ydrochlorothizide is usually available in tablets of 25 mg or more, so half of the smallest tablet is the optimal dose (Spence '05: 127). Drug therapy can now control about 80% of all cases of hypertension. Drugs do not cure, but their control of this disease marks a tremendous change in the outlook for patients whose inflexible fate until 1950 was a stroke, heart failure, or kidney failure (Elvin-Lewis '77: 189). Hydralazine is the old standby among vasodilators, drugs that dilate arteries, which has recently been resurrected for the treatment of heart failure, particularly for African-Americans. When used alone, it causes the heart to speed up and tends to cause throbbing headaches, so it is usually used in combination with beta-blocker (Spence '05: 131). People taking long term diuretic therapy to rid their body of salt and water, often experience adverse effects related to the depletion of the number of ions. Often the rubric hypokalemia (low blood level of potassium) is used to characterize the problem. The problem is however not a low eve of potassium in the blood, it is potassium depletion in the cells throughout the body, including muscles, heart, brain, and elsewhere. Potassium supplements do not restore intracellular potassium unless magnesium is taken at the same time. Maintaining adequate intracellular potassium helps prevent toxicity of digoxin (a heart medication that can cause serious problems if the blood level is too high, or the potassium level in the cells is too low) and minimizes the adverse effects on diabetes and cholesterol. Taking diuretic causes the body to react by turning on hormone systems designed to retain salt and water. Aldosterone causes the kidney to retain sodium and excrete potassium and other ions; when potassium is eventually depleted, there is excretion of hydrogen ions, leading to an alkaline state in the blood (alkalosis). Most individuals with depleted potassium have a normal serum potassium. If taking a diuretic and feel tired, achy, have cramps in extremities, are impotent, and feel faint when standing up, presume depleted potassium. Usually when there is potassium depletion there is also depletion of magnesium, zinc, selenium, rubidium and other ions (Spence '05: 146). Drugs that reduce production of aldosterone by the adrenal gland also are magnesium and potassium sparing. Drugs that block activation of angiotensin by blocking angiotensin-converting enzyme, ACE inhibitors such as captopril, enalapril, lisinopril or any drug with a proper name ending in pril), or by blocking angiotensin II at its receptor angiotensin receptor blockers (ARBs) (losartan irbesartan, candesartan, or other drug ending in sartan) will reduce urinary losses of potassium, magnesium and probably the other ions that are depleted by diuretics. Because potassium loss from the kidney is driven by exchange of potassium for sodium as regulated by aldosterone, salt intake is an important concern. The more salt eaten, the more potassium lost. Every sodium ion reabsorbed from the renal tubule leads to excretion of a potassium ion; high sodium intake aggravates potassium losses, and when potassium is depleted, potassium ions are exchanged for hydrogen ions, leading to acid urine with alkaline blood. Blocking the effect of high renin potassium and magnesiu depletion by blocking the effect of angiotensin II with angiotensin receptor blockers (ARBs) will prevent secondary hyperaldosteronism. This may be the best approach for people who have either congestive heart failure or secondary hyperaldosteronism from renal artery stenosis or other high-renin states. ACE inhibitors, also block formation of angiotensin II, but this effect wears off after a few weeks because there are other pathways for the formation of angiotensin II. If potassium-sparing diuretics and ARBs or ACE inhibitors are used together, there is a real risk of seriously increased levels of potassium in the blood (hyperkalemia). For primary hyperaldosteronism the specific treatment is blockers of aldosterone such as spironolactone and eplerenone; amiloride can also be used and is the specific treatment for hypertension due to abnormalities of the renal tubule such as Liddles syndrome. The problem is not low levels of potassium in the blood (hypokalemia) but potassium/magnesium depletion; potassium supplements do not solve the problem because magnesium is required to restore intracellular potassium. A recommended approach is to: (1) reduce salt intake below 2-3 grams per day; (2) reduce the dose of diuretic, (3) use potassium/magnesium sparing diuretics to prevent losses or (4) use angiotensin blockers to reduce secondary hyperadlosteronism and thus prevent depletion of potassium and magnesium (Spence '05: 147, 148 152). To minimize potassium losses, one can reduce salt intake; use angiotensin-receptor blockers (ARBs) to prevent angiotensin II from causing the adrenal cortex to release aldosterone; or block the effects of aldosterone on the kidney tubule by using potassium-magnesium sparing diuretics. A minority of patients with difficult to treat high blood pressure will require potassium and magnesium supplementation. Potassium depletion is usually managed by a combination of reducing salt intake, reducing the dose of diuretic and using either potassium/magnesium sparing diuretics or drugs that prevent excess aldosterone production such as angiotensin receptor blockers. For most individuals, particularly the elderly, a daily dose of 12.5 mg hydrochlorothiazide (HCTZ) is the commonest and cheapest drug for treating high blood pressure, is enough. Among diuretics that do not deplete the bodys potassium and magnesium, amiloride is generally preferred for men, because men who take spironolactone often have sore nipples and sometimes breast enlargement. This does not appear to be a problem with eplerenone, a new aldosterone antabgonist. Avoid triamterene, because half the people who take it develop an abnormality in the urine (triamterene casts) and it is implicated in kidney inflammation (interstitial mephritis) and kidney stones. If a small does of one of the thiazide family of diuretics if required, a common ratio might be HCTZ 12.5 mg to amiloride 10-20 mg, or spironolactone 100 mg. For people with secondary hyperaldosteronism, overproduction of aldosterone because of high levels of renin and angiotensin - angiotensin receptor blockers are more effective (Spence '05: 149, 150). Any ACE inhibitor will cause a cough in about 8 percent of people and swelling of the face and tongue (angiodedema) in about one in one thousand. One can avoid these adverse effects by switching to angiotensin blockers, which have benefits similar to those of ACE inhibitors. The first dose of any ACE inhibitor or angiotensin blocker can cause a severe drop in blood pressure, particularly in people taking diuretics. They can also cause acute kidney failure in people that have severe narrowing of both kidney arteries. This problem is rare except in very severe high blood pressure or heart failure. Among ACE inhibitors the main difference is due to the presence of a sulfhydryl group in captropril, which is responsible for the loss of taste and a characteristic generalized rash that looks like measles. Both of these problems will disappear if the patient switches to another ACE inhibitor or to an angiotensin blocker. Captopril is very short acting and must be taken two or three times per day to achieve desired effects in all but the least severe cases. Lisinopril, quinapril, and some of the other ACE inhibitors are long acting enough to work well when taken once a day. Captopril is also the most expensive of ACE inhibitors (Spence '05: 145). Beta-blockers block one of the two kinds of adrenaline receptor (a structure on the surface of cells that responds to adrenaline), the beta receptors. Beta receptors are of two types, beta-1 and bta-2. Stimulating beta-1 receptors causes the heart to speed up and beat more forcefullyl. Stimulating the beta-2 receptors causes the bronchi to dilate and the arteries that got to the muscles to dilate. Alpha-blockers block the second of the two kinds of adrenaline receptor, the alpha receptors: the alpha-1 receptor when stimulated causes the arteries to constrict, and the alpha-2 receptor when stimulated inhibits the sympathetic nervous system. Alpha-blockers are used selectively to block the alpha-1 receptors by preventing the arteries from constricting, they tend to lower blood pressure. They also have beneficial effects on cholesterol and diabetes, and are now commonly used for bladder symptoms from prostate gland enlargement. The main ones in use are prazosin, doxazosin, and terazosin. Compared with prazosin, the latter two are longer acting so can be taken less often, and they tend to cause less trouble with a faint feeling on standing. Doxazosin is the longest acting, and probably the best choice for that reason (Spence '05: 128, 129, 130). Beta-blockers have issues in the different ways individual bodies handle the drugs (pharmacokinetics) and the way the drugs interact with adrenaline receptors (pharmacodynamics). Concerns include how drugs metabolize, how long the drug action lasts, how the drugs are absorbed into various body tissues, and how tightly the drug binds to receptors. Propranolol undergoes extensive metabolism during its first pass through the liver (first-pass metabolism); about 70 percent of an oral dose is broken down in the liver and never makes to the rest of the body. Both propranolol and metoprolol have a twenty-fold range in the blood levels achieved with a given dose that in different people can lead to blood levels that range from five to one hundred units. If propranolol and metoprolol dont work well at the dose prescribed hypertension can be controlled, at a much lower cost, with a beta-blocker that is excreted by the kidney or metabolized in a different way. Nadolol and atenolol are two beta-blockers that are excreted by the kidney, creating special problems for the elderly and for people with impaired kidney function. They can build up in the blood-stream, causing relatively slow heart action (bradycardia), and aggravate heart failure, which in turn aggravates the kidney function. If the heart rate has been getting slower and slower switch to a beta-blocker that is not excreted by the kidney, but metabolized by the liver (Spence '05: 140, 141). The best and most convenient beta-blocker is pindolol, it has the most potent ISA, so it does not cause the adverse effects due to blockade of beta-2 receptors. (ISA, intrinsic sympathomimetic activity of drugs that block beta-1 receptors and stimulate beta-2 receptors.) Pindolol is also the best beta-blocker for people with diabetes, high cholesterol, or blocked arteries in the legs; it is less likely to aggravate cholesterol and diabetes, and less likely to cause fatigue and is the least likely to cause rebound hypertension if doses are missed. The downside of pindolol is that small proportion of people (about 5 percent) experience vivid dreams, tremor or anxiety because of the drugs greater penetration into the brain. Beta-blockers penetrate brain tissue to markedly varied extents because of difference in how well they dissolve in fat. These differences explain why pindolol, with its extreme penetration into brain tissue, is the most likely beta-blocker to cause anxiety, tremors and vivid dreams, and why propranolol, which is also concentrated in the brain, is the most likely to cause subjective tiredness and hallucinations. Selective blockade of beta-1 receptors that speed up the heart and cause it to beat harder and stimulation of beta-2 receptors that cause dilation of the large air tubes in the lung and of the arteries that go to muscles. Nonselective drugs such as propranolol, nadolol and timolol are more likely to cause adverse effects due to beta-2 blockade. Drugs that stimulate beta-2 receptors will have a different profile again; pindolol, a relatively potent beta-2 stimulator, had beneficial effects on cholesterol, may benefit diabetes, and is least likely to cause problems with cold extremities and asthma (Spence '05: 141, 142, 144). Calcium-channel antagonists, or calcium-channel blockers, dilate arteries by interfering with the channels that permit calcium to enter cells; they are useful for both hypertension and angina. Calcium-channel antagonists, or calcium-channel blockers, dilate arteries by interfering with the channels that permit calcium to enter cells. Trouble with constipation or shortness of breath or other symptoms of heart failure, is often helped by changing from verapamil or diltiazem to another type of drug, or changing to a dihydropyridine (the largest class of CCBs) such as nifedipine, felodipine, or amlodipine. If the problem is a slow heart rate from diltiazem, changing to a dihydropyridine or another class of drug should help; if it doesnt, check out a pacemaker. Consumers of both diltiazem and a beta-blocker, may need to reduce the dose of beta-blocker. Those having a lot of angina on a dihydropyridine such as felopidipine, are helped by adding a beta-blocker (or switching to diltiazem for those who cant take a beta-blocker). If it doesnt help, find out about endartectomy, angioplasty or bypass surgery, and make sure that all the risk factors are optimally controlled. If the problem is ankle swelling, flushing, or headache, switching from nifedipine or felodipine to amlodipine or another class of drug should help. Diltiazem and verapamil are not very strong and are extremely expensive, so are not advised for treating high blood pressure: the main reason to use them. Verapamil is good for heart-rhythm disturbances such as atrial fibrillation and diltiazem is good for angina (chest pain brought on by exertion, due to narrowing of the coronary arteries) (Spence '05: 139, 140). Drugs in the class called dihydropyridines, the largest group, tend to be the best at lowering blood pressure. Diltiazem is a somewhat weaker vasodilator in the peripheral arteries throughout the body, but it affects the coronary arteries and so may be better for angina. Verapamil is another relatively weak drug that may aggravate heart failure. The main dihydrpyrinidines are nifedipine, felodipine, amlodipine, nisodipine, and nicardipine. Nifedipine and felodipine are quite short acting, and the slow-release pills that have been developed are only partially effective in correcting the problem of peaks and troughs in blood pressure. Nifedipine is relatively expensive, but the best value is felodipine, and if it is causing too many side effects, amlodipine may be better. Nicardipine is very expensive and usually has to be taken several times a day, so it has little advantage. A special problem occurs when dihydropyridines are taken with grapefruit juice that reduce the metabolism of a number of drugs. Felodipine blood levels go up on average about 300 percent with grapefruit juice, nisodipine levels about 500 percent. A number of important interactions occur between grapefruit and other drugs such as cyclosporine, terfenadine (an antihistamine), and propafenone; based on the known metabolism of warfarin and the cholesterol-lowering drugs such as lovastatin and simvastatin, can be anticipated to be affected by grapefruit juice. As a rule of thumb any drug that should not be taken with erythromycin, ketoconazole or itraconazole, should not be taken with grapefruit juice (Spence '05: 162). Grapefruit juice inhibits the metabolism of a number of drugs, whereby a large proportion of the drug is metabolized by oxidation to form another chemical, in the wall of the intestine. This oxidation is performed by a specific form of the family of oxidative enzymes (Cytochrome P450) called CYP3A4. Drugs that are largely metabolized during oxidation are said to have low bioavailability, because a low proportion of the drug is available to the body. When the metabolism of these drugs in the intestinal wall is inhibited, a much larger proportion of the drug is absorbed unchanged, and the blood levels of the drug are much higher. Dihydropyridine calcium-channel antagonists) drugs with high bioavailability such as amlodipine are not much affected by grapefruit juice; nifedipine, which is 60 percent bioavailable, ahs a 30 percent rise in blood levels when taken with grapefruit juice, and nisoldipine, which is 8 percent bioavailbe, goes up on average fivefold up to ninefold. Interesting Florida orange juice has no such effect, although Seville orange juice and lime juice have some effect (though less powerful than grapefruit juice). Other drugs for which the grapefruit juice effect is important include the transplant antirejection drug cyclosporine (a tripling of blood levels); the AIDS drug squinovir (large effects); the sleeping pills midazolam and triazolam; and most importantly, the anti-histamine terfenadine. Both terfenadine and the gut-motility drug cisapride can cause serious heart-rhythm disturbances when their metabolism is inhibited, wherefore they are no longer on the market. Other drugs affected importantly by grapefruit include the anticoagulant warfarin and the heart-rhythm drug propafenone in some individuals, and the cholesterol-lowering drugs lovastatin and simvastatin. Blood levels of both lovastatin and simvastatin can be increased fifteen-fold by a glass of grapefruit juice. Atorvastatin is also affected by grapefruit, although to a much lesser degree, but pravastatin and rosuvastatin are not. A simple rule of thumb is that if a drug should not be taken with erythromycin, ketoconazole or itraconazole, it should not be taken with grapefruit juice. To be safe, don't drink grapefruit juice if taking one of the affected drugs (Spence '05: 162). Adverse Effects of Hypertensive Drugs Drug ClassMain Adverse EffectsACE InhibitorsAcute kidney failure in severe narrowing of both kidney arteries, cough in 8%, swelling of the face and tongue (angiodedema) 1 in 1,000Beta-BlockersBeta 1 to reduce heart rate and contractilityBradycardia and congestive heart failureBeta 2 for vasoconstriction, bronchoconstriction, reduced insulin release, gluconeogenesis and fat metabolismCold extremities, reduced muscle blood flow, Raynauds phenomenon, aggravation of asthma, Type II diabetes, hypoglycemia by insulin and hyperlipidemiaCalcium Channel BlockersVerapamilConstipation, aggravation of congestive heart failureDiltiazemSlow heartbeat (bradycardia)Dihydropyridines (nifedipine, felodipine, amlodipine)Ankle swelling, fast heartbeat (tachycardia), headacheSource: Spence '05: Table 9.1, 9.3; pgs. 139, 145 Decade-old heart attack scars healed after being injected with stem cells from a patients' own bone marrow. So far, eight patients have received the experimental treatment in an ongoing clinical trial. All eight had suffered heart attacks an average of 5 1/2 years prior; one of the patients had his heart attack 11 years earlier. All had dangerously enlarged hearts, with areas of scar tissue from their heart attacks. The researchers harvested bone marrow progenitor cells from four patients and adult stem cells from another four patients. Using a catheter, they then injected the cells into the walls of the patients' hearts. Within three months, the scarred areas of the patients' hearts began to work again. About six months after treatment, and for a year later -- the length of the study so far -- all eight hearts regained a more normal size. They shrank 15% to 20%, three times more than current treatments can achieve. Whether just plain old bone marrow or [adult stem] cells, injected into the scar, and three months later, the area that