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CLINICAL STUDY: HYPERTROPHIC CARDIOMYOPATHY

Relationship of race to sudden cardiac death in competitive athletes with hypertrophic cardiomyopathy

Barry J. Maron, MD, FACC^*,*, Kevin P. Carney, BS^*, Harry M. Lever, MD, FACC, Jannet F. Lewis, MD, FACC, Ivan Barac, MD, Susan A. Casey, RN^* and Mark V. Sherrid, MD, FACC

^* Minneapolis Heart Institute Foundation, Minneapolis, Minnesota, USA
Cleveland Clinic Foundation, Cleveland, Ohio, USA
University of Florida Health Sciences Center, Gainesville, Florida, USA
St. Luke’s-Roosevelt Hospital Center, New York, New York, USA

Manuscript received December 27, 2001; revised manuscript received September 24, 2002, accepted October 25, 2002.

^* Reprint requests and correspondence: Dr. Barry J. Maron, Minneapolis Heart Institute Foundation, 920 East 28th Street, Suite 60, Minneapolis, Minnesota 55407, USA.
hcm.maron{at}mhif.org

	Abstract

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OBJECTIVES: The goal of this study was to determine the impact of race on identification of hypertrophic cardiomyopathy (HCM).

BACKGROUND: Sudden death in young competitive athletes is due to a variety of cardiovascular diseases (CVDs) and, most commonly, HCM. These catastrophes have become an important issue for African Americans, although HCM has been previously regarded as rare in this segment of the U.S. population.

METHODS: We studied the relationship of race to the prevalence of CVDs causing sudden death in our national athlete registry, and compared these findings with a representative multicenter hospital-based cohort of patients with HCM.

RESULTS: Of 584 athlete deaths, 286 were documented to be due to CVD at ages 17 ± 3 years; 156 (55%) were white, and 120 (42%) were African American. Most were male (90%), and 67% participated in basketball and football. Among the 286 cardiovascular deaths, most were due to HCM (n = 102; 36%) or anomalous coronary artery of wrong sinus origin (n = 37; 13%). Of the athletes who died of HCM, 42 (41%) were white, but 56 (55%) were African American. In contrast, of 1,986 clinically identified HCM patients, only 158 (8%) were African American (p < 0.001).

CONCLUSIONS: In this autopsy series, HCM represented a common cause of sudden death in young and previously undiagnosed African American male athletes, in sharp contrast with the infrequent clinical identification of HCM in a hospital-based population (i.e., by seven-fold). This discrepancy suggests that many HCM cases go unrecognized in the African American community, underscoring the need for enhanced clinical recognition of HCM to create the opportunity for preventive measures to be employed in high-risk patients with this complex disease.

Abbreviations and Acronyms   ARVC   arrhythmogenic right ventricular cardiomyopathy   CVD   cardiovascular disease   HCM   hypertrophic cardiomyopathy   LV   left ventricle/ventricular

	Methods

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Selection of subjects.   The Minneapolis Heart Institute Foundation registry was established in 1992 to systematically assemble, prospectively and retrospectively (from 1985), cases of young athletes who died suddenly. These cases were primarily identified from news media accounts, but also from a variety of other sources including informal communications and reports from high schools and colleges (5). A total of 584 young athletes who died suddenly were consecutively enrolled in the registry to April 2000. Subjects were initially considered for inclusion if they were: 1) truly a competitive athlete, that is, a participant in an organized team or individual sport requiring regular training and competition while placing a high premium on excellence and achievement (10), and 2) <35 years old while actively engaged in competitive sports. The number of cases reported to the registry have increased with time: 117 (20%) before 1990; 105 (18%) from 1990 to 1994; and 362 (62%) from 1995 to 1999. The largest number of reported cases in a single year occurred in 1996 (n = 70). Forty-two states were represented, most commonly: California (n = 31 cases), Florida (n = 17 cases), Michigan and New York (n = 16 each cases), Ohio (n = 15 cases), and Texas (n = 13 cases).

