ࡱ> @ 2jbjbqq *Tl    8D`\ j""4j6j6j6j6j6j6j,k mbj-bjbibibibi]4jbi(rr4jbibi4j4jq1\  `4j4jjj4jSnbiSn4jbi Sudden cardiac death in young athletes Causes, athlete's heart, and screening guidelines Jonathan A. Drezner, MD VOL 108 / NO 5 / OCTOBER 2000 / POSTGRADUATE MEDICINE ------------------------------------------------------------------------ CME learning objectives * To review the causes of sudden cardiac death in young athletes * To understand the physiologic changes seen in so-called athlete's heart * To recognize key features of the preparticipation sports evaluation The author discloses no financial interests in this article. ------------------------------------------------------------------------ This page is best viewed with a browser that supports tables. Preview: The sudden, unexpected death of a young athlete from a cardiac cause, while rare, often captures the public's attention and raises questions about the need for more comprehensive screening before athletes are allowed to participate in vigorous sports. In this article, Dr Drezner addresses the questions surrounding such tragedies and discusses the causes of sudden cardiac death, the physiologic adaptations seen in so-called athlete's heart, and guidelines for cardiovascular screening. Drezner JA. Sudden cardiac death in young athletes: causes, athlete's heart, and screening guidelines. Postgrad Med 2000;108(5):37-50 ------------------------------------------------------------------------ When a young athlete dies unexpectedly, the impact often extends beyond the local community and medical establishment to attract regional and national media attention. As a result, primary care and sports medicine physicians are often asked to screen athletes for relatively rare cardiac-related diseases that may predispose an athlete to sudden death. Physicians involved in the care of athletes play the dominant role in prevention of sudden cardiac death and should be familiar with its various causes and the current recommendations for screening of athletes before their participation in sports. This article outlines the major causes of sudden cardiac death, reviews the physiologic cardiovascular adaptations seen in so-called athlete's heart, and defines key features of the preparticipation sports evaluation. Background and prevalence Sudden cardiac death in an athlete has been defined as nontraumatic and unexpected sudden cardiac arrest that occurs within 6 hours of a previously normal state of health (1). In athletes less than 35 years of age, congenital cardiovascular disease is usually responsible. This catastrophic event typically occurs during or shortly after training or competition, suggesting that intense physical exertion is a precipitating factor (2). Recently, the list of recognized cardiovascular risks during athletic competition has been expanded to include cardiac arrest resulting from blunt trauma to the chest wall in the absence of underlying cardiovascular disease (3). The earliest documented case of sudden cardiac death occurred in 490 BC, when Pheidippides, a Greek soldier and conditioned runner, ran from Marathon to Athens to announce military victory over Persia, only to deliver his message, then collapse and die (4). More recently, the sudden deaths of a number of high-profile athletes--Olympic gold medal skater Sergei Grinkov in 1995, professional basketball player Reggie Lewis in 1993, college basketball player Hank Gathers in 1990, Olympic volleyball champion Flo Hyman in 1986--have received national publicity, raising public interest in this infrequent event. Young competitive athletes are generally perceived as the healthiest segment of our society, and their unexpected collapse often sparks public debate on prevention of sudden cardiac death and the appropriateness of established screening guidelines. Fortunately, sudden cardiac death in young athletes is rare. Its exact prevalence is unknown, since there is no national database to track death in athletes. The largest available studies estimate the risk among high school and collegiate athletes to be between 1 per 100,000 and 1 per 300,000 each year (5-7). An estimated 50 to 100 cases occur in the United States annually (6,8). Researchers have also found that sudden cardiac death is about five times more common in males than in females (5). The incidence increases in persons over 35 years of age, largely because of the increasing prevalence of atherosclerotic heart disease. Estimates of the incidence in the older population of joggers or people who exercise vigorously range from 1 per 15,000 to 1 per 18,000 (9,10). Causes of sudden cardiac death Most cases of sudden cardiac death in young people are secondary to congenital cardiac abnormalities. The common denominator in all cases is the development of electrical instability that leads to a fatal arrhythmia (8). Table 1 lists the various causes of sudden cardiac death in young athletes. Table 1. Causes of sudden cardiac death in young athletes Most common Hypertrophic