was completely dead started to contract again. Stem cells are being explored in the treatment of people with recent heart attack damage -- but the "landmark area" is the use of stem cells to treat end-stage heart failure. Stem cells actually reverses the enlargement and their propensity to get worse (DeNoon 11) (Hare '11). In 1868, two investigators from Prussia and Italy were the first to report that bone marrow generates blood cells in mammals. This observation was the starting point of intense efforts to replace malfunctioning marrow through the transplantation of blood-forming (hematopoietic) cells in humans. However, it took an entire century to develop reliable techniques to identify suitable donors, design potent antibiotics, and establish essential supportive care methods to successfully perform clinical hematopoietic cell transplantation (HCT) procedures. This important accomplishment would not have been possible without understanding issues related to graft rejection and the prevention of graft-versus-host disease (GVHD), a serious reaction caused by the donors immune cells attacking the recipients vital organs. In 1968, three patients in the United States and the Netherlands suffering from severe combined immunodeficiency syndromes, in which the ability of the bodys immune system to fight infections is compromised, were successfully transplanted and cured by HCT. Since then, the number of HCT procedures has risen to 50,000-60,000 per year, and the cumulative number of patients treated worldwide has now reached 800,000. The majority of HCT recipients are patients with leukemia, lymphoma, myeloma, myelodysplasia, bone marrow failure conditions, severe red blood cell disorders such as sickle cell disease or thalassemia, and certain solid tumors (Blume '08). Hematopoietic cells can be obtained from suitably matched related or unrelated volunteer donors (allogeneic HCT) or from the patients own tissues (autologous HCT). Sources of hematopoietic cells include the bone marrow, blood, or umbilical cord blood. International unrelated volunteer donor banks containing information on approximately 12 millionvolunteers are interconnected by worldwide computer systems. Approximately 3,500 HCT procedures from unrelated donors are now performed annually, and almost 40 percent of such transplants involve a donor who is from a different country from the recipient. Inparallel, umbilical cord blood banks are rapidly growing in size and usage. To date, some 10,000 HCT procedures with umbilical cord blood grafts have been performed. The choices of which type of HCT (allogeneic or autologous) and the source of the graft (bone marrow, blood, or cord blood) depend mainly on the patients underlying disease and whether it is in remission. Before transplant, the patient is treated with high-dose chemotherapy, with or without radiation therapy, to eradicate the cancerous cells (prior to both autologous and allogeneic HCT), and to suppress the patients immune system to prevent it from attacking the donor hematopoietic cells (prior to allogeneic HCT). Morerecently, it has been established that less intensive pre-transplant treatment also allows successful transplantation, but with less severe side effects. Such reduced intensity transplants prevent later relapses by maintaining the bodys ability to launch an immuneattack by the new marrow against the cancer. This graft-versus-malignancy effect is a critical element for cure through allogeneic HCT. Reduced-intensity regimens have also made it possible to extend HCT to older patients (up to 75 years) and younger patients with health problems that make them ineligible for high-intensity regimens. Significant post-transplant problems can result from toxic effects related to the preparatory treatments, GVHD, infections, and relapse of the underlying disease. Continued research is leading to further improvements and better survival results. The long-term outcome of HCT procedures depends on whether or not the patient is in remission. While 50-80 percent ofleukemia patients can be cured by allogeneic HCT if performed during first remission, the expectation for success is markedly reduced for those whose HCT is carried out in more advanced stages of their disease. Likewise, the long-term results of autologous HCT are strongly influenced by the amount of cancer in the patients body at the time of transplantation, with relapse being the leading cause for treatment failure (Blume '08). Blood transfusions are the transfer of blood, its components, or products from one person (donor) into another persons bloodstream (recipient). Every year in the U.S., more than 20 million units of red blood cells, platelets, and plasma are transfused to treat hematologic conditions such as severe anemia, leukemia, and sickle cell disease. Transfusions have long been associated with some risk to patients. The HIV epidemic during the 1980s was a major cause of fear; regular transfusions, especially of clotting factor concentrates, spread the virus quickly and nearly undetected. That outbreak prompted the developmentof biovigilance or hemovigilance: tracing and tracking transfusion-related adverse events and incidents, both infectious and non-infectious, that affect blood donors and recipients. Another of the most significant issues complicating transfusion safety has been bacterial contamination of blood products, particularly of platelets. However, steps have been taken in the last decade to avoid, detect, and eliminate this complication through improved donor selection, specialized preparation of the arm before needle insertion, and special screening techniques. Blood is regularly tested for infectious disease transmission, particularly for viruses such as Hepatitis B and C, HIV, and West Nile Virus. Serum tests have been replaced by molecular testing called nucleic acid amplification testing (NAT), which finds active viruses in the donors blood to determine infection risk. If an active virus is found, the donor unit is discarded. Experts anticipate that new methods, including new molecular and microarray testing, which can identify many infectious agents rapidly and accurately, will replace or augment serum studies and NAT in the near future. Blood transfusion has never been safer from known infectious risk than it is today (Luban '08). Potential post-transfusion reactions include transfusion-related lung injury (TRALI), during which the donors immune antibodies cause breathing problems in the recipient; transfusion associated cardiac overload (TACO), which is swelling caused by the increased blood volume; and post-transfusion iron overload, which is a buildup of iron in the body, usually caused by multiple or regular transfusions. Immune reactions, which happen when the bodys immune system is affected by the donor blood, also pose several risks to transfused patients. Alloimmunization occurs when the recipient develops an allergic reaction to the donors red blood cells: transfusion-related immune modulation (TRIM) can lead to increased risk of infections and cancer recurrence, post-transfusion graft-versus-host disease (GVHD, when the donors immune system attacks the recipients blood cells), and microchimerism (when a small amount of donor blood persists in the recipients body, causing ongoing low-grade GVHD). Removing white blood cells or radiating blood to prevent white blood cell growth can reduce the likelihood that the recipient will reject the donor blood.New techniques can isolate specialized cell populations from blood most importantly, hematopoietic progenitor cells (HPCs) that are used for stem cell transplantation. Because HPCs are easier to extract and the process is safer for donors, HPC transplantation has replaced bone marrow transplantation for many cancers and other diseases. Researchers are also using umbilical cord stem cells (UCSCs) as a source of HPCs. UCSCs are collected and processed in a method similar to whole blood and are a rich resource for transplantation therapy in pediatric and some adult patients. In the future, these cells may be grown and expanded for clinical use. Furthermore, researchers have isolated specialized cell types other than HPCs that play an important role in cellular therapy because they can modify proliferation and immune responses during the engraftment of transplanted cells (Luban '08). By the early 1980s, human blood, plasma, and plasma-derived products were discovered to be transmitting potentially deadly blood-borne viruses, including hepatitis viruses and HIV. Manufacturers of plasma-derived clotting factor concentrates attempted to kill these viruses with dry heat, solvent-detergent treatment, and pasteurization, with varying degrees of success. By 1985, most patients with hemophilia in the U.S. had been switched to heat-treated concentrates, but many had already been infected with HIV and a large percentage of them succumbed to it. Eventually better screening methods for blood donors were developed, improving the safety of donated plasma. Screening of donors for the hepatitis B virus was already in place, and in 1989 the hepatitis C virus (HCV) was isolated, allowing HCV antibody testing of donors to begin in 1990. HIV was identified in 1984, and by 1985 a blood test for HIV antibodies was instituted in blood and plasma collection facilities. The successful cloning of the factor VIII gene in 1984 was a major breakthrough, allowing production of recombinant human factor VIII (r factor VIII). Clinical trials in humans began three years later, and this was truly an exciting time, especially for families who had lost loved ones to AIDS. By 1992, two pharmaceutical companies had licensed factor VIII products for use in hemophilia A. Cloning of factor IX was first reported in 1982, and a licensed r factor IX product (BeneFIX) became available for people with hemophilia B in 1997. Other significant advances that have been made in recent years include treatment for patients with inhibitors (antibodies that inhibit or interfere with the function of factor VIII or factor IX) and prophylaxis (treatment to prevent disease). Inhibitor antibodies develop in approximately 30-35 percent of people with hemophilia A and 1-3 percent with hemophilia B.Now that we have safer clotting factor replacement products, preventive (prophylactic) treatment has gained acceptance as a means to preserve normal joint and musculoskeletal function inboys and young men with hemophilia (Lucher '08). The Sickle Cell Anemia Control Act of 1972, allotted government health funds for screening, research, and treatment programs. As scientific progress and technology improved, new treatment regimens evolved for sickle cell disease patients. The Prophylactic Penicillin Study (PROPS) found that giving penicillin, an antibiotic, when patients were not sick could prevent death related to serious infections in sickle cell disease. Later, the Multicenter Bone Marrow Transplant Study demonstrated that 84 percent of children with sickle cell disease who received a bone marrow transplant from a matched relative could be cured. Finally, in the mid-1990s, the U.S. Food and Drug Administration approved a new therapy called hydroxyurea as a treatment to decrease complications of the disease. Hydroxyurea works in part by stimulating the body to resume production of fetal hemoglobin (hemoglobin F), a normal hemoglobin in the fetus that prevents sickling. In the 1960s, doctors treating thalassemia patients started to transfuse them with fresh red blood cells every month. This alleviated most of the childhood symptoms and led to a major improvement in survival. It is still used as a treatment today. However, since blood contains large amounts of iron, which the body cannot eliminate naturally, most patients died in their teenage years from damage caused by too much iron. Researchers later found that excess iron could be removed from the body by treatment with a drug called desferoxamine. This drug prevented iron-induced heart disease and helped patients live much longer. Recently, two oral drugs have become available to remove iron. They have dramatically improved the quality of life of patients with iron overload from transfusions for thalassemia (Vichinsky '08). A century ago, two French investigators reported that small amounts of plasma from anemic rabbits injected into normal animals caused an increase in red blood cell production (erythropoiesis) within a few hours. They referred to this activity as hemopoietine. Over time, as investigators became more convinced that this red-blood-cell stimulating activity was caused by a single protein in the blood plasma, they gave it a variety of names erythropoietic-stimulating activity, erythropoietic-stimulating factor, and, ultimately, erythropoietin. Refining the work of the French scientists in the 1950s and 60s, American investigators conclusively showed that a hormone stimulated red cell production, and that the kidneys were the primary source of erythropoietin, and that low oxygen was the main driver of erythropoietin production. Soon, researchers found that patients with anemia responded by increasing their levels of erythropoietin to stimulate increased red blood cell production. Patients who required an increase in red blood cells in order to make up for low oxygen levels in the blood (such as patients with lung disease living at high altitudes, or smoking more than a pack of cigarettes a day) also had elevated erythropoietin levels. In the early 1960s came the development of hemodialysis, a method of removing waste products from the blood when the kidneys are unable to perform this function, to sustain the lives of patients with end-stage kidney disease. As a result of this treatment advance, these patients were able to survive the underlying disease, but their damaged kidneys could no longer make erythropoietin, leaving them severely anemic and in desperate need of Epo therapy. In 1983, scientists discovered a method for mass producing a synthetic version of the hormone. Experiments were conducted to test the safety and effectiveness of the new drug, Epo, for treating anemia in patients with kidney failure. The results of these early clinical trials were dramatic. Patients who had been dependent on frequent blood transfusions were able to increase their red blood cell levels to near-normal within just a few weeks of starting therapy. Patients appetites returned, and they resumed their active lives. It was the convergence of two technologies long-term dialysis and molecular biology that set the stage for anemia management in this group of patients. Since then, millions of patients worldwide have benefited from Epo therapy (Adamsom '08). At any given time, the blood of an average adult carries over a trillion platelets throughout his or her body, each one surviving for about a week before being replenished by new platelets arising in the marrow. Platelets are like microscopic circulating band-aids, constantly looking for leaks in the vascular system and then instantaneously plugging these bleeding sites by sticking to the wound (a process called adhesion), becoming activated locally, and then attracting other circulating platelets to build an impermeable clump (a process called aggregation) at the exact point of damage. This protective mechanism, which is a desirable function of platelets, is called hemostasis. But under some conditions platelets can become harmful, causing plugs to form where there is no bleeding and they are not needed. This typically happens in arteries that have become diseased with atherosclerosis, a condition in which deposits of fat or plaque collect and harden in the arteries, blocking the normal flow of blood. Platelets can stick to atherosclerotic plaques in the coronary and brain arteries and obstruct, or occlude, these vessels causing heart attacks and strokes. This undesirable, pathological process is called thrombosis (Schafer '08). There are two classes of antithrombotic drugs: anticoagulants and antiplatelet drugs. Anticoagulants slow down clotting, thereby reducing fibrin formation and preventing clots from forming and growing. Antiplatelet agents prevent platelets from clumping and also prevent clots from forming and growing. The first antiplatelet drug was aspirin, which has been used to relieve pain for more than 100 years. In the mid-1960s, scientists showed that aspirin prevented platelets from clumping, and subsequent clinical trials showed that it reduces the risk of stroke and heart attack. In 1980, researchers showed that aspirin in very low doses (much lower than that required to relieve a headache) blocked the production of a chemical in platelets that is required for platelet clumping. Antithrombotic therapy has had an enormous impact in several significant ways. Heparin has made bypass surgery and dialysis possible by blocking clotting in external tubing. Antithrombotic therapy has reduced the risk of blood clots in leg veins (also known as deep-vein thrombosis or DVT), a condition that can lead to death from pulmonary embolism (a clot that blocks an artery to the lungs) by more than 70 percent. And most importantly, it has markedly reduced death from heart attacks, the risk of stroke in people with heart irregularities (atrial fibrillation), and the risk of major stroke in patients with mini-strokes (Hirsh '08). It was first noted more than 50 years ago by a private practitioner that aspirin, which had been used in its native form since antiquity to treat fever and pain, was remarkably able to protect individuals from heart attacks. The ability of aspirin to prevent cardiovascular disease was subsequently found by hematologists to be due to its effects on platelets. Beginning in the mid-1960s, several investigators conducted basic hematology research to clearly identify the precise mechanism by which aspirin inhibits platelet activation and aggregation. Aspirin thus became the first effective antiplatelet drug. It is still in wide use today to prevent cardiovascular complications that are caused by pathological platelet occlusion of atherosclerotic arteries. the next clinically effective antiplatelet agent, a monoclonal antibody against the platelet membrane protein that initiates aggregation (the glycoprotein (GP) IIb/IIIa complex). This drug (abciximab) was approved by the FDA in 1994 to reduce the thrombotic complications of coronary angioplasty. Other GP IIb/IIIa receptor antagonists soon followed, and this class of drugs is now in wide use to also treat acute coronary syndromes. Yet another class of antiplatelet drugs called ADP receptor antagonists (ticlopidine, clopidogrel) were first found in 1998 to greatly reduce the occlusion of coronary stents (devices placed inside an atherosclerotic artery to hold it open and prevent further narrowing), a particularly thrombosis-provoking intervention. These new antiplatelet drugs may have wider application in the prevention of vascular disease by improving on or adding to the beneficial actions of aspirin. Excessive interference with platelet function with any of these antiplatelet agents carries with it the risk of causing the opposite of thrombosis, namely bleeding complications (Schafer '08). The anticoagulants heparin and dicumarol were discovered by chance, long before we understood how they worked. Heparin was first discovered in 1916 by a medical student at The Johns Hopkins University who was investigating a clotting product from extracts of dog liver and heart. In 1939, dicumarol (the precursor to warfarin) was extracted by a biochemist at the University of Wisconsin from moldy clover brought to him