Of these 584 subjects, 298 were ultimately excluded from the present study based on: 1) identification of primary noncardiovascular causes of death (e.g., drug abuse, complications of asthma, heat stroke, drowning, head trauma, or ruptured cerebral artery); 2) sudden death due to a blunt chest blow in the absence of structural cardiac disease (commotio cordis) (7); 3) incomplete postmortem or toxicology examination, or one insufficient to establish the probable cause of death based on the available clinical and autopsy data; and 4) inability to track and obtain the necessary diagnostic data due to confidentiality considerations restricting access to autopsy information. The remaining 286 athletes constitute the principal study group. Selected data from 134 athletes are included in a prior report (5).

Data assembly.   Upon initial identification, a systematic tracking process was established to assemble information on each case, including the autopsy report (with complete gross anatomic, histologic, and toxicologic data), as well as pertinent clinical information. In selected instances, primary pathologic materials were requested and analyzed, and, when necessary, the findings were verified by direct communication with medical examiners. Clinical information (e.g., circumstances of collapse and preparticipation screening) was derived from written accounts and from telephone interviews with family members, witnesses, or coaches. The final diagnoses were based almost solely on the autopsy findings in the vast majority of athletes. However, 46 (16%) had cardiovascular evaluations during life, and, when appropriate, those data were considered in formulating the diagnosis and cause of death.

Diagnosis of hypertrophic cardiomyopathy (HCM).   Our primary diagnostic criterion for probable or definite evidence of HCM was a hypertrophied nondilated left ventricle (LV) in the absence of another cardiac or systemic disease capable of producing the degree of hypertrophy present (11–13). Required criteria were, as previously described (5), heart weight of 500 g and 1 supporting clinical or morphologic feature in any of the following categories: 1) family history of HCM with or without premature sudden death; 2) asymmetric pattern of LV hypertrophy such as prominent bulging of the ventricular septum into the outflow tract, or marked wall thickening (ventricular septum 20 mm), and/or enlarged left atrium with small ventricular chambers, fibrous outflow tract contact plaque (on the septum), or markedly elongated mitral valve leaflets; 3) histologic abnormalities of LV, including marked disorganization of cardiac muscle cells (14), abnormal intramural coronary arteries (15,16), and/or replacement scarring (15,16). Alternatively, hearts with weight <500 g but with maximal LV wall thickness 20 mm were also regarded as diagnostic of HCM.

Hearts that showed a modest, but otherwise unexplained, increase in cardiac mass (heart weight 400 g in males and 350 g in females but <500 g) and mild LV wall thickening (15 to 19 mm), but with one or no other supporting diagnostic feature of HCM, were judged as suggestive of HCM, although insufficient to warrant a definitive diagnosis (5).

Clinical HCM cohort.   For comparative purposes, a multicenter population of 1,986 patients with HCM who were diagnosed clinically (12) was assembled from the outpatient records of the University of Florida Health Sciences Center (Gainesville) (n = 75), St. Luke’s-Roosevelt Hospital Center (New York) (n = 107), Cleveland Clinic Foundation (n = 1,314), and Minneapolis Heart Institute (n = 490) specifically to ascertain the distribution of HCM patients with respect to race. Data from these four centers included all HCM patients referred to that institution, both locally and from other regions.

These institutions were selected because of their recognition as HCM centers, as well as location in large metropolitan areas and/or regions generally accessible to large numbers of African American patients. Therefore, the cohort included a prominent component of largely unselected patients, as well as patients who were part of tertiary center referral patterns.

Ages at initial institutional evaluation were 56 ± 19 years; 1,060 of 1,986 (53%) were male. Maximal LV wall thicknesses obtained with two-dimensional echocardiography were 20 ± 5 mm (range, to 55 mm). Outflow obstruction under basal conditions (Doppler-estimated gradient 30 mm Hg) was present in 693 of 1,986 (35%).