cardiomyopathy Idiopathic left ventricular hypertrophy Congenital coronary artery anomalies Less common Ruptured aortic aneurysm Myocarditis Dilated cardiomyopathy Arrhythmogenic right ventricular dysplasia Aortic valve stenosis Tunneled left anterior descending coronary artery Atherosclerotic coronary artery disease Rare Wolff-Parkinson-White syndrome Long QT syndrome Mitral valve prolapse Commotio cordis Drugs Unknown/other ------------------------------------------------------------------------ Hypertrophic cardiomyopathy Hypertrophic cardiomyopathy is the most common cause of sudden cardiac death in young competitive athletes. Maron and associates (2) studied autopsy results of 134 athletes who died of cardiovascular causes and found that hypertrophic cardiomyopathy accounted for 36% of the deaths. This familial autosomal dominant disorder has variable expression. Its prevalence is 1 per 500 in the general US population and higher in blacks (11). Researchers have found more than 100 mutations in genes encoding proteins for the cardiac sarcomere that result in hypertrophic cardiomyopathy (3). Characteristic morphologic features of hypertrophic cardiomyopathy include asymmetric left ventricular hypertrophy (usually involving the ventricular septum), left ventricular wall thickness of 16 mm or more (normal, <12 mm; borderline, 13 to 15 mm), a ratio between the septum and free wall of more than 1.3, and a nondilated left ventricle (12). Thus, the ventricular hypertrophy occurs in the absence of left ventricular cavity dilatation, a feature distinguishing it from the physiologic changes seen in athlete's heart. This pathologic hypertrophy contributes to decreased ventricular compliance and diastolic dysfunction with impaired filling. Results of histologic analysis show a disorganized cellular architecture. Intramural tunneling (myocardial bridging), in which a segment of coronary artery is completely surrounded by myocardium, is present in about one third of cases and has been identified as a risk factor for poor outcome in children with this condition (13). Hypertrophic cardiomyopathy has also been called hypertrophic obstructive cardiomyopathy or idiopathic hypertrophic subaortic stenosis--names which falsely imply that obstruction of the left ventricular outflow tract is an invariable component of the disease. In fact, the nonobstructive form of this disease accounts for about 75% of cases (11). Therefore, previously used criteria, such as obstruction of the left ventricular outflow tract, systolic anterior motion of the mitral valve, and a loud systolic ejection murmur, although suggestive, are no longer required for the diagnosis. Unfortunately, most athletes with hypertrophic cardiomyopathy remain asymptomatic until the time of death and are difficult to identify on the basis of history or physical examination. In one study (2), only 21% of athletes who died from this condition had signs or symptoms of cardiovascular disease before their death. Symptoms may include exertional chest pain, dyspnea, light-headedness, or syncope. Hypertrophic cardiomyopathy should be suspected in any athlete in whom a harsh systolic ejection murmur is heard on examination. This characteristic murmur increases in intensity with any maneuver that decreases venous return, such as a sustained Valsalva's maneuver. Similarly, a systolic ejection murmur that decreases with squatting and increases upon standing is suspicious. Examination may also reveal the presence of a fourth heart sound and a rapid initial upstroke of the carotid pulse. Ultimately, the diagnosis is confirmed by echocardiography. Athletes with a genetic predisposition to hypertrophic cardiomyopathy should undergo serial echocardiography every 12 to 18 months until about age 18, because phenotypic expression may not occur until physical maturation and development are complete (12). Idiopathic left ventricular hypertrophy Idiopathic left ventricular hypertrophy is another cause of sudden cardiac death in young athletes, accounting for 9% to 10% of cases (2,8). It is marked by an unexplained increase in cardiac mass that exceeds the limits of physiologic hypertrophy in athlete's heart. The increase in cardiac mass does not meet criteria for hypertrophic cardiomyopathy because the hypertrophy is symmetric (concentric) and histologic examination does not show the cellular disarray characteristic of hypertrophic cardiomyopathy. Furthermore, no genetic basis of the disease has been established. Controversy exists as to whether idiopathic left ventricular hypertrophy is a separate disease or whether it may be a variant of hypertrophic cardiomyopathy without the latter's characteristic asymmetry or genetic transmission (1). Congenital coronary artery anomalies Congenital anomalies of the coronary arteries account for 17% to 19% of cases of sudden cardiac death (2,8). Origin of the left coronary artery from the right sinus of Valsalva (figure 1: not shown) is the coronary anomaly that most commonly