by a farmer whose prize bull had bled to death after eating the clover. Both of these anticoagulants have been used effectively to prevent clots since 1940. These drugs produce a highly variable anticoagulant effect in patients, requiring their effect to be measured by special blood tests and their dose adjusted according to the results. Heparin acts immediately and is given intravenously (through the veins). Warfarin is swallowed in tablet form, but its anticoagulant effect is delayed for days. Therefore, until recently, patients requiring anticoagulants who were admitted to a hospital were started on a heparin infusion and were then discharged from the hospital after five to seven days on warfarin (Hirsh '08). In the 1970s, three different groups of researchers in Stockholm, London, and Hamilton, Ontario, began work on low-molecular-weight heparin (LMWH). LMWH is produced by chemically splitting heparin into one-third of its original size. It has fewer side effects than heparin and produces a more predictable anticoagulant response. Because LMWH is injected subcutaneously (under the skin) in a fixed dose without the need for anticoagulant monitoring, patients can now be treated at home instead of at the hospital. The first successful synthetic anticoagulants were fondaparinux and bivalirudin. Bivalirudin, a synthetic molecule based on the structure of hirudin (the anti-clotting substance found in leeches), is an effective treatment for patients with heart attacks. Fondaparinux is a small molecule whose structure is based on the active component of the much larger LMWH and heparin molecules. It has advantages over LMWH and heparin and has recently been approved by the FDA. Newer designer drugs that target single clotting factors and that can be taken by mouth are undergoing clinical testing. If successful, we will have safer and more convenient replacements for warfarin, the only oral anticoagulant available for more than 60 years (Hirsh '08). Angiogenesis is the formation of new blood vessels. This process involves the migration, growth, and differentiation of HYPERLINK "http://www.cancer.gov/Common/PopUps/popDefinition.aspx?id=CDR0000044203&version=Patient&language=English" endothelial cells, which line the inside wall of blood vessels. The process of angiogenesis is controlled by chemical signals in the body. These signals can stimulate both the repair of damaged blood vessels and the formation of new blood vessels. Other chemical signals, called angiogenesis inhibitors, interfere with blood vessel formation. Normally, the stimulating and inhibiting effects of these chemical signals are balanced so that blood vessels form only when and where they are needed. Bevacizumab was the first angiogenesis inhibitor that was shown to slow tumor growth and, more important, to extend the lives of patients with some cancers. The FDA has approved other drugs that have antiangiogenic activity, including sorafenib (Nexavar), sunitinib (Sutent), pazopanib (Votrient), and everolimus (Afinitor). Sorafenib is approved for hepatocellular carcinoma and kidney cancer, sunitinib and everolimus for both kidney cancer and neuroendocrine tumors, and pazopanib for kidney cancer. Angiogenesis inhibitors are unique cancer-fighting agents because they tend to inhibit the growth of blood vessels rather than tumor cells. In some cancers, angiogenesis inhibitors are most effective when combined with additional therapies, especially chemotherapy. Angiosarcomas are usually treated with paclitaxel (Taxol), docetaxel (Docefrez, Taxotere), sorafenib (Nexavar), or bevacizumab (Avastin). Lymphangiosarcomas are more difficult to treat. Chemotherapeutic drugs such aspaclitaxel, doxorubicin,ifosfamide, andgemcitabineexhibit antitumor activity. Recently, there has been interest in evaluating the effectiveness of anti-angiogenic drugs in the treatment of lymphangiosarcoma. Early evidence suggests that treatment with one such drug, Bevacizumab, may be effective in treating lymphangiosarcoma.Investigation of bevacizumab in combination with other chemotherapy agents is underway. Interferon-alfa was the first drug specifically approved for the treatment of Kaposi's. It is of particular interest because of its antiproliferative, antiviral (anti-HIV), antiangiogenic, and immune-modulating properties. Etoposide (VP-16) has been evaluated as both an oral and an intravenous treatment for KS. As an oral agent, VP-16 has been evaluated primarily in patients who have undergone prior treatment with multiple cytotoxic agents.When VP-16 is given intravenously (150 mg/m2on days 1 to 3 every 4 weeks), high response rates (78%) have been reported in patients without prior treatment and with good prognosis (no history of opportunistic infection and no constitutional symptoms). The primary toxicity of this agent is myelosuppression, which may necessitate the use of colony-stimulating factors, particularly in patients with advanced disease receiving other myelosuppressive agents. Additionally, alopecia frequently occurs in association with etoposide therapy, and is a consideration for patients who are receiving treatment of their KS for primarily cosmetic purposes. In patients with KS of poor prognosis, bleomycin given intramuscularly (5 mg/day for 3 days) or as a 4-day continuous infusion (6 mg/m2/day) produced a 48% partial response rate. Results of a small, single-institution study in which bleomycin was given as a 72-hour infusion (20 mg/m2/day) to 17 patients indicated a partial response rate of 65%. Bleomycin toxicity appears to be acceptable, with neutropenia an infrequent complication. Doxorubicin (also known by its trade name Adriamycin) is a component of the most widely used combination regimen for HIV-associated KS. In one trial, however, weekly treatment with doxorubicin (25 mg/m2) in patients with AIDS-related KS achieved a partial response rate of only 10%. The primary toxicity of weekly doxorubicin is myelosuppression, even with the relatively low doses prescribed for KS treatment. Alternating vincristine and vinblastine weekly achieves a response rate of 33%. Toxicity includes vincristine-induced neurotoxicity (which limits its usefulness as a single agent) and vinblastine-induced myelosuppression. Paclitaxel A partial response was reported in 13 of 20 patients (65%), with 5 of 6 patients with known pulmonary KS responding, as well as 6 previously treated patients with nonpulmonary KS achieving a partial response. In a second trial, of the 30 evaluable patients, 16 (53%) achieved a partial response. The time to response was short (median of three cycles of treatment). Dramatic improvement in symptomatic lymphedema was noted in 25 of 26 patients. Therapy was well tolerated.Vinorelbine, a semisynthetic vinca alkaloid with a favorable therapeutic index compared to other vinca alkaloids, was evaluated in previously treated patients with progressive AIDS-related KS. Thirty-five evaluable patients were treated with vinorelbine 30 mg/m2 every 2 weeks. Clinical complete and partial remissions were achieved in 43% of patients, with a median progression-free survival of 151 days. The agent was well tolerated, with neutropenia the most frequent dose-limiting toxicity. Two liposomal agents are currently approved for the treatment of KS: liposome-encapsulated daunorubicin (DaunoXome) and liposome-encapsulated doxorubicin (Doxil). Both agents are highly active against KS and have less toxicity than the nonliposomal anthracyclines. Myelosuppression, however, remains the dose-limiting toxicity. Between 1949 and 1954, the first clinical trials that tested combinations of chemotherapy drugs methotrexate and corticosteroids, (and unfortunately 6-MP) for childhood acute lymphoblastic leukemia (ALL) were carried out. Patients lived longer with these new combinations of chemotherapy drugs, but all still died, usually within a year. Because ALL tended to come back in the central nervous system, a major advance was made by aggressively treating the brain and spinal fluid with radiation and drugs that markedly decreased this form of relapse so, one-half of the patients were cured of leukemia. The cure rate now approximates 80 percent and methotrexate is available by prescription for oral consumption (Simone '08). Chronic myeloid leukemia(CML) is one of the four main types of leukemia, affecting approximately 5,000 people per year in the United States. The disease can occur at any age but is primarily a disease of adults. CML is characterized by a massive over-production of white blood cells. A normal white blood cell count ranges between 4,000 and 10,000; in contrast, patients with CML typically have white blood cell counts ranging from 100,000 to as high as 500,000. Because the white blood cells mature and function normally, infections are not a common feature of CML. Rather, symptoms include fatigue due to anemia or abdominal discomfort due to an enlarged spleen. Historically, patients with CML lived no more than three to five years, during which time the disease would quickly transform from a chronic leukemia to an aggressive and fatal acute leukemia. In 1960, Peter Nowell and David Hungerford, working in Philadelphia, described a shortened chromosome in the blood and bone marrow of patients with CML. This was the first consistent chromosomal abnormality associated with a human cancer. Then, in 1973, Janet Rowley showed that this abnormal chromosome, now called the Philadelphia chromosome, came about because of an exchange of genetic material between two chromosomes. In the 1980s, it was demonstrated that the consequence of this chromosome exchange was the production of an abnormal gene calledBCR-ABL fueling the excess growth of white blood cells in CML. With the target identified, a drug discovery program was started, aimed at developing a drug to shut down the activity ofBCR-ABL. The compound that became known as imatinib (Gleevec) was developed in 1992, and studies showed that this compound killed CML cells without harming normal cells. In 1998, the drug was tested in patients with CML who had exhausted standard treatment options and whose life expectancy was limited. Within six months of starting the clinical trials of imatinib, all of the patients had their blood counts return to normal. Remarkably, this once-a-day pill had minimal side effects. These unprecedented results were confirmed in much larger clinical trials, and imatinib was approved by the U.S. Food and Drug Administration (FDA) in 2001, less than three years from the start of the clinical trials. With longer follow-up, this once routinely fatal leukemia now has a five-year survival rate of 95 percent. Newer drugs (dasatinib and nilotinib) have been developed that can shut down most of the mutated forms ofBCR-ABL, and have significant activity in patients with resistance to imatinib; these drugs are also FDA-approved (Druker '08). Chemotherapy for Leukemia and Lymphoma White Cell DiseaseFDA Approved DrugMultiple Myeloma and Plasma Cell DyscraciasOral Thalidomide, with dexamethasome, a corticosteroid. Others: Bortezomib, Carfilzomib, Clafen (Cyclophosphamide), Cyclophosphamide, Cytoxan (Cyclophosphamide), Doxil (Doxorubicin Hydrochloride Liposome), Doxorubicin Hydrochloride Liposome, Dox-SL (Doxorubicin Hydrochloride Liposome), Evacet (Doxorubicin Hydrochloride Liposome), Kyprolis (Carfilzomib), Lenalidomide, LipoDox (Doxorubicin Hydrochloride Liposome), Mozobil (Plerixafor), Neosar (Cyclophosphamide), Plerixafor Pomalidomide (Pomalyst), Pomalyst HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/plerixafor" , Revlimid (Lenalidomide), Synovir (Thalidomide), Thalidomide, Thalomid (Thalidomide), Velcade (Bortezomib), Zoledronic Acid Zometa (Zoledronic Acid).Waldenstrm macroblobulinemia Fludara (fludarabine) andLeustatin(cladribine) first to try.Cytoxan(cyclophosphamide) may be added. Other commonly used chemotherapy drugs areLuekeran(chlorambucil) and prednisone, usually given together, or Adriamycin (doxorubicin). Rituxan(rituximab). Campath(alemtuzumab) has also been an effective treatment, as has Velcade (bortezomib).Langerhans cell histiocytosesOral methotrexate (20 mg/m2) weekly for 6 months or Oral thalidomide 50 mg to 200 mg nightly, with prednisone are taken for low risk disease or vinblastine IV and prednisone for patients with more complicated cases requiring radiation and surgeryAcute LeukemiasAcute lymphoblastic leukemia (ALL)Abitrexate (Methotrexate) HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/ADE" , Adriamycin PFS (Doxorubicin Hydrochloride), Adriamycin RDF (Doxorubicin Hydrochloride), Arranon (Nelarabine), Asparaginase Erwinia chrysanthemi, Cerubidine (Daunorubicin Hydrochloride), Clafen (Cyclophosphamide), Clofarabine, Clofarex (Clofarabine), Clolar (Clofarabine), Cyclophosphamide, Cytarabine, Cytosar-U (Cytarabine), Cytoxan (Cyclophosphamide) HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/dasatinib" , Dasatinib, Daunorubicin Hydrochloride, Doxorubicin Hydrochloride, Erwinaze Asparaginase Erwinia Chrysanthemi), Folex (Methotrexate), Folex PFS (Methotrexate) HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/gemtuzumabozogamicin" , Gleevec (Imatinib Mesylate), Iclusig (Ponatinib Hydrochloride), Imatinib Mesylate, Marqibo (Vincristine Sulfate Liposome), Methotrexate, Methotrexate LPF (Methorexate), Mexate (Methotrexate), Mexate-AQ (Methotrexate), Nelarabine, Neosar (Cyclophosphamide), Oncaspar (Pegaspargase), Pegaspargase, Ponatinib Hydrochloride, Rubidomycin (Daunorubicin Hydrochloride), Sprycel (Dasatinib), Tarabine PFS (Cytarabine), Vincasar PFS (Vincristine Sulfate), Vincristine Sulfate, Vincristine Sulfate LiposomeAcute myeloblastic leukemia (AML)Adriamycin PFS (Doxorubicin Hydrochloride), Adriamycin RDF (Doxorubicin Hydrochloride) HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/alemtuzumab" , Arsenic Trioxide, Cerubidine (Daunorubicin Hydrochloride), Clafen (Cyclophosphamide), Cyclophosphamide, Cytarabine, Cytosar-U (Cytarabine), Cytoxan (Cyclophosphamide), Daunorubicin Hydrochloride, Doxorubicin Hydrochloride, Neosar (Cyclophosphamide) HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/nilotinib" , Rubidomycin (Daunorubicin Hydrochloride) HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/dasatinib" , Tarabine PFS (Cytarabine), Trisenox (Arsenic Trioxide), Vincasar PFS (Vincristine Sulfate), Vincristine Sulfate, combination; ADEMyelodysplastic syndromesChronic myeloid leukemia (CML)Bosulif (Bosutinib), Bosutinib, Clafen (Cyclophosphamide), Cyclophosphamide, Cytarabine, Cytosar-U (Cytarabine) Cytoxan (Cyclophosphamide), Dasatinib HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/daunorubicinhydrochloride" , Gleevec (Imatinib Mesylate), Iclusig (Ponatinib Hydrochloride) HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/fda-ponatinibhydrochloride" , Imatinib Mesylate HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/chlorambucil" , Neosar (Cyclophosphamide), Nilotinib, Omacetaxine Mepesuccinate, Ponatinib Hydrochloride HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/ofatumumab" , Sprycel (Dasatinib), Synribo (Omacetaxine Mepesuccinate) HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/dasatinib" , Tarabine PFS (Cytarabine), Tasigna (Nilotinib) Chronic lymphocytic leukemia (CLL)Alemtuzumab, Ambochlorin (Chlorambucil), Amboclorin (Chlorambucil), Arzerra (Ofatumumab), Bendamustine Hydrochloride, Campath (Alemtuzumab), ChlorambucilClafen (Cyclophosphamide), Cyclophosphamide HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/cytarabine" , Cytoxan (Cyclophosphamide), Fludara (Fludarabine Phosphate), Fludarabine Phosphate, Leukeran (Chlorambucil), Linfolizin (Chlorambucil), Neosar (Cyclophosphamide) HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/nilotinib" , Ofatumumab Treanda (Bendamustine Hydrochloride), combinations CHLORAMBUCIL-PREDNISONE, CVPMeningeal LeukemiaCytarabine, Cytosar-U (Cytarabine) HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/cyclophosphamide" ,Tarabine PFS (Cytarabine), MethotrexateHairy cell leukemiaCladribine (2-chlorodeoxyadenosine, 2-CdA), PentostatinPolycythemia veraAnagrelide (Agrylin), Ruxolitinib (Jakafi)LymphomaHodgkin's lymphomaAdcetris (Brentuximab Vedotin), Adriamycin PFS (Doxorubicin Hydrochloride), Adriamycin RDF (Doxorubicin Hydrochloride), Ambochlorin (Chlorambucil), Amboclorin (Chlorambucil), HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/BEACOPP"  Blenoxane (Bleomycin), Bleomycin, Brentuximab Vedotin, HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/bleomycin"  Chlorambucil, Clafen (Cyclophosphamide), Cyclophosphamide, Cytoxan (Cyclophosphamide), Dacarbazine, Doxorubicin Hydrochloride, DTIC-Dome (Dacarbazine), Leukeran (Chlorambucil), Linfolizin (Chlorambucil), Lomustine, Matulane (Procarbazine Hydrochloride), Neosar (Cyclophosphamide), Procarbazine Hydrochloride, Velban (Vinblastine Sulfate), Velsar (Vinblastine Sulfate), Vinblastine Sulfate, Vincasar PFS (Vincristine Sulfate), Vincristine Sulfate, combinations; ABVD, ABVE, ABVE-PC, BEACOPP, COPP, ICE, MOPP, STANFORD and VAMP.Non-Hodgkin's lymphomaAbitrexate (Methotrexate), Adcetris (Brentuximab Vedotin), Adriamycin PFS (Doxorubicin Hydrochloride), Adriamycin RDF (Doxorubicin Hydrochloride), Ambochlorin (Chlorambucil), Amboclorin (Chlorambucil), Arranon (Nelarabine), Bendamustine Hydrochloride, Bexxar (Tositumomab and Iodine I 131 Tositumomab), Blenoxane (Bleomycin), Bleomycin, Bortezomib, Brentuximab Vedotin, HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/bortezomib"  Chlorambucil, Clafen (Cyclophosphamide), Cyclophosphamide, Cytoxan (Cyclophosphamide), Denileukin Diftitox, DepoCyt (Liposomal Cytarabine), Doxorubicin Hydrochloride, DTIC-Dome (Dacarbazine), Folex (Methotrexate), Folex PFS (Methotrexate), Folotyn (Pralatrexate), Ibritumomab Tiuxetan, Intron A (Recombinant Interferon Alfa-2b) HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/ibritumomabtiuxetan" , Istodax (Romidepsin), Leukeran (Chlorambucil), Linfolizin (Chlorambucil), Liposomal Cytarabine, Matulane (Procarbazine Hydrochloride), Methotrexate, Methotrexate LPF (Methotrexate), Mexate (Methotrexate), Mexate-AQ (Methotrexate), Mozobil (Plerixafor), Nelarabine, Neosar (Cyclophosphamide), Ontak (Denileukin Diftitox), Plerixafor, Pralatrexate, Recombinant Interferon Alfa-2b HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/pralatrexate" , Rituxan (Rituximab), Rituximab, Romidepsin, Tositumomab and Iodine I 131 Tositumomab, Treanda (Bendamustine Hydrochloride), Velban (Vinblastine Sulfate), Velcade (Bortezomib), Velsar (Vinblastine Sulfate), Vinblastine Sulfate, Vincasar PFS (Vincristine Sulfate), Vincristine Sulfate, Vorinostat, Zevalin (Ibritumomab Tiuxetan), Zolinza (Vorinostat) and combinations CHOP, COPP, CVP, EPOCH, ICE, R-CHOP.Source: FDA The cure of Hodgkin lymphoma in the 20th century is another one of cancers biggest success stories. Breakthroughs in radiation therapy and chemotherapy paired with careful clinical research transformed an invariably fatal disorder into one that is routinely cured.The recognition of late adverse effects from radiation therapy and chemotherapy in the form of second cancers, heart and blood vessel disease, and sterility shaped subsequent research efforts to maintain or improve cure rates with fewer complications, an important goal in a disease that primarily affects individuals in their 20s and 30s. Today, as more than 80 percent of patients are cured after primary treatment. Sir Thomas Hodgkin is credited with the initial description of the clinical disorder that bears his name. In 1832, he reported on a group of patients with enlargement of lymph