Statistical methods.   Data are expressed as mean ± SD. Proportions were compared with the chi-square test, where appropriate.

	Results

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Demographic profile of athletes.   In the 286 athletes who died of CVD, ages were 9 to 40 years (mean, 17 ± 3); 256 (90%) were male. Distribution according to race was: white (n = 156; 55%); African American (blacks of African descent) (n = 120; 42%); and other races (n = 10; 3%), including Asian (n = 5; 2%); Hispanic (n = 4; 1%); and Native American (n = 1; 0.3%). Most athletes were competing in organized high school (n = 188; 66%) or college sports (n = 53; 19%), and 12 (4%) were professional athletes. The remaining 33 athletes (12%) were 14 years and engaged in organized youth or junior high school sports. Nineteen athletes (7%) were regarded as elite, having achieved national or international levels of competition.

A variety of 18 competitive sports were represented, most commonly basketball and football (combined: 192, 67%); only in basketball were African American athletes more common than whites (i.e., 63:35). Of the 286 athletes who died suddenly of heart disease, 204 (71%) collapsed during or immediately after a training session (n = 129) or a formal athletic contest (n = 75). The remaining 82 athletes (29%) died either during mild recreational physical activities (n = 46), or while sedentary (n = 36; including 11 during sleep). Only 55 athletes (19%) were known to have experienced symptoms that could have been cardiovascular in origin (e.g., chest pain, exertional dyspnea, syncope, or recurring dizziness).

Of the 286 athletes, information regarding preparticipation medical evaluations were available in 252. Customary personal and family history and physical examination, or other clinical evaluations, were performed as part of medical clearance for high school or college sports in 247 of the 252 athletes (98%). Preparticipation examinations were documented in 98.6% of whites and 97.3% of African Americans (p = NS).

Cardiovascular causes of sudden death in athletes.   A variety of CVDs were identified as the cause of sudden death in the 286 athletes (Table 1). In three of these, standard autopsy examination did not identify a cause of death, but a clinical evaluation had previously documented or strongly suggested long QT syndrome (17). Three other athletes with Marfan’s syndrome did not have autopsies, but the clinical circumstances of their death was judged most consistent with aortic dissection and rupture (18).

The second most frequent cardiovascular cause of sudden death was coronary artery anomalies of wrong sinus origin (22,23) that were present in 37 athletes (13%); these were left main coronary artery originating from the right (anterior) sinus of Valsalva (n = 32) and right coronary artery from the left sinus of Valsalva (n = 5) (Table 1). The remaining 118 athletes died suddenly of a variety of cardiac diseases or malformations, each of which comprised 7% of the overall study group. These included most commonly, myocarditis (n = 20), ruptured dissecting ascending aortic aneurysm with or without evidence of Marfan’s syndrome (n = 12), and arrhythmogenic right ventricular cardiomyopathy (ARVC) (n = 11) (Table 1) (24).

Relation of race to HCM and other CVDs.   Athletes with sudden death
Of the 102 competitive athletes who died suddenly of HCM, most (56; 55%) were African American and 42 (41%) were white (p = 0.002); the remaining 4 (4%) were of other races (Table 1, Fig. 1). African American and white athletes with HCM did not differ significantly with respect to age (17.1 ± 2 years vs. 16.7 ± 2 years), gender (98% vs. 95% male), maximum LV wall thickness (23.0 ± 5 mm vs. 22.2 ± 5 mm), nor competitive sport at the time of death (most commonly basketball; 57% vs. 33%; p = NS). Arrhythmogenic right ventricular cardiomyopathy and aortic valve stenosis were both significantly more common in white than African American athletes (Table 1, Fig. 2). Of 102 athletes who died of HCM, the correct diagnosis was ultimately made during life in only 3 (3%), of whom 2 were white and 1 was African American.