leads to sudden death. Among athletes who died of this disorder, only 31% were found to have symptoms before death (2). Symptoms included exertional syncope or near-fatal arrhythmia, dyspnea, chest pain, pressure, and tightness. Possible mechanisms of ischemia in anomalous origin of the left coronary artery include a slitlike ostium that narrows with aortic dilatation during exercise, an acute-angled takeoff, and impingement of the artery as it passes between the aorta and pulmonary trunk (1,2,4). Anomalous coronary artery origin can be investigated by echocardiography and exercise testing but ultimately may require coronary arteriography for diagnosis. Other coronary anomalies include origin of the right coronary artery from the left sinus of Valsalva or from the pulmonary artery, presence of a single coronary artery, hypoplasia (ie, small size or short course), aneurysm, and acute-angled takeoff of the left main coronary artery (1,2,5). Intramural tunneling of the left anterior descending coronary artery has also been implicated as a cause of sudden death. However, necropsy studies have shown that this condition exists in about 20% of all persons, and its role in sudden cardiac death remains uncertain (1). Aortic rupture Rupture of an aortic aneurysm is a less common cause of sudden cardiac death. Half of these cases occur in athletes with Marfan syndrome (1,2), which is an autosomal dominant, systemic connective tissue disorder with a prevalence in the general US population of 1 per 10,000 (14). A defect in the gene for the structural protein fibrillin leads to intrinsic weakening of the aortic wall, known as cystic medial necrosis. The diagnosis of Marfan syndrome is based on clinical features and confirmed by eye examination and echocardiography. Skeletal features include tall stature with arm span greater than height, arachnodactyly (long fingers and toes), hyperextensible joints, scoliosis, a high arched palate, and anterior chest-wall deformities, such as pectus excavatum. Ophthalmologic examination may show myopia and ocular lens subluxation (ectopia lentis), and echocardiography may reveal a dilated aortic root or mitral valve prolapse. Myocarditis and dilated cardiomyopathy Myocarditis is another infrequent cause of sudden cardiac death in young athletes. This inflammatory condition of the myocardium is most commonly viral. Coxsackievirus B is implicated in more than 50% of cases (4). Other viral origins of myocarditis include echovirus, adenovirus, and influenza. Chlamydia pneumoniae has been noted in several cases in Sweden (15). Characteristic symptoms of myocarditis include a prodromal viral illness followed by progressive exercise intolerance and congestive symptoms of dyspnea, cough, and orthopnea. Sudden cardiac death may occur in the presence of either active or healed myocarditis. Thus, a convalescent period of at least 6 months is recommended before a return to sports (16). Dilated cardiomyopathy may result from viral infections or be secondary to infiltrative diseases (eg, sarcoidosis, amyloidosis, hemochromatosis) or toxins (eg, ethanol). Arrhythmogenic right ventricular dysplasia Arrhythmogenic right ventricular dysplasia involves fatty infiltration and fibrosis of the right ventricle, which predisposes an athlete to exercise-induced ventricular tachyarrhythmias. Although rare in the United States, this disease causes 22% of sudden cardiac deaths in the Veneto region of northern Italy, implying a genetic basis (17). Diagnosis is made by echocardiography or magnetic resonance imaging, which demonstrates fatty infiltration of the myocardium. Aortic valve stenosis Aortic stenosis in young athletes results from congenital abnormalities, such as a bicuspid valve. Diagnosis should be suspected in the presence of a systolic ejection murmur or early systolic click heard on cardiac examination. The murmur of aortic stenosis can be distinguished from the murmur of hypertrophic cardiomyopathy because it will diminish with maneuvers that decrease venous return. These include Valsalva's maneuver or assumption of the standing position (opposite to the findings in hypertrophic cardiomyopathy). Aortic stenosis can be evaluated by Doppler echocardiography, but cardiac catheterization may be required to distinguish moderate from severe disease (16). Cardiac conduction abnormalities Supraventricular tachyarrhythmias are no more frequent in athletes than in the general population (18,19). Wolff-Parkinson-White syndrome, or ventricular preexcitation, is present in 0.15% to 0.20% of persons and predisposes an athlete to sudden cardiac death (8). Athletes may complain of palpitations, light-headedness, or syncope. The electrocardiogram (ECG) may show an initial slurred upstroke (delta wave), short PR interval, and wide QRS complex. Sudden death results from the development of atrial fibrillation with rapid atrioventricular conduction via a bypass tract and subsequent ventricular fibrillation. Long QT syndrome involves prolonged ventricular