nodes and spleen that differed from the major known maladies of the day. The introduction of the linear accelerator (a radiation machine used to treat cancer) in the treatment of Hodgkin lymphoma at Stanford University resulted in cures of early-stage lymphoma. Meanwhile, a team at the National Cancer Institute safely combined four chemotherapy drugs (mustard, vincristine, procarbazine, and prednisone) known as the MOPP regimen and reported the first cures of advanced Hodgkin lymphoma in 1964. Steadily improving techniques for defining the extent and location of disease (staging) has allowed appropriate modalities of treatment to be selected for individual patients. The late 1970s and 80s presented new challenges in the recognition of adverse effects associated with MOPP and radiation therapy, some of which were not apparent for decades after treatment. This time period also featured another major advance in an alternative four-drug chemotherapy regimen (doxorubicin, bleomycin, vinblastine, and dacarbazine), known as ABVD, that proved to be more effective than MOPP in treating advanced disease and had fewer side effects. In the 1990s, even more effective and less toxic treatments for early-stage lymphoma were devised by reducing the dose and area of the body treated with radiation therapy in combination with briefchemotherapy such as ABVD. The German Hodgkin Study Group introduced an intensive seven-drugchemotherapy program, BEACOPP, to address thefact that approximately 30 percent of advancedHodgkin's lymphoma was not cured with ABVD. Although associated with more severe early toxicity andsterility, a higher cure rate and improved survival were achieved with BEACOPP in a randomized clinicaltrial (Horning '08). The development of the drug rituximab as a therapy for B-cell lymphoma (a type of cancer affecting cells of the immune system) provides an excellent illustration of how great improvements in patient care were made through the discovery of a therapy that destroys cancer cells without harming other cells in the body. The discovery of rituximab, an antibody that recognizes CD20, a target shared by malignant lymphoma cells from almost all patients, but also found on normal, immune B cells. Rituximab proved to be effective in treating B-cell lymphoma, and the elimination of normal B cells was surprisingly not harmful. Because rituximab does not affect other normal cells in the body, it can be combined with other therapies. Today, rituximab is part of the regular treatment for almost all patients with B-cell lymphoma, and it has prolonged the lives of many of them. Rituximab can also treat many non-cancerous diseases caused by overactive B cells of the immune system. Rituximab has been used to treat rheumatoid arthritis, multiple sclerosis, and a growing list of non-cancerous conditions (Levy, Malony & Miller '08). Bone pain, known as myeloma, or multiple myeloma if there are multiple bone infections, is an extremely common serious complication because it is crippling and untreated infections can break through the bone to marrow causing leukemia or through soft tissue to the lymphatic system, causing lymphomas. Bone pain is the primary physical symptom of leukemia and is the most painful symptom in lymphoma. Oral Thalidomide, used in conjunction with dexamethsaome, a corticosteroid, are the first FDA approved chemotherapeutic drugs usually taken by people diagnosed with multiple myeloma and plasma cell dyscracias. Others include: Bortezomib, Carfilzomib, Clafen (Cyclophosphamide), Cyclophosphamide, Cytoxan (Cyclophosphamide), Doxil (Doxorubicin Hydrochloride Liposome), Doxorubicin Hydrochloride Liposome, Dox-SL (Doxorubicin Hydrochloride Liposome), Evacet (Doxorubicin Hydrochloride Liposome), Kyprolis (Carfilzomib), Lenalidomide, LipoDox (Doxorubicin Hydrochloride Liposome), Mozobil (Plerixafor), Neosar (Cyclophosphamide), Plerixafor Pomalidomide (Pomalyst), Pomalyst HYPERLINK "http://www.cancer.gov/cancertopics/druginfo/plerixafor" , Revlimid (Lenalidomide), Synovir (Thalidomide), Thalidomide, Thalomid (Thalidomide), Velcade (Bortezomib), Zoledronic Acid Zometa (Zoledronic Acid). Radiation therapy may be done to relieve bone pain or treat abone tumor. Two types of bone marrow transplantation may be tried: Autologous bone marrow or stem cell transplantation makes use of ones own stem cells. Allogeneic transplant makes use of someone elses stem cells. This treatment carries serious risks but offers the chance of improved survival. Many patients with myeloma develop bacterial infections that may be serious, and infectious complications remain the most common cause of death in myeloma patients. In the past, gram-positive organisms (eg,Streptococcus pneumoniae, Staphylococcus aureus) andHaemophilus influenzaewere the most common pathogens. More recently, however, infections with gram-negative organisms, anaerobes, and fungi have become frequent. The increased susceptibility of patients with multiple myeloma to bacterial infections, specifically with encapsulated organisms, has been attributed to impairments of host-defense mechanisms, such as hypogammaglobulinemia, qualitative deficiency in immunoglobulin function, granulocytopenia, decreased cell-mediated immunity, and the prolonged use of steroids and a prescription to metronidazole (Flagyl ER) is needed to treat bacterial infection of the bone. Myeloma is best treated quickly with a three week, twice a day application of $1 antifungal foote crme (clotrimazole) over the affected bone that should be instantly relieved of the crippling fungal infection enabling a normal minimal exercise routine, but the full twice a day, three week course, about 3 tubes, plus an extra for the infectious, probably mycotically intoxicated, friend, will be necessary to completely eliminate the infection for completely pain free physical exertion. Cancer is an idiopathic disorder. Drug info removed the explanation that antineoplastic cancer drugs are antibacterial, antiviral and antifungal. Initial necrosis is usually caused by exposure to toxic chemicals, such as benzene, or physical trauma to the bone. Untreated with basic antibiotics and antifungals, the necrotic tissue becomes septic and doesn't heal and the diseases progresses and becomes worse, and the mycotic infection of the necrotic tissue breaks through the bone and induces mutations distorting the peripheral complete blood count and white blood cell differential, although there is no more exposure to the toxic substance. The patient may be quite confused about their disease due to an affinity for the well-documented mind altering, intoxicating, effects of fungi such as brewer's yeast and psychedelic mushrooms. The pathogenesis of neoplastic white cell disease relies heavily upon the failure to treat the large fungal cells causing neoplastic mutation in human cells sensed by the patient as painful bone infections known as myelomas as well as lymphoma. Although the bacteria and virus would happily infiltrate any crack in the bone to get at the marrow where they can cause hematopietic disorders, fungus cells are the most likely to break through the bone, and induce mutations by releasing the enzymes that drive their two stage sexual fungal life cycle. Their large size however gives them away and fungal infections often cause excruciating bone pain in white cell disease. Athletes foot crme (clotrimazole) is generally effective at keeping the patient able to jog, used twice daily for three weeks, is likely to completely eliminate the fungal infection causing the arthritis anywhere the topical preparation can penetrate, it can however be a frustrating 3 weeks chasing multiple myelomas as the fungi translocate from one location to another to escape the topical cream. Another antifungal foot powder spray (toftate), powder being prescribed for elders, however caused a diffuse pain to occur, and elders are definitely recommended to use clotrimazole (athlete's foot cream) as their basic antifungal, reminded of the fact they are not cured until they can run without any undue pain. Athlete's foot cream can be purchased for $1 and lasts about one of three weeks recommended for the treatment of athlete's foot, jock itch and bone pain. There are several oral antifungal drugs such as Lamisil and Grifulvin V available for the treatment of athlete's foot and toenail and fingernail onchymycosis but a scientist cannot be sure they have used an effective antifungal for the treatment of Candida, the most common fungal pathogens, or invasive pulmonary and extrapulmonary Aspergillosis, sold to academic laboratories as A. niger, and other insidious fungal pathogens until they have tried a fingernail pulse of Sporanox (itraconazole), a highly effective broad spectrum oral antifungal used in the treatment of both pulmonary and extra pulmonary invasive aspergillus as well as the common onchymycosis and histoplasmosis - 200 mg 3 times daily for 3 days, then 200 mg twice daily until no longer immune-compromised. For primary prophylaxis of aspergillosis in immunocompromised individuals at high risk of invasive disease such as neutropenic patients with acute myelogenous leukemia (AML) or myelodysplastic syndrome (MDS) or hematopoietic stem cell transplant (HSCT) recipients with graft-versus-host disease (GVHD). IDSA considers posaconazole the drug of choice; alternatives are itraconazole or micafungin. The prophylaxis of invasive Aspergillus and Candida infections in patients, 13 years of age and older, who are at high risk due to being severely immunocompromised, such as hematopoietic stem cell transplant (HSCT) recipients with graft-versus-host disease (GVHD) or those with hematologic malignancies with prolonged neutropenia from chemotherapy and also fororopharyngeal candidiasis. Sporanox is hepatoxic and liver enzymes must be monitored on a monthly basis and is highly contraindicated in heart failure. IV amphotericin B is the preferred alternative to oral Sporonox (itraconazole). The effectiveness of oral antifungals is 60-80%. There is still a chance of re-infection after finishing the course of the medication. The re-infection rate is 15% but can be as high as 25% in diabetics. Serious adverse reactions are less than 0.5%. There are some interactions between these medication and other drugs such as cyclosporine, cimetidine, rifampin, terfenadine, and caffeine (Debrowolski 04: 14-16). 5. Vegan Diet A vegan diet is necessary to recover from heart disease, to lose weight more reliably than any fad diet and particularly to avoid excessive atherosclerotic accumulation when exposed to a cardiac glycoside or natural hyperlipidemia from the overconsumption of fatty foods. Anyone who senses angina pectoris should keep a strictly vegan diet brown rice and vegetables boiled in water is a nutritious staple that can be eaten twice a day perhaps with green salad with vinaigrette dressing, and a large fruit salad for breakfast. A vegan is someone who avoids all animal products; milk, eggs and all dairy products and by-products as well as all foods that contain these ingredients. The vegetable protein tolerance for heart disease is much higher than for cancer but complete vegetable proteins found in wheat gluten and vegetable combinations such as rice and beans and beans and corn can be cardiotoxic and should be avoided or minimized to less than 10% of meal mass. Careful attention must be paid to maintaining levels of caloric intake expended by exercise and vegans tend to have better appetites than the obese people. A vegetarian is someone who does not eat meat. A lacto-ova vegetarian is someone whose diet includes milk and eggs. This type of vegetarian diet is well accepted and proven to be healthy in children, heart patients should however not eat eggs that are high in cholesterol, much lower in egg whites. Eggs are as good as meat as a source of vitamins and minerals found only in animal products and are a fairly powerful medicine for the reversal of vegan diet induced diarrhea, anemia, osteoporosis and dental cavities, not to be taken daily if there is any cardiac intolerance. A lacto-vegetarian is someone who includes milk and milk products in their diet but not eggs or foods that have eggs in them. This diet is a healthy diet for children and because a long term vegan diet requires supplementation to keep the stool firm and prevent cavities a lacto-vegetarian diet provides the minimal amounts of animal product nutrition necessary to sustain gastrointestinal health in vegans over the long term. Two dairy products are particularly safe and effective source of animal nutrition, cheese aged over two months does not tend to cause intolerance because the lactose has converted to lactic acid, and probiotioc yoghurt and drinks supply the gut with friendly bacterial cultures that comprise 30% of healthy fecal volume and protect against dominating proliferations of fast growing bad bacteria. Vegetarian cultures, including the Hunza, Seventh Day Adventists, and various Indian sects, have a long history. Among these communities, vegetarianism is firmly grounded in a cultural setting, sufficient nutritional knowledge is embedded in daily and yearly rituals, ensuring continued health. In the United States, the Seventh Day Adventists were the first large group to develop and maintain a healthy vegetarian lifestyle (Yntema 95: 40, 41, 68). Food of high fat, sugar and protein content should be avoided. Cholesterol comes from eating food of animal origin, when ingested in the form of fat, this substance is absorbed form the intestinal tract, converted in the liver, and added to the total amount of cholesterol already circulating in the serum. When the amount of cholesterol becomes high, arteries begin to show an increase in fatty deposits. A healthy person can tolerate 6 ounces of liquor over a one hour period, but more than this amount rapidly weakens muscle contraction and can lead to alcoholic myocarditis. The risk of developing myocardial infarction is about twice as great for heavy coffee drinkers as it is for individuals who drink no coffee at all. Elevated blood pressure, stress may increase serum cholesterol thereby causing atherosclerosis. The use of oral contraceptives involves an increased risk of clotting disorders, increases hypertension and thrombotic strokes and sharply increases the risk of stroke when cigarette smoking is also practiced. Excessive licorice (Glycyrrhiza glabra) ingestion for example can lead to cardiac dysfunction and severe hypertension. Vitamin E deficiency is also implicated in heart disease, and homogenized milk may be involved in atherosclerosis and other cardiovascular disease. Everything I enjoy in life runs the ancient lament, is either illegal, immoral or fattening (Elvin-Lewis 77: 181, 182). To make the elimination diet for heart disease as simple as possible - no animal products, no angina pectoris. Eating the standard American diet thats based on meat and dairy products, with plenty of white flour and white sugar, one-third of the women and one-half of the men in the US population die of heart disease. Meanwhile, vegetarians and vegans (vegetarians who consume no dairy products or eggs) not only have far less heart disease, but also have lower rates of cancer, hypertension, diabetes, gallstones, kidney disease and obesity. Not only is mortality from coronary artery disease lower in vegetarians than non-vegetarians, but vegetarian diets have been successful in arresting coronary artery disease. The daily intake of cholesterol by non-vegetarians is 300-500 mg/daily, lacto-ovo-vegetarians 150-300 mg/ daily and vegans zero, their cholesterol levels were 210, 161 and 133 respectively, safe levels of cholesterol are less than 150. The ideal ratio of total cholesterol to HDL (high-density lipoproteins) is 3.0 to 1 or lower, the average American males ratio is 5.1 to 1 and the average vegetarians ratio, on the other hand, is 2.9 to 1. When it comes to heart disease the evidence is against animal products. Vegans live on average six to ten years longer than the rest of the population and in fact seem to be healthier on every measurement we have of assessing health outcomes. A low-fat plant based diet would lower the heart attack rate about 85 percent, and cancer rate 60 percent (Robbins 01: 14 , 15, 21, 22, 47). The cardinal risk factors for coronary disease in the United States are hypercholesterolemia, hypertension, inactivity and anti-smoking propaganda. Modified nutritional habits of high-risk American men, substituting diets moderate in calories, total fat, and carbohydrate, low in saturated fat, cholesterol, and simple sugars reduced heart disease mortality by about one-half and the sudden death rate was only one-fourth as great, and total mortality was lower by 40%. In a study of coronary heart disease in seven countries only the concentration of cholesterol in the blood proved to be the outstanding risk factor within and between national groups. As these data indicate, Japanese men have the lowest incidence of coronary heart disease of any industrialized nation, they smoke heavily and they have high blood pressure, but they eat a low cholesterol diet (Elvin-Lewis 77: 201, 202, 182-183). In North America there are about six hundred heart attacks per 100,000 population annually, compared with 60 per 100,000 in China. People of Chinese origin who live in North America; however, have just as many heart attacks as do other Americans. This means the major difference is environmental, not genetic, the main difference is diet. The typical North American diet tends to be too high in total fats (approximately 39 percent of total calories consumed) (Spence 06: 108, 109, 111, 110). Although lactose intolerance is estimated at 10 percent amongst people of Caucasian descent, it is much higher in other races, 90-100 percent in Asians, 65-70 percent in Africans, 65-70 percent in Italians, and 50-60 percent in Hispanics. Countries with the highest levels of dairy products have the highest levels of osteoporosis Finland, Sweden, United States and England. The hip fracture rate for African-Americans, who consume more than 1,000 mg of calcium a day, compared with black South Africans is 9 times greater. Calcium intake in rural China is one-half that of people in the US but the bone fracture rate is one-fifth of that in the US. Soy is a calcium rich substitute for dairy. It is important to buy organic or non-GM (genetically modified) soy products to avoid potentially unhealthy levels of pesticides. There are no antibiotics in soy milk. Soy milk is cholesterol-free, while cows milk contains 34 mg of cholesterol per cup. 44 percent of children with chronic constipation so intractable that it cant be treated successfully by laxatives, are cured by switching from cows milk to soy milk. While the average American estimates that 1 percent of the world population does not drink milk the actual number is 65 percent (Robbins 01: 99, 104, 107). Cheese aged longer than two months contains no more lactose, having been converted into lactic acid, and cheese is a nice high calorie food with a lot of calcium and phosphorus for the bones and teeth. Furthermore probiotic yoghurt, milk drinks and supplements are very good for gastrointestinal health, teeth and bones, because around 30% of normal fecal matter is composed of mostly dead gut flora. A new study of 137 mummified bodies, some as old as 3,500 years, found a high prevalence of hardening of the arteries, which often presages heart attack or stroke. The researchers used computer tomography (CT) scanners to detect calcium in arteries. They looked in the aorta, which