View larger version (37K): [in this window] [in a new window]   Figure 1 Distribution according to race shown separately for the overall autopsy-based study population of 286 trained competitive athletes who died suddenly from a variety of cardiovascular diseases (left), for those 102 athletes studied at autopsy who died of hypertrophic cardiomyopathy (HCM) (center), and a clinically identified, multicenter hospital-based cohort of 1,986 patients with HCM (right). SCD = sudden cardiac death.

View larger version (47K): [in this window] [in a new window]   Figure 2 Impact of race on cardiovascular causes of sudden death in the population of 286 competitive athletes, with data shown for those seven structural heart diseases represented by at least 10 deaths. Ao = aortic; ARVC = arrhythmogenic right ventricular cardiomyopathy; CAD = atherosclerotic coronary artery disease; HCM = hypertrophic cardiomyopathy.

Therefore, the prevalence of African Americans among athletes who died suddenly of HCM (56 of 102; 55%) was significantly greater than the representation of African Americans in the cohort of HCM patients clinically diagnosed within outpatient and inpatient hospital settings (158 of 1,986; 8%; p < 0.001). Also, clinically identified African American patients with HCM were older (59.5 ± 16 years) and more commonly women (64%), and less frequently had outflow obstruction (25%), compared with the HCM patients of other races (54.0 ± 19 years, 45% and 36%, respectively; p < 0.001, 0.001, and 0.01. African Americans and those of other races with HCM did not differ with respect to maximum LV wall thickness (20.5 ± 5 mm vs. 20.8 ± 6 mm, respectively).

	Discussion

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Demographics and causes of athletic field deaths.   Sudden death on the athletic field in young participants has been of considerable interest in the lay and medical communities (1–7,10,25). Indeed, in studies from the U.S. (including the present one), a variety of predominantly congenital CVDs have been documented to be responsible for most of these deaths, with HCM the most common condition occurring in about one-third of cases (1,3–5,25).

Our large prospective registry of sudden deaths in young athletes proved instructive with regard to the epidemiology of these catastrophic events and particularly the significance of race in HCM. We found that the majority of athletes who died of HCM were African Americans (i.e., 55%). While characterization of the racial composition of the entire athlete population in the U.S. is well beyond the scope of the present study, this predominance of African Americans with HCM cannot be solely attributable to relative rates of sports participation among the races. Indeed, there are about 8 million high school and college athletes (of both genders) in the U.S. each year, and the overall U.S. population includes 2.7 million male and 2.7 million female African Americans between the ages of 15 and 24 years. Therefore, for African Americans to comprise 55% of high school and college athletes, fully 80% of all African Americans in the U.S. age 15 to 24 years would have to be members of organized athletic programs. Obviously, because this cannot be the case, it is most reasonable to assume that participants in organized sports nationally are not predominantly black, and that African Americans probably have a representation in the overall athlete population similar to that in the general U.S. population (i.e., about 15%) (26).

HCM in African Americans.   Historically, HCM has been regarded as a condition that uncommonly affects and rarely is diagnosed in black patients. The published medical literature reflects this view in that HCM patients reported by race are very uncommonly identified as black (27). This may be explained, in part, by the fact that the tertiary center referral institutions that have traditionally assessed the largest numbers of HCM patients (in the U.S., Canada, and Europe), and contributed substantially to the literature, have generally evaluated relatively few black patients with CVD (12,28,29).

Indeed, the observation that clinically diagnosed HCM patients are uncommonly African American is supported by the large multicenter HCM population assembled for the present analysis in which only 8% of about 2,000 patients with this disease were reported as African American (range, 2% to 15% for each of the four institutions). Therefore, HCM was seven times more common in African Americans when the disease was identified for the first time at autopsy after a sudden death on the athletic field than when recognized within a clinically diagnosed patient cohort. This suggests that many HCM cases in African Americans go undetected in the community. Furthermore, African Americans appear to comprise a smaller proportion of our multicenter clinical HCM population (i.e., 8%) than would be expected from their representation in the general U.S. population (i.e., 16%) (26).