repolarization and may lead to the development of polymorphic ventricular tachycardia (torsades de pointes). The syndrome can be congenital (Romano-Ward and Jervell and Lange-Nielson syndromes) or may be acquired from administration of certain drugs (eg, group IA antiarrhythmics, tricyclic antidepressants, antifungals, nonsedating antihistamines, antibiotics, promotility agents) or from certain metabolic abnormalities (eg, hypokalemia, hypomagnesemia). Commotio cordis Although sudden cardiac death in young athletes is most often associated with congenital heart disease, the cardiovascular risk to athletes playing either organized or recreational sports includes cardiac arrest resulting from direct, nonpenetrating trauma to the chest wall. This occurrence, known as commotio cordis, results in almost instantaneous cardiac death following blunt chest impact over the heart. Trauma is usually caused by a projectile, such as a baseball or ice hockey puck, or a direct blow from an opposing player. In contrast to other causes of sudden cardiac death, commotio cordis occurs in the absence of underlying cardiovascular disease or structural injury to the heart itself. The timing of chest-wall impact as it relates to the cardiac cycle appears to be critical in producing commotio cordis. The precise mechanism of death is unknown but is believed to involve an exquisitely timed precordial blow that occurs during a period of electrically vulnerable ventricular repolarization and leads to a fatal dysrhythmia (20). Only about 10% of reported victims of commotio cordis are known to survive (21). Recently, an experimental model reproducing commotio cordis in swine found that softer-than-standard baseballs reduced the risk for ventricular fibrillation (22). This finding suggests that modified athletic equipment may prevent some deaths in athletes. Other causes of sudden cardiac death Mitral valve prolapse occurs in 5% to 10% of the general US population (1). Its association with sudden cardiac death has not been clearly established. Physical examination may reveal a midsystolic click and a late systolic murmur. Athletic participation need not be restricted unless mitral valve prolapse is associated with syncope, exertional chest pain, moderate or severe mitral regurgitation, or a family history of sudden cardiac death (16). Illicit drugs that cause coronary vasospasm, such as cocaine, have also been linked to sudden cardiac death (4). Interestingly, atherosclerotic coronary artery disease, the cause of more than 75% of sudden cardiac deaths in athletes over 40 years of age, accounts for only 2% to 3% of sudden deaths in young athletes (2,5). Athlete's heart The heart of an athlete involved in long-term athletic training undergoes normal physiologic and morphologic changes, known as athlete's heart or the athletic heart syndrome (23). These adaptations are considered a normal response to repetitive exercise. Physiologic hypertrophy The myocardial adaptations that occur in athlete's heart depend on the frequency, duration, and intensity of physical conditioning (24). An athlete can place either of two types of load on the heart--volume or pressure--depending on the type of exercise (23). Athletes involved in isotonic (dynamic) exercise, such as running, cycling, or swimming, present a volume load to the heart. Isotonic exercise increases venous return and thus left ventricular end-diastolic diameter, allowing for a larger stroke volume and cardiac output. In response to a chronic volume demand, the left ventricular wall thickens proportionately in order to normalize wall stress. Changes occur according to Laplace's law (wall stress = [pressure X radius]/[wall thickness X 2]) (23), and the myocardium hypertrophies in an eccentric fashion such that the mass-to-volume ratio remains unchanged. Athletes involved in isometric (static) exercise, such as weight lifting or shot-putting, place a pressure load on the heart by brief increases in systemic blood pressure during training. Wall thickness increases in response to a chronic pressure demand in accordance with Laplace's law. Without an increase in left ventricular end-diastolic diameter, the myocardium hypertrophies in a concentric fashion such that the mass-to-volume ratio increases. Because training for most competitive athletes involves a combination of both isotonic and isometric exercise, cardiac adaptations are usually a blend of eccentric and concentric hypertrophy. The result is an overall increase in cardiac mass due to an increase in left ventricular diastolic cavity dimension, wall thickness, or both (12). Physiologic hypertrophy in athlete's heart is always symmetric and reversible with deconditioning (decreasing about one third in 3 weeks) (23). Asymmetry or a failure of myocardial hypertrophy to resolve with the cessation of regular exercise suggests the presence of hypertrophic cardio-myopathy. Pathologic versus physiologic hypertrophy Left ventricular wall thickness in athlete's heart is usually