is the bodys main arterial trunk; the coronary arteries of the heart; the carotid arteries of the neck; and the arteries of the thigh and the lower leg. When calcium was present, they concluded the person had atherosclerosis a diagnosis supported bystudies of living patients. Probable or definite atherosclerosis was evident in 34percent of the mummies. Only 4percent, however, had atherosclerosis in the coronary arteries, where it can cause heart attacks. The condition was more common in people who died in middle and old age, but was also seen frequently in those dying in their 30s. The 51 ancient Peruvians, who in life presumably ate a lot of beans and complex carbohydrates such as sweet potatoes and manioc, had atherosclerosis in 25percent of their mummies. Three of the five Aleutian hunter-gatherers who ate a paleo diet high in meat and devoid of sweets and grains, showed atherosclerosis and one woman who died in her late 40s had the kind of disease seen in people with bypass surgery (Brown 13). Around 75 percent of the days exposure to cholesterol and harmful fat is determined by diet. The Lyon Diet Heart Study showed that a Mediterranean diet from Crete reduced heart attacks and death by 60 percent in four years, compared to the diet usually prescribed in North American coronary care units. A Cretan Mediterranean diet is low in cholesterol and animal fat, high in beneficial oils such as olive and canola, and high in fruit vegetables and whole-grain fiber. Never eat an egg yolk (use whites or egg substitutes or organic tofu). Avoid trans-fats and fried foods such as chips and fries. Heart patients who eat meat at all should keep meat intake to two ounces per day, or one serving of animal flesh every other day. Use a nonhydrogenated canola margarine, preferably one that also contains olive oil, or coconut oil. Have fun making vegetarian meals delicious (Spence 06: 164). The National Academy of Science recommends a 2,000 calories diet for 128 pound woman, and 2,900 for a 175 pound man. One pound of fat consists of 3,500 calories stored. One serving of anything fat-based, such as meat, cake, pie, ice cream, nuts, chips or fries, is about 400 calories, a serving of starches such as potatoes, pasta, rice, bread, juice, fruit, four crackers, half a bagel , or a can of pop is 100 calories. Avoid cake, pie, ice cream (except on your birthday), nuts, chips and fries. The trick is finding alternatives you like (Spence 06: 165) and eat a lot more pounds of food and more frequently than a carnivore or omnivore to get enough calories from fruits, vegetables and whole grains. Vegetable Calories and Macro-Nutrients VegetableServingCaloriesCarbs (g)Protein (g)Fat (g)Asparagusraw, 4 medium spears, 2oz112.21.30.1Beans, Kidneyboiled, 1/2 cup, 3oz10819.47.20.4Broccoli1 cup chopped, 3oz355.62.40.3Cabbage1 cup shredded, 5oz419.82.10.1Carrots1 cup chopped5212.31.30.3Cauliflower1 cup chopped, 3.5oz234.11.80.4Celery1 cup chopped, 3.5oz143.60.70.2Corn (kernels)1/2 cup kernels, 3.5oz35482.310.84.3Corn on cob1 large ear, 5.5oz14033.34.71.1Cucumber1/2 cup slices (with skin), 2oz71.30.30.1Lentils1/2 cup boiled, 3.5oz11519.98.90.4Lettuce (iceberg)1 cup shredded, 1.9oz81.70.50.1Mushrooms1/2 cup pieces, 2.5oz203.81.40.4Onion1/2 cup chopped, 3oz368.60.80.1Rice, Brown cup boiled, 3.5 oz321142.914.75.4Peas1/4 cup, 1.5oz366.72.30.1Peppers (bell or sweet)1 cup sliced, 3.2oz184.20.80.2Potatoes1 potato, baked with skin, 7oz25558.17.00.4Pumpkin1/2 cup mashed, 4oz235.60.80.1Spinach1/2 cup, 3oz203.22.60.3Sweet potato1 cup, baked, with skin, 7oz18041.44.00.4Tomato1 tomato, raw, 2.2oz112.40.60Source: Freedieting.com calories from rice and vegetables A calorie is the heat required to raise the temperature of 1g of water 1C. The energy value of food and human energy requirements are expressed as caloric equivalents. Fatty acids are used by the body as a source of energy and are provided for in our diet by animal fat and vegetable oils that when metabolized supply 9 cal/g. Carbohydrates are complex compounds made up of sugars that when metabolized yield 4 cal/g. Proteins, are complex chains of amino acids, supplied in our diet chiefly by animal proteins meat, milk, cheese and eggs and to a lesser degree by plants such as legumes and nuts. Protein requirements vary, with children, pregnant and lactating women, and men undergoing strenuous exercise requiring larger amounts. Beyond infancy a child requires about 10% of his caloric intake in protein. Protein deficiency, especially during the first year of life, has been associate with decreased brain development and lowered IQ (Elvin-Lewis 77: 201 200). The adverse health impacts of excessive meat-eating stem in part from what nutritionists call the great protein fiasco a mistaken belief of many Westerners that they need to consume large quantities of protein. This myth has resulted in Americans and other members of industrial societies ingesting twice as much protein as they need. Among the affluent, the protein myth is dangerous because of the saturated fats that accompany protein and dairy products. Those fats are associated with most of the disease of affluence that are among the leading causes of death in industrial countries: heart disease, stroke, breast, lung and colon cancer. The amount of protein in a mothers breast milk is 5 percent of calories. According to the World Health Organization (WHO) the human minimum protein requirement is 5 percent of total calories, according to the US Recommended Dietary Allowance for adults 10 percent of total calories. For optimum protein intake WHO recommends 10-15 percent of calories. Although much smaller than lipids, protein is by its very nature too large to be absorbed into human cells which are themselves composed of protein and must be broken down into amino acids to pass through the cell walls. Vegans recovering from coronary artery disease generally try not to mix large quantities of certain vegetables together, like rice and beans or beans, to avoid making the complete proteins, most Americans eat in excess (Robbins 01: 71, 67). An important way of looking at foods made from grains involves the glycemic index, which deals with how quickly foods are converted to sugar. On a scale of 0 to 100, table sugar is 100; white bread, white rice, and potatoes are about 80; brown rice about 60; and whole-grain pasta about 20. Learning to prepare vegetable dishes make it easier to reduce the intake of meat and other animal products or highly processed sugary foods. When selecting margarine and cooking oils it is important to choose a non-hydrogenated margarine or oil high in polyunsaturated and monounsaturated fats, and low in saturated fats (Spence 06: 108, 109, 111, 110). Omega-3 fats, can also be an issue. You have to eat twenty of todays supermarket eggs to get as much Omega-3s as are provided by a single egg from a free range chicken. Omega 3s are plentiful in flax seeds and oil, in fatty fish such as salmon, herring, mackerel and sardines, and can be found in lesser amounts in walnuts, hemp seeds, green leafy vegetables and in canola oil (Robbins 01: 91). To the heart patient fish are Japanese junk food. Conventional wisdom tends to recommend olive oil as the heart friendly oil and categorizes coconut oil as a saturated fat but coconut oil is easy on the heart and has antifungal properties. Garlic also has antibiotic, antifungal and antiviral properties that make it a useful seasoning with or, preferably for the heart patient, without any oil. Heart patients should buy organic food although unlike cancer and neurological conditions organophosphate pesticides do not necessarily cause angina pectoris, although in sufficient quantity sometimes found in GM products and waxed fruits they can cause chest pain. Around 3 million pounds of antibiotics are administered to people in the United States to treat diseases. 24.6 million pounds are administered to livestock for purposes other than treating disease. Before Denmarks ban on the routine use of antibiotics the prevalence of antibiotic-resistant bacteria in chickens was 82 percent and after the ban 12 percent (Robbins 01: 141). More than 90 percent of US beef cattle receive hormone injections and in the larger feedlots the figure is 100 percent. The European Union refuses to import US hormone-treated beef. After the European Union banned the sale of hormone-treated meat within European Union countries, the United States complained to the World Trade Organization (WTO) where a three-lawyer panel ruled that the European Union was required to pay the US $150 million a year as compensation for lost profit although scientists called such hormones as so carcinogenic as to cause cancer by themselves. The 1999 the EU found that 12 percent of the US hormone free cattle had in fact been treated with sex hormones (Robbins 01: 143, 144). According to Monstantos own tests, Roundup Ready soybeans contain 29 percent less of the brain nutrient choline and 27 percent more trypsin inhibitor, a potential allergen that interferes with protein metabolism. The GM soybeans have lower levels of phylalanine, and essential amino acid that affects levels of phytoestrogens. And levels of lectins, which are frequently allergens are nearly double. In December 1999 a statement was posted to the cafeteria of the Monsanto Corporations United Kingdom headquarters in High Wycombe, England In response to concerns raised by our customerswe have decided to remove, as far as is practicable, genetically modified soy and maize from all food products served in our restaurant. We will continue to work with our suppliers to replace GM (genetically modified) soy and maize with non-GM ingredients We have taken the above steps to ensure that you, the consumer, can feel confident in the food we serve (Robbins 01: 336, 345, 346). Iron deficiency is probably the most common nutritional disorder in the world. Although more common in developing countries this form of anemia is also common in the United States. Normally, the total body iron content is in the range of 2gm in women and up to 6 gm in men. Approximately 80% of the functional iron is found in hemoglobin, myoglobin and iron-containing enzymes such as catalase and the cytochromes contain the rest in pools of hemosiderin and ferritin containing approximately 15 to 20% of total body iron. Because women have substantially smaller stores of iron than males they have a much more precarious iron balance and are vulnerable to excessive loss or increased demands associated with menstruation and pregnancy. In iron deficiency, serum ferritin is always below 12 g/liter, whereas in iron overload very high values approaching 5000 g/liter may be obtained. With liver damage and inflammatory states, serum ferritin levels may be high despite normal body stores. Storage iron pool is readily mobilized in the event of an increase in body iron requirements, as may occur following loss of blood. Iron is transported by transferrin which delivers iron to the cells, including erythroid precursors, where iron is required for hemoglobin synthesis. Immature red cells possess high-affinity receptors for transferrin. The most active site of iron absorption is the duodenum, but the stomach, ileum, and colon may also participate to a small degree. Approximately 25% of the heme iron derived from hemoglobin, myoglobin, and other animal proteins is absorbed, but only 1 to 2% of nonheme iron found in green leafy vegetables is absorbed. Daily losses of iron range between 1 and 1.5 mg. Thus to maintain a normal iron balance, approximately 1 mg of iron must be absorbed from the diet every day. Because only 10 to 15% of the ingested iron is absorbed, the daily iron requirement for adult males is 5 to 10 mg and for adult females 7 to 20 mg. The average daily dietary intake of iron in the Western World is about 15 to 20 mg. An iron deficiency may result from (1) dietary lack; (2) impaired absorption; (3) increased requirement; or (4) chronic blood loss. Dietary inadequacy is found in the elderly, very poor, infants because milk contains very small amounts of iron and children who need dietary iron to accommodate growth and expansion of blood volume. Impaired absorption is encountered in sprue, intestinal steetorrhea and chronic diarrhea. Chronic blood loss is the most important cause of iron deficiency in the Western world but is common in vegans complaining of diarrhea. Bleeding within the tissues or cavities of the body may be followed by total recovery and recycling of iron, however, external hemorrhage depletes the reserves of iron. Iron deficiency induces a hypochromic microcytic anemia and may cause other changes, including koilonychias, alopecia, atrophic changes in the tongue and gastric mucosa and intestinal malabsorption. The diagnosis of iron deficiency anemia rests on laboratory studies. Both hemoglobin and hematocrit are depressed, usually to moderate levels, and are associated with hypchromia, microcytosis and some poikilocytosis. The serum iron and serum ferritin are low, and the total plasma iron-binding capacity is high. Low serum iron with increased iron-binding capacity results in a reduction of transferrin saturation levels to below 15%. Reduced heme synthesis leads to elevation of free erythrocyte protoporphyrin. Unexplained iron deficiency anemia can be caused by an occult lesion or cancer (Saunders 94: 610-613). Vegans with diarrhea should take an iron supplement as well as the highly solicited vitamin B12 supplement. A vegetarian diet may be the minimum animal products necessary to treat chronic diarrhea from the overconsumption of vegetables, but supplementation may help. A balanced diet with enough fruits and vegetables to digest some animal products provides sufficient amounts of vitamins and few individuals have deficits. One of the biggest concerns of vegetarians, for which reason they stray from the heart healthy vegan diet, is providing adequate levels of B12 which is almost entirely unavailable in vegetable. There is typically no problems in the growth and development of vegetarian and vegan children who eat varied diets with enough calories and adequate intake of vitamin B-12. The recommended Dietary Allowance for vitamin B-12 is 2 micrograms, 2 millionths of a gram. Because soils have been sprayed with chemical fertilizers and pesticides, they are devoid of the B-12 that was once abundant in the dirt (Robbins 01: 85). Vitamin B 12 is found in tempeh, dulse and kombu (two varieties of seaweed), many fortified soy products and in dairy products. The recommended daily dietary allowance for B12 is Children 1-3 years 0.7 micrograms/day, 4-6 years 1.0 micrograms/day and 7 and up 1.4 micrograms/day. Approximately 13 micrograms of B12 can be derived from 100 grams of dried seaweed (Yntema 95: 94). A deficit in vitamin B12 can result from various causes with disparate results. Vegetarians and the elderly are often deficient in B12 because the main dietary source is meat and they should therefore take a vitamin B12 supplement. An estimated 15-20 percent of the elderly have B12 deficiency. Pernicious anemia is a condition in which vitamin B12 is not properly absorbed because the stomach does not produce a factor required for its absorption in the distal intestine. Individuals who lack this factor can develop anemia, because we need vitamin B12 to make new red blood cells; they can also develop a problem in the spinal cord and peripheral nerves that results in numbness and tingling of the extremities, and if untreated, in paralysis and dementia. Another cause of vitamin B12 depletion is long-term use of drugs that suppress the production of acid by the stomach, such as omeprazole. Gastric acid is needed to strip vitamin B12 off food so we can absorb it; because crystalline vitamin B12 can also be absorbed from tablets without acid, it will be effective. Individuals taking omeprazole or related rugs for longer than a few months should probably take a B12 supplement. Folic acid is particularly important for the development of the nervous system of the fetus and the typical North American diet may not provide enough folic acid found in green leafy vegetables for pregnant women, and it is now apparent that folic acid fortification of cereal grain products (mandated in the U.S. since 1998) has reduced by half abnormalities of the brain and spinal cord that lead to spina bifida and related abnormalities (neural tube defects) (Spence '05: 156, 155). Megaloblastic anemias constitute a diverse group of entities, having in common impaired DNA synthesis and distinctive morphologic changes in the blood and bone marrow. The erythroid precursors and erythrocytes are abnormally large, thought to be related to impairment of cell maturation and division. Vitamin B12 and folic acid are coenzymes in the DNA synthetic pathway. A deficiency of these vitamins or impairment in their utilization results in deranged or inadequate synthesis of DNA that may lead to megaloblastic anemia and usually presents in the form of chronic diarrhea. Vitamin B12 is a complex organometallic compound known as cobalamin, for the cobalt atom attached to a corrin ring, therapeutically synthesized as stable cyanocobalamin. Vitamin B12 is required for methylcobalamin to convert homocysteine to methionine and to metabolize polyglutamate forms of folate. Under normal circumstances, human are totally dependent on dietary animal products for the vitamin B12. Strictly vegan or macrobiotic diets do not provide enough of this essential nutrient. The daily requirement is 2 to 3 g daily and the normal balanced diet contains significantly larger amounts which takes years of vegan diet to deplete (Saunders 94: 603-607). The hypothesis that lack of folate is the proximate cause of anemia in vitamin B12 deficiency is supported by the observation that the anemia improves with the administration of folic acid. Folate is most necessary for (1) the synthesis of purines.; (2) the synthesis of methionine from monocysteine, a reaction that also requires vitamin B12; and (3) the synthesis of deoxythymidylate monophosphate (dTMP). Folic acid deficiency results in megaloblastic anemia without the neurological changes, but is not common, except with a very marginal diet, without adequate green vegetables. Despite their abundance in raw foods folate is sensitive to heat and cooking foods for 5 to 10 minutes destroy up to 95% of the folate. Folic acid antagonist drugs such as methotrexate, 6-mercaptopurine and cyclophosphamide inhibit folate function leading to ulcerative lesions in the gastrointestinal tract as well as megloblastic anemia. Human require 50 to 200 g of folate daily especially due to the increased demand for folate during pregnancy and dietary inadequacies found in chronic alcoholics, the indigent and very elderly. Megaloblastic anemia resulting from folic acid and vitamin B12 deficiency are identical (Saunders 94: 605-610). Dark leafy greens and brown rice, seem to be the most effective vegan staple, before diarrhea calls for animal products. The feature that sets pernicious anemia apart from dietary vitamin B12 deficiency is that the cause of the malabsorption is atrophic gastritis with failure of the production of intrinsic factor (IF). Chronic atrophic gastritis is marked by a loss of parietal cells, a prominent infiltrate of lymphocytes and plasma cells, and megaloid and atypical changes to the mucosal cells. It is an auto-immune disorder resulting from the presence of blocking, binding and gastric antibodies. Absorption of vitamin B12 requires IF, which is secreted by the parietal cells with HCl. Diagnostic features include (1) a marked to severe megalobastic anemia; (2) leukopenia with hypersegmented granulocytes; (3) mild to moderate thrombocytopenia; (4) neurologic changes related to involvement of the posterolateral spinal tracts; (5) achlorhydria even after histamine stimulation; (6) inability to absorb an oral dose of cobalamin (assessed by urinary excretion of radiolabeled cyanocobalamin given orally, called the Schilling test; (7) low serum levels of vitamin B12 ; (8) excretion of methymalonic acid in the urine; and (9) a striking reticulocytic response and improvement in hematocrit levels following parenteral administration of vitamin B12 (Saunders 94: 605, 608). Vitamins and Minerals Essential to Cardiovascular Health VitaminIndicationB1 (thiamin)Supports energy metabolism and nerve function. Found in spinach, green peas, tomato juice, watermelon, sunflower seeds, lean ham, lean pork chops, soy milkB2 (riboflavin)Supports energy metabolism, normal vision and skin health. Found in spinach, broccoli, mushrooms, eggs, milk, liver, oysters, clamsB3 (niacin)Supports energy metabolism, skin health, nervous system and digestive system. Found in spinach, potatoes, tomato juice, lean ground beef, chicken breast, tuna (canned in water), liver, shrimpB6 (pyridoxine)B complex, amino acid and fatty acid metabolism, red blood cell production. Found in bananas, watermelon, tomato juice, broccoli, spinach, acorn squash, potatoes, white rice, chicken breastB9 (folate)Supports DNA synthesis and new cell formation. Found in tomato juice, green beans, broccoli, spinach, asparagus, okra, black-eyed peas, lentils, navy, pinto and garbanzo beansB12Used in new cell synthesis, helps break down fatty acids and amino acids, supports nerve cell maintenance. Found in meats, poultry, fish, shellfish, milk, eggsC (ascorbic acid)Collagen synthesis, amino acid metabolism, helps iron absorption, immunity, antioxidant. Found in spinach, broccoli, red bell peppers, snow peas, tomato juice, kiwi, mango, orange, grapefruit juice and strawberries.Vitamin EAntioxidant, regulation of oxidation reactions, supports cell membrane stabilization. Found in polyunsaturated plant oils (soybean, corn and canola oils), wheat germ, sunflower seeds, tofu, avocado and sweet potatoes.Vitamin KSynthesis of blood-clotting proteins, regulates blood calcium. Found in Brussels sprouts, leafy green vegetables, spinach, broccoli and cabbage.MineralIndicationSeleniumAntioxidant. Works with vitamin E to protect body from oxidation. Found in grains.Source: Sanders '12 The B complex vitamins seem to have the greatest relationship with cardiovascular health. Niacin, also known as vitamin B3, has for years been widely prescribed to lower "bad" LDL cholesterol and raise levels of "good" HDL cholesterol. Niacin -- in doses about 100 times higher than the recommended amount from food -- was thought to be helpful. A combination drug containing these medicinal doses of niacin failed to lower the risk of heart attacks or strokes and even proved harmful for some with vascular disease. Indeed, the combination drug used in the study -- made by US pharmaceutical giant Merck and combining extended release niacin with laropiprant -- is already approved in 70 countries, though not the US. But when tested against a placebo in more than 25,000 patients, it failed to reduce the numbers of heart attacks, strokes or other serious cardiovascular problems. Even more worryingly, the study showed unexpectedly higher levels of bleeding and infections in the group taking the drug versus the placebo. And the group taking the study drug also showed higher levels of other side effects, including new cases of diabetes and complications for previously-diagnosed diabetes, as well as rashes and diarrhoea. It was unlikely the poor outcome could be linked to the second component of the drug, laropiprant, which was included to reduce the facial flushing caused by niacin. The lack of benefit on heart attacks and strokes is consistent with another recent, smaller-scale study of niacin, which did not use laropiprant, and many of the side effects are known to be due to niacin. Because of the results of this research, Merck has withdrawn its application for FDA approval of the drug and suspended its sale around the world (Armitage 13). Niacin should not be taken in doses many times the Recommended Daily Allowance (RDA) found in multi-vitamins. Folic acid 2.5 mg daily will normalize blood levels of homocysteine in about half the cases; a combination of folic acid 1 mg, vitamin B6 10 mg, and vitamin B12 1 mg (1000 mcg) will normalize levels in more than 95 percent of cases. A high dose of B12 is needed. Blood levels of B12 should be above 300 pmol/L. In some cases it is necessary to add a fourth supplement called betaine, and vitamins are not as effective for individuals with kidney failure. Overnight daily dialysis is more effective at lowering homocysteine than routine dialysis three times a week, and sulfur containing compounds called thiols may be useful (Spence '05: 157, 158). Vitamin E, C and beta carotene, which reduce oxidation, may be protective. A Cambridge study showed a significant reduction in recurrent heart attacks in individuals given vitamin E after a heart attack, but without a reduction in deaths. Vitamin E, when it accepts a free radical, itself becomes a free radical (the tocophyryl radical); it then needs vitamin C to detoxify it. A Finnish study showed that combining vitamin E with 250 mg daily of slow-release vitamin C reduced the progression of artery thickening as measured by ultrasound. It is probably best to get vitamins and antioxidants from food rather than from tablets. Vitamin C in orange or grapefruit juice brings along with it other potentially beneficial antioxidants and bioflavonoids- hesperitin in orange juice and naringin in grapefruit juice are related to genistein in soy beans. These have anticancer and cholesterol-lowering effects. The antioxidant lycopene is what gives the red color in tomatoes, watermelon, and strawberries; blueberries get their color and flavor from anotehr brightly colored antioxidant. Eat fruits and vegetables of all colors to get a variety of antioxidants (Spence '05: 159, 160). Selenium is an antioxidant found in grains needed to help the absorption of vitamin E to protect body from oxidation. In general vitamin supplementation is ineffective for the treatment of heart disease and dietary vitamins and minerals should suffice in the absence of bone loss, dental cavities, diarrhea or anemia due to deficiency. If the diet is not nutritious a multivitamin may help, but is poor substitute for a balanced diet. Obesity is certainly a factor in shortening the life span and increasing the incidence of diabetes, cholelithiasis, hypertension, gallbladder disease, and vascular disorders including atherosclerosiss, but obese people make the best vegans due to their large stores of iron and vitamin B12 they can fully enjoy a vegan diet without much fear of diarrheal sprue or anemia until they have lost their belly fat. That obesity is due to an excess of caloric intake over metabolic need is accepted by nearly everyone. But the significance of the vegan diet as the weight loss and heart attack diet has been suppressed. In 1862 the famous Dr. William Harvey imposed the then radical carbohydrate restrictive diet on his obese patient and friend, William Banting, an overweight London cabinet maker and undertaker to royalty, after diet and exercise failed to help with Bantings problem. The regiment was so successful that in 1864 Banting published a booklet A Letter on Corpulence Addressed to the Public extolling its virtues. The booklet sold over 60,000 copies and his diet became as widely known and controversial in Britain and Later America. Banting maintained his normal weight on his low carbohydrate diet until his death at 81. Atkins, a young cardiologist in 1963 found that for him a low carbohydrate diet worked to assuage his hunger and control his tendency to gain weight. In 1972 just as the American Medical Association and the American Heart Association started the low cholesterol/low fat juggernaut a little-known doctor by the name of Robert Atkins started his own trajectory, named Diet Revolution. He sold millions of copies of his book promising that a diet completely contradictory to the medical establishment recommendations was the way to go. He promised the public they would lose weight by eating steak, eggs and butter to their hearts desire because fat was harmless. It was the carbohydrates, the pasta, rice, bagels and sugar that caused obesity and heart disease. The result is our present obesity epidemic (Graveline 04: 86, 76). While one can tolerate more fat without carbohydrates and more carbohydrates without fat the heart patient is trying to neutralize the effects of "cardiac glycosides" by reducing the intake of fat and sugar to create low levels in the blood so that fatty calcified atherosclerotic plaques can be dissolved into the bloodstream by osmosis and finally be used as fuel. Height Weight Tables for Prior and Non-Prior Service Height (inches)Non-Prior Service Prior ServiceMaximum weight by years of age for femalesMaximum weight by years of age for males17-2021-2728-3940 and over17-2021-2728-3940 and over58Non-Prior112115119122----Prior109112115119----59Non-Prior116119123126----Prior113116119123----60Non-Prior120123127130139141143146Prior11612012312713213613914161Non-Prior124127131135144146148151Prior12012412713113614014414662Non-Prior129132137139148150153156Prior12512913213714114414815063Non-Prior133137141144153155158161Prior12913313714114514915315564Non-Prior137141145148158160163166Prior13313714114515015415816065Non-Prior141145149153163165168171Prior13714114514915515916316566Non-Prior146150154158168170173177Prior14114615015416016316817067Non-Prior149154159162174176179182Prior14514915415916516917417668Non-Prior154159164167179181184187Prior15015415916417017417918169Non-Prior158163168172184186189193Prior15415816316817517918418870Non-Prior163168173177189192195199Prior15916316817318018518919271Non-Prior167172177182194197201204Prior16316717217718518919419772Non-Prior172177183188200203206210Prior16717217718319019520020373Non-Prior177182188193205208212216Prior17217718218819520020520874Non-Prior183189194198211214218222Prior17818318919420120621121475Non-Prior188194200204217220224228Prior18318819420020621221722076Non-Prior194200206209223226230234Prior18919420020621221722322677Non-Prior199205211215229232236240Prior19319920521121822322923278Non-Prior204210216220235238242247Prior19820421021622322923523879Non-Prior209215222226241244248253Prior20320921522222923524124480Non-Prior214220227232247250255259Prior208214220227234240247250Height will be measured in stocking feet on a flat surface with the chin parallel to the floor. The body should be straight but not rigid, similar to the position of attention. The measurement will be rounded to the nearest inch with the following guidelines: If the height fraction is less than 1/2 inch, round down. If the height fraction is 1/2 inch or greater, round up. Weight should be measured and recorded to the nearest pound. All measurements will be taken in the APFT uniform. Add 6 pounds per inch for males and 5 pounds per inch for females measuring over 80 inches tall.  Maximum Allowable Body FatMale Age GroupFemale Age GroupAge17-2021-2728-3940+17-2021-2728-3940+Prior20%22%24%26%30%32%34%36%Non-Prior24%26%28%30%30%32%34%36Source: Army Study Guide Changing one's diet, even to save one's life, is very similar to weaning a baby and probably doesn't happen overnight resulting in chronic atherosclerotic illness reversible with a vegan diet but for a long time. Nursing babies under eight or nine months, that derive all their nutrition from mothers milk, cannot tolerate it is she eats an unhealthy diet. When a child is weaned, his eating schedule is usually adapted to that of the rest of the family. By 1 years most children can eat by themselves. By 2 years the child continues to need help feeding and likes to play with the food at meals. Three year olds can feed themselves and food dislikes are rarer, and most children will choose food based upon familiarity with it. At 3 they like to complain about their food. By four years, sweetness is the most important factor determining food preference. By 5 years they have basically a normal adult eating pattern. It is important introduce a wide variety of foods. Bear in mind that hunger and fatigue can affect mealtime behavior. Remember young children usually prefer unmixed foods. Remember that socially determined habits may not work for all people. Remember that everyone has food likes and dislikes (Yntema 95: 28-30). The diet for the heart patient is limited to the vegan diet of fruits, vegetables and whole grains. The diet for the anemic, diarrheal and tooth decaying vegan heart patient is vegetarian. 6. Basic Training The American College of Sports Medicine defines physical fitness as a set of attributes that people have, or achieve, that relates to the ability to perform physical activity. The fitness components of cardio-respiratory endurance, muscular strength and endurance, flexibility, and body composition are all inherent within a generalized exercise prescription. The Surgeon Generals Report, Physical Activity and Health, states: significant health benefits can be obtained by including a moderate amount of physical activity (e.g. brisk walking, running, resistance training, recreational sports) on most, if not all, days of the week. Additional health benefits can be gained through greater amounts of physical activity. People who can maintain a regular regimen of activity that is of longer duration, or of more vigorous intensity, are likely to derive greater benefit. The vast majority of physically active adults are not involved in structure, formal exercise programs, nor do they need to be. There is however excellent evidence that good physical fitness reduces all-cause mortality, and coronary artery disease; good evidence that it reduces disease rates of hypertension, obesity, colon cancer, non-insulin dependent diabetes and osteoporosis; some evidence that it reduces disease rates of stroke, breast, prostate and lung cancer; although there is no apparent difference in disease rates across activity categories in peripheral vascular disease, rectal, stomach or pancreatic cancer, or osteoarthritis (Mahler et al '95: 3, 6). More than 20 cardiac pathologies have been identified as causes of Sudden Coronary Death (SCD) in athletes. Findings at autopsy reveal a predominance of an enlarged heart, hypertrophic cardiomyopathy (HCM) (26%), commotion cordia (20%) and aberrant coronary arteries (13%) as the underlying cause of death (Lawless '11: 3). Congestive heart failure is a constellation of symptoms with a poor prognosis of about 3 years, from onset, whose primary diagnostic criteria is an inability to exercise because angina pectoris becomes worse with exertion and this inability to exercise is ultimately invariably lethal to the heart patient. The herb Hawthorne is the only medicine that treats all the symptoms and without any known side-effects is highly recommended for the treatment of congestive heart failure. Exercise is generally contraindicated in acute inflammatory cardiac disease, uncontrolled congestive heart failure, acute myocardial infarction, acute pulmonary disease, severe systemic hypertension, acute renal disease, acute hepatitis or drug overdose affecting cardiorespiratory response to exercise (Mahler et al '95: 222). Exercise is the cure for atherosclerosis, 90% of heart disease. In general, the minimal standards of military basic training must be exceeded to have a fighting chance to perform daily duties when exercise must be reduced to 60% of normal or less due to crippling injury or illness. One of the first studies to suggest the benefits of exercise was the London bus drivers study about thirty-five years ago. The investigators compared the drivers and conductors on the big red double-decker buses in London, England. They found that, in comparison to bus conductors, drivers had more heart attacks and died younger; they concluded that the reason was probably that the driver sat behind the wheel all day, while the conductor ran up and down the stairs taking tickets (Spence 06: 94). The essential components of a systematic, individualized exercise prescription include the appropriate mode(s), intensity, duration, frequency, and progression of physical activity. These five components apply when developing exercise prescriptions for persons of all ages and functional capacities, regardless of the presence or absence of risk factors and disease. The optimal exercise prescription for an individual is determined from a objective evaluation of that individual's response to exercise, including observations of heart rate (HR), blood pressure (BP), ratings of perceived exertion (RPE), subjective response to exercise, electrocardiogram (ECG) when applicable, and functional capacity measured during a graded exercise test (GXT). The art of exercise prescription requires modification in accordance with observed individual responses and adaptations because physiological and perceptual responses to acute exercise vary. Improvement of the ability of the body to utilize oxygen efficiently, resulting in improved endurance, is one component of physical fitness. The increase in maximal oxgygen intake (VO2max) may range from 5 to 30% and is most dramatic in people with low initial levels of fitness, cardiac patients and those exhibiting weight loss. The greatest improvement VO2max occurs when exercise involves the use of large muscle groups over prolonged periods and is rhythmic and aerobic in nature (e.g. walking, hiking, running, stair climbing, swimming, cycling, rowing, dancing, skating, skiing, rope skipping, or endurance game activities). Circuit weight training, which involves 10 to 15 repetitions with 15 to 30 seconds rest between weight stations results in an average improvement of about 5% and is not generally recommended as an activity for improving cardiorespiratory endurance. Intensity and duration of exercise determine the total caloric expenditure during a training session. To reduce the risk of orthopedic injury progams emphasizing low- to moderate-intensity exercise with a longer training duration are recommended for most individuals. The recommended intensity of exercise should be prescribed as 60 to 90% of maximum heart rate, or 50 to 85% of VO2max. However individuals with a very low initial level of fitness respond to a low exercise intensity, for example, 40 to 50% of VO2max. Although improvement in cardiorespiratory endurance have ben demonstrated with 5 to 10 minutes of very high intensity (>90% VO2max) exercise, at least 20 to 60 minutes of continuous aerobic activity is recommended (Mahler et al '95: 153, 155, 156, 157, 165). Optimal musculoskeletal function requires that an adequate range of motion be maintained in all joints. There are different types of stretching techniques that can be performed. Static stretching involves slowly stretching a muscle to the point of mild discomfort and then holding that position for an extended period of time (usually 10 to 30 seconds). Ballistic stretching uses the momentum created by repetitive bouncing movements to produce muscle stretch. Proprioceptic neuromuscular facilitation (PNF) stretching involves a combination of alternating contraction and relaxation of both agonist and antagonist muscles. As a rule stretches, with an emphasis on the lower back and thigh area, should