This finding of a large disparity in the clinical identification of HCM between African Americans and whites is provocative and can possibly be explained in a number of ways. First, in general terms, there is a disproportionate access to subspecialty medical care between the black and white communities, specifically with regard to referral for specialized cardiovascular procedures (30–36). This perception suggests that underdiagnoses of HCM in young African Americans may be attributable, in large measure, to socioeconomic factors that potentially limit access to medical specialty referral (and echocardiography), which is usually a prerequisite for the clinical diagnosis of HCM. Consequently, it may be much less likely for young black males (compared with their white counterparts) to be identified with HCM, particularly if asymptomatic. Of note, our clinically identified African American patients with HCM were not predominantly male (as is consistently the case in white patients with this disease) (12,13,19,28), but, rather unexpectedly, were more commonly female (i.e., 64%). Finally, the well-recognized difficulties in diagnosing HCM in generally healthy asymptomatic populations (1,25) are likely to be accentuated in African Americans for whom HCM-related LV hypertrophy may be ascribed erroneously to mild degrees of systemic hypertension (37).

Preparticipation screening.   Our findings may also be relevant to the issues surrounding preparticipation screening for competitive athletes in the U.S. (25). We found no obvious differences in the frequency with which standard screening and cardiovascular evaluations were carried out between African American and white athlete populations. The failure to identify during life a substantial number of athletes (either black or white) who died suddenly with HCM raises the question of the efficacy attributable to customary screening as it is generally practiced in the U.S. with only a history and physical examination (38,39). Certainly, the rigor of preparticipation screening has been of concern for both high school (38) and college-age (39) competitive athlete populations, as well as the implicit limitations of the history and physical examination in identifying or raising the suspicion of HCM (and other CVDs). Of note, in Italy, preparticipation screening employs an obligatory 12-lead electrocardiogram (40), which has been shown to increase the likelihood that HCM will be diagnosed before competitive athletics are undertaken (41).

Significance of the findings.   Alternatively, it is possible that HCM in African Americans may represent a more virulent form of the disease, possibly due to a malignant genetic substrate when associated with exercise (42,43), and, thereby, predisposing to sudden death on the athletic field in susceptible individuals. However, regardless of these considerations, it is our aspiration that the present report will trigger greater awareness that HCM not uncommonly occurs and is an important cause of sudden death in young African American males, thereby creating a higher index of suspicion and ultimately more frequent clinical HCM diagnoses in such athletes. Indeed, the failure to identify HCM in young African American athletes has important and potentially life-threatening consequences. Specifically, there is the possibility that such individuals will not be afforded important options, that is, disqualification from intense competitive sports (in accord with recommendations of Bethesda Conference #26) (10,44) to reduce sudden death risk during physical activity, nor employment of potentially life-saving prophylactic interventions such as the implantable cardioverter-defibrillator in high-risk HCM patients (45).

Study limitations.   The present study is a retrospective autopsy-based analysis, comprised largely of athletes without cardiovascular evaluation or diagnosis during life, for whom we had no access to family screening or laboratory-based genetic analysis (12,42,43). These patient selection factors make any comparisons of clinical expression and outcome, between our autopsy series of competitive athletes and the hospital-based patient cohort, exceedingly difficult. Therefore, in this study, our multicenter cohort of clinically identified HCM patients was reserved solely for comparisons of prevalence.

The assembly of this large series of athletic field deaths required substantial reliance on news media accounts for the identification of cases. We recognize that this process could have created certain selection biases relevant to our autopsy-based series. For example, the sudden deaths of non-elite athletes are probably less likely to achieve media visibility, thereby underestimating the frequency with which sudden deaths occur. Due to these selection factors, as well as the absence of a systematic national reporting registry for such deaths, precise estimates of the prevalence of athletic field catastrophes in young athletes of all races are beyond the scope of the present study.

