ࡱ> HJG7 V*bjbjUU "@7|7|V&lZZZZZZZn4n       XZZZZZZ$ ~Z     ~ZZ   jZ Z X XPXZZX  rzn2tFXX0XENEXnnZZZZThursday, January 4, 2001 Scribe: Justin Reid Pathology 1PM Proof: Justin Reid Dr. Graham ISCHEMIC HEART DISEASE (contd) I. Reperfusion effects A. If injured tissue is reperfused within an hour to several hours there maybe no death of tissue B. Tissue: dead, stunned (semi alive), and alive 1. Reperfusion can save stunned but not dead tissue C. Contraction bandsirreversibly injured myocytes 1. Histologically appear to be alive but sarcomeres are non-functional 2. Mark of reperfusion injury D. Many times there is obvious dead tissueRemember>Red is Dead 1. Hypereosinophilic and wavy b/c other fibers around this dead tissue is contracting while it isntnot the same as contraction bands (good picture in the book!) D. Hemorrhage will occur with reperfusion to injured tissue E. Injured tissue adjacent to alive tissue will appear wavy due to its lack of contraction F. Cardiac enzymes will appear worse with reperfusion because of additional damage to myocytes by O radicals G. Stunned (reversibly injured) myocytes may take a while to recover and therefore there functional recovery should be monitored II. Cardiac Enzymes A. Released by the myocardium as the tissue dies B. Creatine Kinase (CK) dimers M/B 1. CK-MB fraction is specific for cardiac muscle 2. Pro: peaks in 18 hr 3. Con: gone in 2-3 days C. Troponin I and T (TnI;TnT)associated with sarcomeres of cardiac and skeletal muscle but selectivity to cardiac muscle can be achieved through antibodies 1. Pro: peaks in 18 hr 2. Pro: lasts 7 to 10 days D. Most people are moving toward TnI b/c of its lasting power SLIDE: 3-6 day heart; hypertrophy of left ventricle (LV); ant. transmural yellowing; old subendocardial scarring SLIDE: ant. MI; yellowing with some hemorrhaging probably 3-5 days old; transmural in the septum SLIDE: viable myocardium with cellular granulation tissue (appear as early as 3 days); macrophages, neutrophils SLIDE: mononuclear cells cleaning the place up III. Complications of MI A. Early complications are very rare B. Lethal complications are cardiac rupture syndromes SLIDE: LV with a transmural infarction of left circumflex with complete rupture of the wall SLIDE: large rent (?) in the free wall of the LV 1. Free wall rupture-- lead to hemopericardium (which acutely can occlude intake and therefore output) 2. Interventricular septum rupturelead to increased load on the right ventricle SLIDE: transmural rupture into the free wall of the ventricle SLIDE: heart bathed in cloud of blood--hemopericardium SLIDE: heart ruptured through the right ventricle (RV) 3. Ruptures can lead to papillary muscle damage with acute mitral insufficiency, which can lead to acute hemodynamic changes on the left side C. Ventricular aneurysm 1. Thinned scar and therefore it doesnt work and just takes up space 2. Late complication 3. Rarely ruptures SLIDE: old (white) heart with a very thin wall distinct of an aneurysm SLIDE: LV aneurysm, which isnt contributing anything to cardiac output but is a source of emboli and is taking up space SLIDE: LV with huge laminated mural thrombus; removal can prolong life SLIDE: Huge ballooning aneurysm looks like another chamber D. Early pericarditis can occur in a transmural infarction as well as an autoimmune pericarditis which can cause friction rubs and pain a couple of weeks after an MI therefore producing a different pain syndrome E. Mural thrombussource of emboli and results from aneurysms or any injured surface F. Infarct extension 1. Hypotension 2. Additional ischemic extension of the infarction 3. Attempts are made to prevent these secondary symptoms G. Papillary muscle dysfunction and therefore valvular dysfunction IV. Mortality A. Make hospital: only 7-13% die B. Dont make hospital: 40% die C. 30% of people who have an MI die within year one D. 3-4% of people die each year thereafter Side notes: After you have gotten through the first few weeks after an MI, what happens? You will scar downyou eat up the bad dead stuff, the macrophages leave, the vessels hang around while you continue to scar, and vessels lessen in number until there gone when the scarring is complete. Some MIs take longer to scar than others depending on the size of the MI. After approximately a month, the scarring is finished and whether the MI was 3 months ago or 10 years ago we wouldnt be able to tell b/c a scar is a scar. Thin scars can result in dilatations (aneurysms). Scars with many cells containing macrophages are symbolic of a new scar. Trichrome is used to stain collagen green, which is the component of scars. V. Chronic Ischemic HD A. Diffuse dysfunction from