within normal limits or only mildly increased (<12 mm). Some athletes, however, have larger increases, approaching pathologic values (>16 mm) and raising the possibility of hypertrophic cardiomyopathy (12). Wall-thickness values in the range of 13 to 15 mm are described as the morphologic gray zone, and criteria have been outlined to distinguish pathologic from physiologic hypertrophy in these cases (12). An unusual pattern of left ventricular hypertrophy, a left ventricular end-diastolic cavity dimension of less than 45 mm, left atrial enlargement, bizarre ECG patterns, abnormal left ventricular filling, and a positive family history support a diagnosis of hypertrophic cardiomyopathy. In contrast, a left ventricular end-diastolic cavity dimension of more than 55 mm and a decrease in thickness with deconditioning support a diagnosis of athlete's heart. ECG changes Athlete's heart is also associated with many common ECG alterations (table 2). Changes are related to either an increase in resting parasympathetic (vagal) tone or an increase in cardiac mass from physiologic hypertrophy. The most common ECG finding related to increased vagal tone is a resting sinus bradycardia, which is found in the majority of aerobically trained athletes (18,19,23,25). Sinus arrhythmias, first-degree atrioventricular block, Mobitz type I (Wenckebach) second-degree atrioventricular block, and junctional rhythms are also seen more often in athletes than in the general population (23). These changes are readily reversed with exercise as increased sympathetic drive overcomes baseline parasympathetic tone. Increased QRS voltage, related to an increase in cardiac mass, is present in up to 80% of well-conditioned athletes (19,23) and should be considered a normal variant in young normotensive, asymptomatic athletes with normal findings on examination. Table 2. Common electrocardiographic changes in athlete's heart Changes due to increased resting vagal tone* Sinus bradycardia Sinus arrhythmia Wandering atrial pacemaker First-degree atrioventricular block Mobitz type I (Wenckebach) second-degree atrioventricular block Junctional rhythms Changes due to physiologic hypertrophy** Increased P-wave amplitude Increased QRS voltage (LVH*** or RVH+ criteria) Early repolarization (J-point ST-segment elevation)* Tall, peaked T waves T-wave inversion* Prominent U waves Incomplete RBBB (intraventricular conduction delays) Vertical QRS axis ------------------------------------------------------------------------ LVH, left ventricular hypertrophy; RBBB, right bundle branch block; RVH, right ventricular hypertrophy. *Changes normalize with exercise. **Changes regress with cessation of regular exercise. ***LVH criteria = S in V1 + R in V5 >35 mm. +RVH criteria = R in V1 + S in V5 >10.5 mm. Compiled from Zehender et al (19) and Huston et al (23). ------------------------------------------------------------------------ Other common changes secondary to physiologic hypertrophy include voltage criteria suggestive of left or right ventricular hypertrophy; early repolarization with J-point ST-segment elevation and tall, peaked T waves; T-wave inversion; and a vertical QRS axis (19,23). These ECG changes should regress with the cessation of regular exercise as the myocardium returns to its previous, smaller size. A representative ECG tracing of athlete's heart is shown in figure 2 (not shown). Some ECG findings are clearly abnormal and should be further investigated for the presence of organic heart disease. ECG warning signs are listed in table 3. Table 3. Electrocardiographic warning signs for risk of sudden cardiac death in athletes Downsloping ST segment or horizontal depression Left ventricular hypertrophy with downsloping ST segment and T-wave inversion that does not normalize with exercise Persistent second-degree atrioventricular block with exercise Third-degree atrioventricular block Complex ventricular arrhythmias Dramatic increase in QRS voltage* Prominent Q waves* Deep negative T waves* ------------------------------------------------------------------------ *Changes may suggest hypertrophic cardiomyopathy. ------------------------------------------------------------------------ Preparticipation physical evaluation The American Heart Association Science Advisory and Coordinating Committee developed consensus recommendations and preparticipation screening guidelines in 1996 (26). The purpose of screening is to identify preexisting cardiovascular abnormalities that place athletes at increased risk for sudden cardiac death and to provide medical clearance by means of routine and systematic evaluations. The committee recommended that a screening history and physical examination be performed on all athletes before participation in high school and collegiate sports. For high school athletes, the screening should be repeated every 2 years and an interim history should be obtained in the intervening years. For college athletes, a history and blood pressure measurement should be obtained