	References

Top Abstract Methods Results Discussion References

 
1. Maron BJ. Cardiovascular risks to young persons on the athletic field. Ann Intern Med. 1998;129:379–386[Abstract/Free Full Text]

2. Maron BJ. Sudden death in young athletes: lessons from the Hank Gathers affair. N Engl J Med. 1993;329:55–57[Free Full Text]

3. van Camp SP, Bloor CM, Mueller FO, Cantu RC, Olson HG. Nontraumatic sports death in high school and college athletes. Med Sci Sports Exerc. 1995;27:641–647[Medline]

4. Burke AP, Farb V, Virmani R, Goodin J, Smialek JE. Sports-related and non-sports-related sudden cardiac death in young adults. Am Heart J. 1991;121:568–575[CrossRef][Medline]

5. Maron BJ, Shirani J, Poliac LC, Mathenge R, Roberts WC, Mueller FO. Sudden death in young competitive athletes: clinical, demographic and pathological profiles. JAMA. 1996;276:199–204[Abstract/Free Full Text]

6. Corrado D, Thiene G, Nava A, Rossi L, Pennelli N. Sudden death in young competitive athletes: clinicopathologic correlations in 22 cases. Am J Med. 1990;89:588–596[CrossRef][Medline]

7. Maron BJ, Poliac L, Kaplan JA, Mueller FO. Blunt impact to the chest leading to sudden death from cardiac arrest during sports activities. N Engl J Med. 1995;333:337–342[Abstract/Free Full Text]

8. Becker LB, Han BH, Meyer PM, et al. Racial differences in the incidence of cardiac arrest and subsequent survival: the CPR Chicago project. N Engl J Med. 1993;329:600–606[Abstract/Free Full Text]

9. Cowie MR, Fahrenbruch CE, Cobb LA, Hallstrom AP. Out-of-hospital cardiac arrest: racial differences in outcome in Seattle. Am J Public Health. 1993;83:955–959[Abstract/Free Full Text]

10. Maron BJ, Mitchell JH. 26th Bethesda conference: recommendations for determining eligibility for competition in athletes with cardiovascular abnormalities. J Am Coll Cardiol. 1994;24:845–899[Medline]

11. Roberts CS, Roberts WC. Morphologic features. In: Zipes DP, Rowlands DJ, editors. Progress in Cardiology. Philadelphia, PA: Lea and Febiger, 1989:2-2;3–22

12. Maron BJ. Hypertrophic cardiomyopathy: a systematic review. JAMA. 2002;287:1308–1320[Abstract/Free Full Text]

13. Klues HG, Schiffers A, Maron BJ. Phenotypic spectrum and patterns of left ventricular hypertrophy in hypertrophic cardiomyopathy: morphologic observations and significance as assessed by two-dimensional echocardiography in 600 patients. J Am Coll Cardiol. 1995;26:1699–1708[Abstract]

14. Maron BJ, Roberts WC. Quantitative analysis of cardiac muscle cell disorganization in the ventricular septum of patients with hypertrophic cardiomyopathy. Circulation. 1979;59:689–706[Free Full Text]

15. Tanaka M, Fujiwara H, Onodera T, et al. Quantitative analysis of myocardial fibrosis in normals, hypertensive hearts, and hypertrophic cardiomyopathy. Br Heart J. 1986;55:575–581[Abstract/Free Full Text]

16. Maron BJ, Wolfson JK, Epstein SE, Roberts WC. Intramural ("small vessel") coronary artery disease in hypertrophic cardiomyopathy. J Am Coll Cardiol. 1986;8:545–557[Abstract]

17. Vincent CM, Timothy KW, Leppert M, et al. The spectrum of symptoms and QT intervals in carriers of the gene for the long-QT syndrome. N Engl J Med. 1992;327:846–852[Abstract]

18. Marsalese DL, Moodie DS, Vacante M, et al. Marfan’s syndrome: natural history and long-term follow-up of cardiovascular involvement. J Am Coll Cardiol. 1989;14:422–428[Abstract]