long term subacute disease or postinfarction decompensation B. Chronic CAD of varying degrees C. Patchy or old transmural fibrosis D. Myocardial hypertrophy b/c as myocardium is lost other myocardium needs to make up for the loss E. Diffuse subendocardial vacuolization--long-term low-grade injury that may be reversible in the subendocardial cells VI. Sudden Cardiac Death---death occurring within one hour of a cardiac event A. 300,000 to 400,000 deaths/year in the US B. Arrhythmias C. Causes: 1. Critical stenosis i.e. occlusion of a coronary vessel >75% (80-90% of cases) a. Acute plaque disruption, which is not occlusive but subocclusive D. Younger patients--other non-ischemic causes VII. Systemic hypertension A. Causes: 1. Idiopathic in 90-95% of cases 2. Increased vascular resistance 3. <5% of cases caused by nonidiopathic causes: endocrine or renal vascular disease B. Complex Pathogenesis C. Effects 1. Left ventricular hypertrophy 2. Small vessel disease especially the kidney resulting in mild to significant renal disease 3. Accelerates atherosclerosis 4. Potentiates aortic dissection 5. Strokes (Cerebrovascular accidents-CVAs) VIII. Acquired Valvular Heart Disease (primarily the left sided valves) A. Aortic stenosis (AS)makes up 2/3 of all valve disease 1. Chronic process (usually) --b/c it involves scarring down calcification process of the valves B. Valvular insufficiency 1. Hole in the valve 2. Blowout of the valve 3. Common complication of acute bacterial endocarditis 4. Blowout or dilation of assoc. structures 5. Marfans syndromedilates the aortic ring 6. Syphilisdilates the aortic ring C. Mitral stenosis 1. #1 cause is rheumatic HD D. Mitral regurg/insuff 1. Mitral valve prolapse E. Aortic stenosis (contd from A) 1. Senile calcific ASoccurs in the elderly 2. Bicuspid valve with calcificationoccurs in 50s and 60s but rare 3. Rheumatic HD F. Aortic regurg/insuff 1. Blowout of a valve in effective endocarditis 2. Dilated aorta 3. Left ventricular hypertrophy b/c of volume and pressure increase **POSSIBLE EXAM QUESTION** Know that if a patient has isolated aortic stenosis it will very unlikely be rheumatic HD. Virtually everytime you have aortic stenosis associated with rheumatic HD you will have mitral valve stenosis!!!! G. Aortic stenosis (contd from E) 1. Left ventricle will become hypertrophic b/c of mimicking of HTN SLIDE: normal tricuspid valve (no vessels b/c flowing blood bathes the leaflets; calcification appearing as thickened and irregular; irregular valves but still separate leaflets are characteristic of acquired senile AS; rheumatic HD causes fusion of leaflets up to a certain point shown in the pictur SLIDE: calcification of valves SLIDE: normal aortic valve and insufficient valve looking ratty SLIDE: aortic stenosis producing massive LV hypertrophy TREATMENT of aortic stenosis should be treated ASAP as compared to some of the mitral valve stenoses(this will be covered later) H. Mitral Valve 1. Annular calcification a. Most common in women >60, mitral valve prolapse, high left ventricular pressure, and complications are usually related to poor movement of the valves I. Mitral Stenosis 1. #1 cause is chronic Rheumatic HD 2. 75% of cases the mitral valve alone is involved in rheumatic HD 3. 25%(the rest) involves both aortic and mitral valve stenosis 4. **The left ventricle does not become hypertrophic with isolated mitral valve stenosis.** 5. **What is significant and becomes gigantic is the right atrium** 6. Also associated is secondary pulmonary hypertension b/c of massive backup of blood into the lungs 7. SLIDE: slitlike appearancefishmouth mitral valvebuzzword for mitral stenosis assoc. with chronic rheumatic HD J. Mitral valve prolapse 1. #1 valvular HD in industrialized countries-3%; Females>males 2. Developmental abnormality 3. Notable for a mid-systolic click b/c of a big ballooning mitral valve leaflet that in the middle of systole goes SNAP! and it clicks and you can hear it through your stethoscope +/- murmur Mitral insufficiency 4. Dilated ring with some myxoid changes 5. Atrial mural thrombi assoc. with jetflows of blood in abnormal fashion causing scarring resulting in thrombi (classic one is in the left atrium) SLIDE: mitral valve with big ballooning leaflets that snap up when they close SLIDE: picture from the atrium shown into the ballooning leaflet 6. Complications: ~3% RARE a. Infective endocarditis b. Mitral insufficiency c. Arrhythmia with sudden death seen but RARE If you have questions concerning the scribe e-mail me at  HYPERLINK "mailto:medsjjr@ttuhsc.edu" medsjjr@ttuhsc.edu and Ill try my best to resolve the issue. 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