be done at least 3 days week, to a position of mild discomfort, 10 to 30 seconds for each stretch, 3 to 5 repetitions. The maintenance or enhancement of muscular strength and muscular endurance enables an individual to perform such taks with less physiological stress. Resistance training should be an integral part of adult fitness and rehabilitative exercise programs to benefit increases in muscle strength and mass, bone mass, strength of connective tissue, modest improvements of cardiorespiratory fitness, reductions in body fat, modest reductions in blood pressure, improved glucose tolerance and improved lipoprotein profiles. Muscular strength and endurance are developed by the overload principle, by increasing the resistance to movement or the frequency or duration of activity to levels above those normally experiences (Mahler et al '95: 170-174). Exceeding 300,000 cases annually, sudden cardiac death (SCD) is the leading cause of death in the U.S. Studies of exercise by apparenty healthy adults report an acute event rate of 1 per 187,500 person-hours of exercise and death rate of male joggers of 1 per 396,000 man-hours of jogging. The incidence of cardiac arrest while jogging is approximately 1 episode per year for every 18,000 healthy men, by appears to be lower for men with higher levels of habitual physical activity. While the risk of sudden cardiac death is increased during vigorous exercise, this risk is lower among those habitually active. There are no scientific studies on execise-related cardiac events in women. The major cause of cardiovascular complications during exercise is coronary artery disease (CAD). During medically supervised cardiac rehabilitation exercise programs , the risk of death in the U.S. is approximately 1 per 60,000 participant hours, maybe one death every four years per program (Mahler et al '95: 8, 9). The risk of SCD in joggers and marathon participants is estimated to 1/15,000 and 1/50,000 respectively. Preparticipation exercise testing should be reserved for men >40-45 years of age and women>50-55 year with moderate to high cardiovascular risk. The probability of an exercise induced cardiac event is greater in athletes with atherosclerotic coronary disease and left ventricular dysfunction and older athletes should be discouraged from participation in high intensity sports if they have left ventricular ejection fraction <50% or evidence of exercise-induced ischemi, ventricular arrhythmia or systolic hypotension (Lawless '11: 391). Make sure exercise clothes are cardiac glycoside free. SCD is also the leading cause of death in athletes. Exercise-related SCD occurs in one to five cases per one million athletes per year. Of the approximately 25 milion competitive athletes in the U.S. there are 25-125 document cases of SCD per year, this is likely a significant underestimation because vigorous exercise does not require participation in organized athletics and independent athletes must guard their heart in certain cardiac conditions. It is estimated that there are 10-25 cases of SCD per iear in individuals younger than 30 years. The overall occurrence rate of SCD in high school athletes is estimated to be 1: 100,000-1:300,000 athletes/year. SCD in older athlets (>35 years of age) is most often related to atherosclerotic coronary arterial disease with myocardial infarction. However, in younger athletes (<35 years of age) the majority of these cases are caused by defined and hereditary cardiovascular disorders. Cardiac electrical instability, due to an underlying pathology, deteriorating into fatal ventricular tachycardia or ventricular fibrillation appears to be the most common immediate cause of death. In one study of SCD in competitive athletes from 1985 to 1995 it was found that the majority of these athletes were involved in high school sports (62%) with collegiate athletes in a distant second (22%) and professional athletes ranking third (7%). 90% of athletes suffering SCD were male. 68% of these deaths occurred during football and basketball. Ninety percent of athletes collapsed during or immediately after a training session or competition. Although symptoms or a family history may of SCD may precede the event, most epidosdes of cardiac arrest are the first manifestation of disease in an "apparently health" individual. Many athletes are capable of exceptionally high levels of performance for long periods of time, even while harboring occult and potentially lethal cardiovascular malformations. More than 20 cardiac pathologies have been identified as causes of SCD in athletes. Findings at autopsy reveal a predominance of an enlarged heart, hypertrophic cardiomyopathy (HCM) (26%), commotion cordia (20%) and aberrant coronary arteries (13%) as the underlying cause of death. Responsible for 20% o SCD in U.S. athletes commotion cordis can be caused by a sudden forceful impact to the chest wall that can elicit electrical instability leading to asystole or ventricular fibrillation, the mean age of victims is 13 years, and the resuscitation rate is only 15%. Only 18% of fatalities had symptoms attributed to the cardiovascular system in the preceding 36 months prior to death, although as many as 10 of 12 older athletes had symptoms prior to death although all had normal ECG findings. SCD in older athletes (<35 years old) is most often related to coronary artery disease with the incidence of SCD increasing with age, including older populations of vigorous exercisers, estimates of SCD incidence approach 1:15,000-1:18,000. Most of these deaths, of young and old athletes, are thought to be related to electrical instability leading to ventricular tachycardia and eventually, ventricular fibrillation. Inflammation, typically related to Coxsackie B virus in 50% of cases, or bacterial infection in the myocardial tissue can lead to electrical instability leading to fatal complete heart block after considerable chest pain and dizziness. Accounting for only 2% of SCD in U.S. athletes, Marfan's syndrome is an autosomal dominant inherited connective tissue disorder cocurring in approximately one in 10,000 individuals, who are characteristically very tall and thin, often with disproportionately long limbs, with an arm span greater than their height and have an increased risk of progressive dilation or the aortic root, potentially leading to dissection or rupture, that should monitored every 6 months by ECG. Approximately one in 10,000 Americans have prolonged QT syndrome exhibited by an abnormal ECG, 60% have a family history of long QT or SCD, one-third of patients present with palpitations, seizures and syncope. The trigger depends on the mutation, that can be detected by genetic testing, in QT1, the common trigger is swimming, in QT2 it is extreme emotion, in QT3 it is inactivity, in QT4 it is a loud noise, such a an alarm clock. Treatment often involves therapy with Beta-blockers, a pacemaker or ICD, typically then refraining from activity although 70% of athletes with ICDs make a return to play. In one study of an athletic department on the use of automated external defribulators (AEDs) found it has been used on 20% for student athletes, 33% for athletic department staff and 47% for fans, with survival rates of 0% for students, 75% for staff, 57% for fans, and 61% overall (Lawless '11: 3-17). Arrhythmogenic right ventricular dysplasia or cardiomyopathy (ARVD or ARVC) is characterized by fibrofatty infiltration of the myocardium, estimates range from 2.8% of SCD in athletes in the U.S. to as high as 22% in Europe. Athletes with this condition are disqualified from sports and must investigate the benefits of moderate levels of exercise. A rest period of approximately 6 months is recommended following the onset of myocarditis, an inflammatory disease of the myocardium. Similarly a diagnosis of acute pericarditis disqualifies athletes from participation in competitive sports, however, once the condition is resolved, sports may be allowed. Sinus bradycardias, sinus tachycardia, premature atrial contraction and nonsustained supraventricular arrhythmias are generally manageable non-lethal rhythm disturbances and for symptomatic athletes with no evidence of underlying high-risk disease, all sports are allowed. Athletes with pacemakers however should not participate in collision sports. Sports participation for athletes with aortic stenosis depends on the severity of the stenosis. All sports are allowed for athletes with mild aortic stenosis and moderate and low intensity sportsa re allowed for athletes with moderate aortic stenosis. However play is not allowed for athletes with severe aortic stenosis or occlusion. Mitral valve prolapse accounts for 2% of SCD in athletes (Lawless '11: 394-396, 398, 399). Activities during the first 48 hours following cardiac surgery or acute heart attack that gets worse with exertion, should be restricted to self-care activities, arm and leg range of motion movement, and other low-resistance activities. The posture should progress from lying, to sitting, to standing. Treadmills are highly recommended for uncomplicated patients, about 3 to 5 days postevent. Prior to discharge the patient shold be able to perform such acitivites as stair climbing and most home activities and should demonstrate a knowledge of those activities that are inappropriate or excessive and a safe, progressive plan of exercise and optimal risk reduction should be formulated for patients to take home. Patients should be able to manage their rehabilitiation independently and report cardiovascular symptoms promptly. The goals of outpatient programs are to provide appropriate patient supervision to ensure detection of problems and potential complications and provide timely feedback to the referring physician in order to enhance effective medical management, vocational and athletic rehabilitation. General principles for progressing the patient include an increase in exercise, as tolerated by the patient, every 1 to 3 weeks, with a goal of achieving 20 to 30 minutes of continuous exercise before prescribing additional increases in intensity. Patients with higher functional capacities respond well to more rapid progression. Patients with low functional capacity respond favorably to lower intensity activity emphasizing frequent short bouts of exercise with intermittent rest periods, progressing from intermittent to continuous exercise. For most patients progression toward an independent self-management program is desirable but some patients may need to remain in a clinically supervised program (Mahler et al '95: 177-187). Over 50 million Americans are hypertensive with a resting BP>140/90 mm Hg and/or currently use anti-hypertensive medication. The prevalence of hypertension rises sharply with age and is higher in men than in women and in blacks compared with whites, all stages are associated with increased ris of nonfatal cardiovascaulr events and renal disease. Endurance exercise training will elicit an average reduction of 10 mm Hg for both systolic and diastolic blood pressures in individuals with mild essential hypertension (blood pressures in the range of 140 to 180/90 to 105 mm Hg) and eve greater reduction in blood pressure in patients with secondary hypertension due to renal dysfunction. The recommended mode, frequency, duration and intensity of exercise is generaly the same as those for apparently healthy individuals. Exercise at somewhat lower intenstities (e.g. 40 to 70% VO2max) appers to lower blood pressure as much, or more, than exercise at higher intensities, which may be especially important in specific hypertensive populations, such as the elderly. Individuals with marked elevations in blood pressure should add endurance training to their treatment regimen only after initiating pharmacologic therapy; exercise may reduce their blood pressure further, allow them to decrease their antihypertensive medications, and attenuate their risk for premature mortality. Resistance training is not recommended as the primary form of exercise training for hypertensive or manic individuals. With the exceptin of circuit weight training resistance training has not consistently been shown to lower blood pressure and upper body strength has a tendency to incite belligerence the more balanced athlete would run away from. Thus resistance training is recommended as a component of a well-rounded fitness program (Mahler et al '95: 207, 208). Patients with peripheral vascular disease such as arteriosclerosis, often associated with hyperlipidemia, hypertension and diabetes, arterial stenosis, Raynaud's phenomenon (an abnormal vasomotor tone exacerbated by cold exposure) and Buerger's disease (an inflammation of the sheath encapsulating the neurovascular bundle in the extremities) experience ischemic pain (claudication) during physical activity as a result of a mismatch between active muscle oxygen supply and demand. The various manifestations of the symptoms may be described as burning, searing, aching, tightness, or cramping. The pain is most often experienced in the calf of the leg but can begin in the buttock region and radiate down the leg. The symptoms typically disappear upon cessation of exercise. Severe occlusive disease is treated initially with exercise and mediacation sthat decrease blood viscosity. Weight bearing and repetitive non-weight bearing exercise is preferred because of four grades of crippling pain. Daily exercise to maximum tolerable pain with intermittent rest periods is advised. Multi-stage discontinuous protocol may be necessary to achieve necessary O2 consumption (Mahler '95: 209-213). There are two major types of diabetes mellitus, juvenile onset Insulin dependent diabetes mellitus (IDDM) and maturity onset non-insulin dependent diabetes mellitus (NIDDM). The response to exercise in juvenile onset insulin dependent diabetes (IDDM) varies. If the diabetic is under appropriate control or only slightly hyhperglycemic without ketosis, exercise decreases blood glucose concentration and a lower insulin dosage may be required. However, a lack of sufficient insulin prior to exercise may impair glucose transport into the muscles limiting the availability of glucose as an energy substrate leading to ketosis, resulting in greater glucose production further exacerbating the hyperglycemic state. Serum glucose concentrations in the general range of 200 to 400 mg/dL require medical supervision during exercise, while exercise is contraindicated for htose with fasting serum values >400 mg/dL pending medical follow-up. Exercise induced hypoglycemia is the most common problem experience by exercising diabetics. Hypoglycemia not only occurs during exercise, but may occur up to 4 to 6 hours following an exercise bout. To counteract this response, the diabetic may need to reduce insulin dosage or increase carbohydrate intake prior to exercising. Proper footwear and good foot hygiene is important. eta-blockers and other medication may interfere with the ability to discern hypoglycemic symptoms and/or angina. Exercise in excessive heat may cause probles in diabetic with peripheral neuropathy. Patients with advanced retinopathy should not perform activities which cause excessive jarring or marked increases in blood pressure. NIDDM diabetic may benefit from oral hypoglycemic agents rather than injections of insulin, although exogenous insulin is sometimes used. Since insuling facilitate the cellular absorption of glucose a lack of sufficiently circulating insulin usually results in hyperglycemia (Mahler et al '95: 213-215). Metabolic and cardiorespiratory adaptations to pregnancy may alter the responses to acute exercise and the adaptations that result from exercise training. Benefits of a properly designed prenatal exercise program include improved aerobic and muscular fitness, facilitatin of recovery form labor, enhanced maternal psychological well-being, and establishment of permanent healthy lifestyle habits. There is no data indicating that pregnant women whould limit exercise intensity because of potential adverse effects. Women should avoid exercise in a supine position after the first trimester. Pregnant women should stop exercising when fatigued, not exercise to exhaustion and discontinue exercising and seek medical advice at any signs of bloody or fluid discharge form the vagina, swelling of hands, feet, or face, persistant headaches, elevation of pulse or blood pressure that persists after exercise, chest pain, contractions that may suggest onset of premature labor, unexplained abdominal pain or insufficient weight gain (<1.0 kg/month during last two trimesters. Any type of exercise involving the potential for even mild abdominal trauma should be avoided. Pregnancy requires an extra 300 kcal/day in order to maintain metabolic homeostasis. There is no objective evidence that woman who exercises has shorter or less complicated labor and delivery. However, studies have shown that women who exercise regularly return to their pre-pregnancy weight, strength and flexibility levels faster than their sedentary counterparts (Mahler et al '95: 235-239). Reducton of body weight is a frequently desired outcome in exercise programs. Obesity may be functionally defined as the percent of body fat at which disease risk increases. Body fat is reduced when a chronic negative caloric balance exists. It is recommended that both an increase in caloric expenditure through exercise and a decrease in caloric intake by used to accomplish this goal, a vegan diet is useful. Exercise increases energy expenditure and slows the rate of fat-free tissue loss that occurs when a person loses weight by severe caloric restriction. Exercise also helps maintain the resting metabolic rate and thsue the rate of weight loss. Obese individuals are invariably sedentary and many have had poor experiences with exercise in the past. The initial exercise prescription should be based on low intensity and progressively longer durations of activity. Central obesity, fat deposited primarily in the trunk or abdominal region is particularly problematic. Obesity often carries a negative social stigma and is associated with a reduced physical working capacity. Reduction of body fatness is a need or a goal of many exercise program participants. One pound of fat is equivalent to approximately 3500 kcal of energy (1kg =7700 kcal). In designing the exercise component of a weight loss pogram, the balance between intensity and duration of exercise should be manipulated to promote a high total caloric expenditure (300 to 500 kcal per session and 1000 to 2000 kcal per week for adults). Obese individuals are at an increased relative risk for orthopedic injury and thus may require that the intensity of exercise be maintained at or below the intensity recommended for imporovement of cardiorespiratory endurance. Non-weightbearing activity and rotation of exercise modalities may be necessary and frequent modification in frequency and duration may also be required (Mahler et al '95: 216-219). The wide range of health and fitness levels observed among older adults make generic exercise prescription difficult. Major objectives in planning exercise for the aging adult and the person with dementing and disabling illness are to increase muscle tone to improve physical functioning, to increase flexibility and balance, to improve physical stamina or endurance, and to reduce stress and promote a feeling well-being. Aerobic activity, at least 3 times a week for 20 minutes, must be spaced throughout the week. If the person cannot tolerate 20 minutes of continual movement, recent research is showing that exercise can be broken