each year after the initial evaluation (27). A standardized questionnaire is helpful in guiding examiners. Parents are the persons who should be responsible for completing the questionnaire for athletes of high school age or younger. The monograph Preparticipation Physical Evaluation (28) provides a useful form that is widely accepted. This monograph was updated in 1996 by the American Academy of Family Physicians, American Academy of Pediatrics, American Medical Society for Sports Medicine, American Orthopaedic Society for Sports Medicine, and American Osteopathic Academy of Sports Medicine. The cardiovascular history should include questions about prior exertional chest pain or discomfort, exertional syncope or light-headedness, dyspnea or fatigue disproportionate to the degree of exertion, and any history of palpitations or irregular heart beats. Previous detection of a heart murmur or elevated blood pressure and the use of cocaine or other drugs should be noted. Questions pertaining to a family history of premature sudden death (before age 50) or cardiovascular disease and the presence of specific conditions, such as hypertrophic cardiomyopathy, Marfan syndrome, or long QT syndrome, should also be investigated. Physical examination should include brachial blood pressure measurement in the sitting position, palpation of the femoral artery pulses to exclude coarctation of the aorta, recognition of the physical stigmata of Marfan syndrome, and precordial auscultation in both supine and standing positions in a quiet environment (26). Detectable heart murmurs should be further elucidated by Valsalva's maneuver or by the athlete moving from a squatting to a standing position to identify changes consistent with hypertrophic cardiomyopathy. The American Heart Association does not recommend noninvasive diagnostic tests such as electrocardiography or echocardiography in the routine screening of asymptomatic athletes for cardiovascular disease (26). Recommendations are based on practicality and cost efficiency, given the large number of competitive athletes in the United States and the relatively low incidence of cardiovascular disease and sudden cardiac death. Because of the low incidence of disease and the relatively high frequency of normal morphologic and ECG alterations occurring in athlete's heart, the specificity of electrocardiography and echocardiography in correctly diagnosing cardiovascular disease is poor. The number of false-positive results, which would very likely exceed the number of true-positive results, would lead to the unnecessary disqualification of athletes (26). Electrocardiography or echocardiography has been used in several studies (29-32) to screen large populations of athletes. Few definitive examples of potentially lethal cardiovascular abnormalities were detected. Two studies (29,30) used screening echocardiograms of 3,262 athletes, and a third study (31) used screening ECGs of 501 collegiate athletes, 90 of whom underwent subsequent echocardiography. No athlete in these studies was thought to be at high risk for sudden cardiac death or was barred from competition. In another study (32), electrocardiography was added to the preparticipation evaluation of 5,615 high school athletes. Echocardiography was performed on 146 athletes thought to have abnormal screening ECGs, and no abnormalities were found. Sixteen (0.3%) of the athletes were not approved for competition because of conduction abnormalities found on ECG, but no results of follow-up studies to determine final eligibility were provided. Screening echocardiography is very costly. For example, taking the prevalence of hypertrophic cardiomyopathy in the general US population as 1 per 500 and the cost of an echocardiogram as $500 per study, it would cost an estimated $250,000 to detect just one previously undiagnosed case of hypertrophic cardiomyopathy (26). Although a properly performed preparticipation evaluation is the best and most practical screening tool, several limitations exist. In a retrospective study of 134 athletes who died suddenly of cardiovascular-related disease (2), only 18% had cardiovascular symptoms in the 36 months preceding death. In this study, 115 athletes had undergone standard preparticipation screening and 15 had undergone individualized medical evaluation for signs or symptoms of disease. Among these, an appropriate diagnosis was made in only eight (6%) prior to death. Despite the American Heart Association recommendations, not all athletes are being properly screened. A 1997 survey of high school athletic associations from the 50 states and the District of Columbia (33) revealed that 8 states did not have approved history and physical questionnaires to guide examiners, 12 states had questionnaires that were judged to be inadequate according to the American Heart Association recommendations, and 1 state had no formal screening requirement. Referral to a specialist is indicated for any cardiovascular abnormality that is identified or