into shorter blocks which total 20 to 30 minutes for the day. Usually walking, even slow walking, is aerobic for many aging adults. As age increases, the heart rate needed to perform aerobically decreases. A 10 second pulse rate between 15 and 19 will be more than adequate to sustain aerobic functioning in an adult between the ages of 70 and 90. Exercises designed to promote flexibility, range of motion and balance daily. Without stretching and utilizing all muscles, some will become stretched and others contracted, resulting in inability to utilize some muscles altogether. Typically, problems occur in the shoulders, arms, and legs. Caregivers must realize how extremely painful it is when muscles become weak, contracted, and out of alignment from lack of use (Bridges '98: 91-92). Resistance training to improve muscular strength and endurance offer considerable benefit to older adults enabling them to perform activities of daily living with greater ease and counteract muscle weakness and frailty in very old persons. Some minimal level of muscular fitness is critical for individuals to retain their independence. It is believed that resistance training provides significant musculoskeletal benefits for men and women of all ages, and an appropriate level of muscular fitness is integral to ensuring that individuals are able to spend their latter years in a self-sufficient, dignified manner. Sessions lasting longer than 60 minutes may have a detrimental effect on exercise adherence and sessions should probably be limited to 20 to 30 minutes. An adequate range of motion in all the joints of the body is important and stretching helps to reduce injury (Mahler '95: 228-234). Exercises designed to tone all body muscles, including work with light weights, should be done no less than three times per week. At the beginning stages of weight exercises, it is best to perform the motions without weights for at least two weeks. Gradually add weights at monthly intervals starting with one pound and increase as tolerated up to a maximum of three pounds. Most older women can improve muscle performance with continous work with one pound weights. Men may require more. The numbers of repetitions should be no more than eight to ten. With any complaints of pain, muscle tenderness, or soreness, weight activities should be stopped. Exercise bicycles can be utilized with ease. Stair climbers and treadmills may be too vigorous for most older people to utilize for cardiovascular conditioning (Bridges '98: 93, 94). In children under no circumstances should a weight be used that allows for less than eight repetitions to be completed per set, since heavy weight can be potentially dangerous and damaging to developing skeletal and joint structures. Resistance exercise may not be appropriate for some patients, including those with congestive heart failure (CHF), severe valvular disease, uncontrolled arrhythmias, or significant left ventricular dysfunction. Resistance training should generally be deferred until 4 to 6 weeks of supervised cardiorespiratory endurance exercise have been completed. Less myocardial ischemia and fewer arrhythmias occur with resistance exercise compared with endurance (Mahler et al '95: 225, 189). The aging adult, and particularly a person with dementing illness, has increasing difficulties with maintaining physical fitness. The person with good muscle tone and endurance prior to illness or injury will recover much more quickly than the person without. Good muscle tone is essential for maintaining normal body functions such as evacuating bowel movements, and for maintaining posture and mobility. There are three aspects of maintaining muscle tone that are important to the caregiver. One is that utilizing all possible muscles while performing every day activities, the second is in encouraging muscle usage when the person is relaxing, and the third is initiation of a more formal exercise program. It is extremely important that the patient perform any and all activities independently, if possible. Independent performance of activities will increase feelings of achievement and accomplishment, and serve to enhance the quality of life for the person with dementing illness. There are many times during the day when caregivers can encourage persons to strengthen muscles by being a little more creative (Bridges '98: 88-90). Exercise testing is performed in many setting for nondiagnositic purposes, such as worksite health promotion programs, YMCAs and YWCAs, health clubs and other community exercise programs. This testing tends to be functiona, in many the ECG is not monitored, and is aimed at assessment of physical fitness, providing a basis for exercise prescription, or monitoring of progress in an exercise program (Mahler et al '95: 10). In a stress test, one exercises on a treadmill while the ECG is monitored. Walking or running speed is progressively increased along with the grade (or slope) as the doctor continuously analyzes blood pressure as well as the ECG. The doctor may perform a nuclear stress test in which a nuclear agent (radioisotope) is injected into your vein and images of your heart are acquired to identify whether areas in the heart muscle are receiving enough blood. Stress tests are useful for sedentary patients before they begin an exercise regimen, to evaluate whether exercise is safe for them. For all stress tests and invasive procedures the patient must have nothing by mouth (NPO) for at least 6 hours prior to the procedure. In addition, the doctor may ask the patient to stop taking blood thinners, such as warfarin (Coumadin) and antiplatelet medications, such as acetylsalicylic acid (aspirin) and clopidogrel (Plavix), before a procedure (Cohen 10: 63, 64, 65). The 1-1-1 Physical Fitness Assessment, consists of one minute of push-ups, one minute of sit-ups, and a timed, one-mile run. Soldiers are allowed a minimum of 5 minutes and a maximum of 10 minutes to recover between events. 100 push-ups, 100 sit-ups and three mile run in less than 28:00 minutes is the goal. Clients often start out doing push-ups on their knees and work up to 40 to 50 regular push-ups without stopping to rest. To enter Marine Corp basic training men have to do 2 pull-ups, 44 sit-ups in two minutes and 1.5 mile run in 13:30 minutes; women do a flexed arm hang for 12 seconds, 44 sit-ups in two minutes and one mile run in 10:30 minutes. The Marine Corp Physical Fitness Requirements for men are three pull-ups, 50 crunches diminishing with age to 40 and 3-mile run in 28:00 minutes diminishing with age to 33:00. For women it is a 15 second flexed arm hang and 50 crunchs diminishing to 40 with age and 3-mile run in 31:00 minutes diminishing to 36:00 minutes with age. There is no reason women can't do three whimpy pull-ups when cross-trainers do 50 before continuing to the next challenge, nor is there any reason men can't develop their arm muscles doing arm hangs for a minute. To make minimal visual improvement in pectoral and arm muscle mass and achieve a flat abdomen (in an already thin person), it generally takes around 300 push-ups and crunches, 500 is enough for "six pack abs" on a working day, doing sets of 100 between chapters, and 1,000 on rainy days when it is impossible to swim twenty laps, jog five to ten miles, cycle 65 miles or run a marathon. Partners are helpful for motivation and in case of injury. Marine Corp Age Adjusted Physical Fitness Requirements AgePush-ups 1 minuteCrunches 3 minutesPull-ups3-Mile RunGoalSets of 50-100Sets of 50-100Sets of 10-2025:00Male 17-26 5050328:0027-394545329:0040-454545330:0046+4040333:00Females 17-265050Flexed Armed Hang 15 seconds31:0027-39454515 seconds32:0040-45454515 seconds33:0046+404015 seconds36:00Source: Army Study Guide The military physical training prescription takes approximately 45 minutes per day, and should be done everyday. Whether following walk-to-run guidelines or training at a higher level, the military program will help to ensure minimal standards of physical fitness. Training does not require a gym or expensive equipment. It is best to start with just the resistance of the body to develop proper form. Each standardized physical training session expends approximately 300-400 kilocalories found in a cup of cooked rice, cereal, or pasta about the same size as your fist. Do not perform exercises that cause indigestion that could lead to ulceration such as running, or sit-ups, immediately after a large meal, although push-ups may not cause discomfort and other slower exercises can actually aid digestion (TRADOC '03). A review of3,832 autopsiesdone on troops who died in combat or of unintentional injuries in the Iraq and Afghanistan wars found that 9 percent had atherosclerosis in the coronaries. Thats a dramatic drop from the prevalence found in autopsies of casualties of the Korean (77 percent) and Vietnam (45 percent) wars (Brown 13). Food is believed to have improved dramatically and the 45 minute physical training program works, but is at least an hour too short for the completely sedentary pensioner to recover from a heart attack or to prevent all angina pectoris for eight hours of sedentary work behind a computer screen. For most adult sedentary workers it takes a five mile run (10k a day), 500 push-ups and crunches, in sets of 100, interspersed throughout the sedentary working day, and because their work is sedentary by nature, should run a marathon or triathlon on the Sabbath. The Boston marathon is one of the last marathons in the United States to require qualifying times be run before the race which are 3:05 for men and 3:35 for women between the ages of 18-34, rising five minutes every four year increments to 80+ times of 4:55 for men and 5:25 for women. The Walk-to-Run Program is for people whose 1-mile time was slower than 8:30 or a female with a 1-mile time slower than 10:30 minutes. During the first four weeks alternate walking and running for 10:30 minutes and repeat the walk-run routine five times in each training session. At week five run continuously for the time period listed on the training schedule. Run at a pace that can be maintained for the entire time or distance without feeling out of breath. The ability to carry on a conversation while running (the talk test), indicates the right pace. Males with 1-mile times 8:30 or faster or a female 10:30 or faster should practice speed running or carry a backpack if they don't increase the distance to the minimal daily distance of 10 km to 10 miles used by most athletes trying to stay healthy and keep the marathon within reach. The recommended rate of progression in an exercise conditioning program has three stages, the initial conditioning stage, improvement stage and maintenance stage (Mahler '95:169). The initial conditioning stage includes light muscular endurance activities and moderate-level cardio respirator endurance activities that produce minimal muscle soreness and control injuries. This stage usually lasts up to four weeks and is dependent upon the individuals adaptation to exercise. The duration of the main activity during the initial stage will begin with approximately fifteen to twenty minutes and may progress to thirty minutes or more. The goal of the improvement stage is to provide a gradual increase in the overall exercise stimulus to allow for more significant improvements in your fitness level. The goal of the maintenance stage is the long-term maintenance of the cardio-respiratory and muscular strength and endurance fitness developed during the weeks spent in the improvement stage. Exercise must be conducted daily at the proper intensity to bring about the desired changes in the body. Missing a whole week of sessions, will probably set the program back a week. If unable to perform certain exercises perform more of those able to do in order to ensure minimal cardiorespiratory exertion. Adequate nutrition, rest and recovery must be studied to optimize health, physical fitness improvement, and control injuries. A standardized physical training session consists of three essential elements: warm-up, activity, and cool-down. Basic military training is not very demanding by athletic standards however many recruits become permanently disabled in boot camp and are discharged due to chronic bone disease before having made a significant contribution, possibly due to shortage of highly safe and effective $1 athlete's foot cream (clotrimazole) rather than $1 antifungal foot powder spray (toftate) that causes diffuse pain and angina. Rheumatism that occurs in conjunction with angina pectoris, usually alternating between angina that gets better with exercise and hip pain that gets worse with exercise, known as rheumatic heart disease, is caused by Streptococcus pyogenes 50% of the time, which responds best to penicillin but any antibiotic, with probiotic supplementation during and for two weeks after finishing a course, should eliminate rheumatism, helping to achieve minimal athletic standards, which heightens the sensitivity to and hastens treatment of new rheumatic infections so that they do not cripple the work-out. Antibiotic resistance is only issue for Staphylococcus aureus that infects the heart and vertebrae with large lesions 1 cm in diameter and is effectively treated with doxycycline as well as infections involving fecal coliform best treated with metronidazole (Flagyl ER). In general, to avoid injury, before running 3 miles it is necessary to warm up with a minimum of 100 push-ups, sit-ups and some movement drills and after running 3 miles it is necessary to stretch. All organized exercise programs do yoga to help improve flexibility, balance and strength to prevent injury during and after the high intensity endurance activity of the day. A mat may be necessary to avoid injury doing crunches. Socks must not make running shoes tight, flat soled cross-trainers make calf muscles stronger and are best for troublesome weather and conditions of the foot. A ripped pectoral muscle, possibly from doing excessive pull-ups beyond the point of flopping, might lead to an aortic aneurysm and causes pain that is indistinguishable from angina pectoris. Army warm up and cool down exercises 1. The Bend and Reach (5 repetitions - slow) 2. The Rear Lunge (5 repetitions - slow) 3. The High Jumper (5 repetitions - moderate) 4. The Rower (5 repetitions - slow) 5. The Squat Bender (5 repetitions - slow) 6. The Windmill (5 repetitions - slow) 7. The Forward Lunge (5 repetitions - slow) 8. The Prone Row (5 repetitions - slow) 9. The Bent-leg Body Twist (5 repetitions - slow) 10. The Push-up (5 repetitions - moderate) Military Movement Drill for warming up 1. Verticals (1 repetition) 2. Laterals (1 repetition) 3. The Shuttle Sprint (1 repetition) The Stretch Drill for cooling down 1. The Overhead Arm Pull (hold 20 seconds) 2. The Rear Lunge (hold 20 seconds) 3. The Extend and Flex (hold 20 seconds) 4. The Thigh Stretch (hold 20 seconds) 5. The Single-leg Over (hold 20 seconds) Source: Training and Doctrine Command (TRADOC) Standardized Physical Training Guide. United States Army Physical Fitness School.  HYPERLINK "http://www.armystudyguide.com/imagesvr_ce/1203/tradoc-prebct-physical-tr.pdf" 5 November 2003 Bibliography Armitage, Jane. Niacin therapy unhelpful, occasionally harmful: study. Channel News Asia. Washington. 10 March 2013 Bronstein, Alvin; M.D. et al. 2010 Annual Report of the American Association of Poison Control Centers National Poison Data System (NPDS). 28th Annual Report. Table 18. Informa Healthcare USA Inc.  HYPERLINK "http://www.aapcc.org/dnn/Portals/0/2010%20NPDS%20Annual%20Report.pdf" 2011 Brown, David. Hardening of the Arteries Common in Ancient Mummies. Health and Science. Washington Post. March 10, 2013 Cohen, Todd J. M.D. F.A.C.C., F.H.R.S. A Patients Guide to Heart Rhythm Problems. The Johns Hopkins University Press. Baltimore. 2010 Debrowolski,Christine MD. Doctor of Podiatric Medicine. Those Aching Feet: Your Guide to Diagnosis and Treatment of Common Foot Problems. Revised Edition. Ski Publishing. San Francisco. 2004 DeNoon, Daniel J. Martin J. Laura, MD. Failing Hearts Healed With Stem Cells. WebMD Health News. 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Infobase Publishing. 2007 Peterson, Faith Young. Alterations in Immune Function. Chapter 10. Pathophysiology. Third Edition. Edited by Loo-Ellen C. Copstead and Jacquelyn L. Banasik. Elsevier Inc. St. Louis, Missouri. 2005, 2000, 1995. Pgs. 244-264 Robbins, John. The Food Revolution: How Your Diet Can Help Save Your Life and Our World. Foreword by Dean Ornish M.D. Conari Press. San Francisco, California. 2001 Robinson, Morton J., M.D.; Greenberg, Jack J., M.D.;Korn, Morton, M.D.; Rwylin,Arkadi M., M.D. Infective endocarditis at autopsy: 19651969. American Journal of Medicine.  HYPERLINK "http://www.amjmed.com/article/0002-9343(72)90040-X/abstract" 10 November 1970 Sanders, Tony J. American Heart Month since February 1963. Hospitals & Asylums  HYPERLINK "http://www.title24uscode.org/heart.htm" HA-14-2-08 -- Radioactive Polygraph.  HYPERLINK "http://www.title24uscode.org/radiation.doc" HA-3-6-11 -- Medicinal Herbs and Probiotics  HYPERLINK "http://www.title24uscode.org/herb.htm" HA-31-10-12 Saunders-Elsevier et al. Kumar, Vinay, M.D., M.B.B.S.; Abbas, Abul K. M.B.B.S.; Fausto, Nelson, M.D.; Aster, Jon C. M.D., Ph.D. Robbins and Cotran Pathologic Basis of Disease. Saunders-Elsevier. Philadelphia, PA. 2010 --Alpers, Charles E., M.D. Kidneys. Chapter 20. Robbins and Cotran Pathologic Basis of Disease. Saunders-Elsevier Imprint. Philadelphia, PA. 2010 Saunders, W.B. et al. Robbins Pathologic Basis of Disease. Cotran, Kumar, Robbins. 5th Edition. W.B. Saunders Company. Philadelphia. 1994 -- Diseases of Red Cells and Bleeding Disorders. Cbapter Thirteen. Robbins Pathologic Basis of Disease. Cotran, Kumar, Robbins. 5th Edition. W.B. Saunders Company. Philadelphia. 1994 --Diseases of White Cells, Lymph nodes and Spleen. Chapter Fourteen. Robbins Pathologic Basis of Disease. Cotran, Kumar, Robbins. 5th Edition. W.B. Saunders Company. Philadelphia. 1994 --Kidneys. Chapter Twenty. Robbins Pathologic Basis of Disease. Cotran, Kumar, Robbins. 5th Edition. W.B. Saunders Company. Philadelphia. 1994 -- Samuelson, John, M.D.; Von Lichtenberg, Franz, M.D. Infectious Disease. Chapter Eight. Robbins Pathologic Basis of Disease. Cotran, Kumar, Robbins. 5th Edition. W.B. Saunders Company. Philadelphia. 1994 --Schoen, Frederick J. M.D., Ph.D. Blood Vessels. Chapter Eleven. Robbins Pathologic Basis of Disease. Cotran, Kumar, Robbins. 5th Edition. W.B. Saunders Company. Philadelphia. 1994 --Schoen, Frederick J., M.D. The Heart. Chapter Twelve. Robbins Pathologic Basis of Disease. 5th Edition. Cotran, Kumar, Robbins. W. B. Saunders Company. Philadelphia. 1994 Shute, Nancy. Side Effects Prompt Patients To Stop Cholesterol Drugs. NPR. April 3, 2013 Spence, David J., M.D. How to Prevent (A) Your Stroke. Vanderbilt University Press. Nashville, Tennessee. 2006 Training and Doctrine Command (TRADOC) Standardized Physical Training Guide. United States Army Physical Fitness School.  HYPERLINK "http://www.armystudyguide.com/imagesvr_ce/1203/tradoc-prebct-physical-tr.pdf" 5 November 2003 Venzmer, Gerhard. 5000 Years of Medicine. Translated by Marion Koenig. Taplinger Publishing Company. New York. 1968, 1972 Wilson, Bruce C., MD, Childre, Doc. The Heart Math The Proven, Natural Way to Lower Your Blood Pressure Forward by Mimi Gaurneri, MD. New Harbinger Publications, Inc. Oakland. 2006 Yntema, Sharon. Vegetarian Children: A Supportive Guide for Parents. McBooks Press. 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