suspected on the preparticipation evaluation, any systolic murmur grade 3/6 or higher, any diastolic murmur, or a family history of sudden cardiac death. Further evaluation includes electrocardiography and selective use of echocardiography, exercise testing, and coronary arteriography. Temporary disqualification must be considered until workup is complete. When cardiovascular abnormalities are found, eligibility for competition should be determined in accordance with the joint recommendations of the American College of Cardiology and the American College of Sports Medicine at the 26th Bethesda Conference (16). The objective of this conference was to identify, by way of consensus and review of available studies, the types and degree of severity of cardiovascular abnormalities that place a competitive athlete at increased risk for disease progression or sudden death and, therefore, justify a medical recommendation against participation. The guidelines consider the type and intensity of exercise performed, the risk of bodily injury from collision, and the estimated stress of the sport on the cardiovascular system. A review of the Bethesda recommendations is beyond the scope of this article, but the guidelines should be used by the primary care physician and consulting specialist when determining eligibility for competition in athletes with identified cardiovascular abnormalities. Summary Sudden cardiac death of a young competitive athlete is a rare but tragic event. Hypertrophic cardiomyopathy and coronary artery anomalies are the most frequent causes. Most cardiovascular abnormalities go unrecognized until the time of death owing to the lack of preceding signs or symptoms suggestive of disease. Physicians responsible for the care of athletes should be familiar with the various causes of sudden cardiac death, the physiologic adaptations seen in so-called athlete's heart, and existing cardiovascular screening guidelines. The preparticipation evaluation, although it has limitations, is the major instrument readily available for prevention of sudden cardiac death. Effort should be made to follow established consensus guidelines. References 1. Maron BJ, Epstein SE, Roberts WC. Causes of sudden death in competitive athletes. J Am Coll Cardiol 1986;7(1):204-14 2. Maron BJ, Shirani J, Poliac LC, et al. Sudden death in young competitive athletes: clinical, demographic, and pathological profiles. JAMA 1996;276(3):199-204 3. Maron BJ. Cardiovascular risks to young persons on the athletic field. Ann Intern Med 1998;129(5):379-86 4. Rich BS. 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Holly RG, Shaffrath JD, Amsterdam EA. Electrocardiographic alterations associated with the hearts of athletes. Sports Med 1998;25(3):139-48 26. Maron BJ, Thompson PD, Puffer JC, et al. Cardiovascular preparticipation screening of competitive athletes: a statement for health professionals from the Sudden Death Committee (clinical cardiology) and Congenital Cardiac Defects Committee (cardiovascular disease in the young), American Heart Association. Circulation 1996;94(4):850-6 27. Maron BJ, Thompson PD, Puffer JC, et al. Cardiovascular preparticipation screening of competitive athletes: an addendum to a statement for health professionals from the Sudden Death Committee (Council on Clinical Cardiology) and Congenital Cardiac Defects Committee (Council on Cardiovascular Disease in the Young), American Heart Association. Circulation 1998;97(22):2294 28. American Academy of Family Physicians, American Academy of Pediatrics, American Medical Society for Sports Medicine, American Orthopaedic Society for Sports Medicine, American Osteopathic Academy of Sports Medicine. Preparticipation physical evaluation. 2d ed. New York: McGraw-Hill, 1996 29. Lewis JF, Maron BJ, Diggs JA, et al. Preparticipation echocardiographic screening for cardiovascular disease in a large, predominantly black population of collegiate athletes. Am J Cardiol 1989;64(16):1029-33 30. Weidenbener EJ, Krauss MD, Waller BF, et al. Incorporation of screening echocardiography in the preparticipation exam. Clin J Sport Med 1995;5(2):86-9 31. Maron BJ, Bodison SA, Wesley YE, et al. Results of screening a large group of intercollegiate competitive athletes for cardiovascular disease. J Am Coll Cardiol 1987;10(6):1214-21 32. Fuller CM, McNulty CM, Spring DA, et al. Prospective screening of 5,615 high school athletes for risk of sudden cardiac death. Med Sci Sports Exerc 1997;29(9):1131-8 33. Glover DW, Maron BJ. Profile of preparticipation cardiovascular screening for high school athletes. JAMA 1998;279(22):1817-9 Dr Drezner completed a sports medicine fellowship and is now clinical instructor in the department of family medicine, University of Washington School of Medicine, Seattle. Correspondence: Jonathan A. Drezner, MD, Family Medical Center, University of Washington, Box 354775, 4245 Roosevelt Way NE, Seattle, WA 98105. E-mail: jdrezner@u.washington.edu. 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