19. Wigle ED, Sasson Z, Henderson MA, et al. Hypertrophic cardiomyopathy: the importance of the site and extent of hypertrophy—a review. Prog Cardiovasc Dis. 1985;28:1–83[CrossRef][Medline]

20. Yetman AT, McCrindle BW, MacDonald LC, et al. Myocardial bridging in children with hypertrophic cardiomyopathy—a risk factor for sudden death. N Engl J Med. 1998;339:1201–1209[Abstract/Free Full Text]

21. Roberts WC, Glick BN. Congenital hypoplasia of both right and left circumflex coronary arteries. Am J Cardiol. 1992;70:121–123[CrossRef][Medline]

22. Cheitlin MD, De Castro CM, McAllister HA. Sudden death as a complication of anomalous left coronary origin from the anterior sinus of Valsalva. Circulation. 1974;50:780–787[Abstract/Free Full Text]

23. Basso C, Maron BJ, Corrado D, Thiene G. Clinical profile of congenital coronary artery anomalies with origin from the wrong aortic sinus leading to sudden death in young competitive athletes. J Am Coll Cardiol. 2000;35:1493–1501[Abstract/Free Full Text]

24. Thiene G, Nava A, Corrado D, et al. Right ventricular cardiomyopathy and sudden death in young people. N Engl J Med. 1988;318:129–133[Abstract]

25. Maron BJ, Thompson PD, Puffer JC, et al. Cardiovascular preparticipation screening of competitive athletes. Circulation. 1996;94:850–856[Free Full Text]

26. U.S. Census 2000; U.S. Census Bureau Home Page, Department of Commerce, Population Division, RACE DATA

27. Lewis BS, Agathangelou NE, Flax H, Taams MA, Barlow BJ. Hypertrophic cardiomyopathy in South African blacks. S Afr Med J. 1983;63:266–269[Medline]

28. Elliott PM, Poloniecki J, Dickie S, et al. Sudden death in hypertrophic cardiomyopathy: identification of high risk patients. J Am Coll Cardiol. 2000;36:2212–2218[Abstract/Free Full Text]

29. Maron BJ, Spirito P. Impact of patient selection bias on the perception of hypertrophic cardiomyopathy and its natural history. Am J Cardiol. 1993;72:970–972[CrossRef][Medline]

30. Peterson ED, Wright SM, Daley J, Thibaul GE. Racial variation in cardiac procedure use and survival following acute myocardial infarction in the Department of Veterans Affairs. JAMA. 1994;271:1175–1180[Abstract/Free Full Text]

31. Schulman KA, Berlin JA, Harless W, et al. The effect of race and sex on physicians’ recommendations for cardiac catheterization. N Engl J Med. 1999;340:618–626[Abstract/Free Full Text]

32. Okelo S, Taylor AL, Wright JT Jr., Gordon N, Mohan G, Lesnefsky E. Race and the decision to refer for coronary revascularization: the effect of physician awareness of patient ethnicity. J Am Coll Cardiol. 2001;38:698–704[Abstract/Free Full Text]

33. Goldberg KC, Hatz AJ, Jacobsen SJ, Krakauer H, Rimm AA. Racial and community factors influencing coronary artery bypass graft surgery rates for all 1986 Medicare patients. JAMA. 1992;267:1473–1477[Abstract/Free Full Text]

34. Whittle J, Conigliaro J, Good CB, Lofgren RP. Racial differences in the use of invasive cardiovascular procedures in the Department of Veterans Administration medical system. N Engl J Med. 1993;329:621–627[Abstract/Free Full Text]

35. Wenneker MB, Epstein AM. Racial inequalities in the use of procedures for patients with ischemic heart disease in Massachusetts. JAMA. 1989;261:253–257[Abstract/Free Full Text]

36. Burke AP, Farb A, Pestaner J, et al. Traditional risk factors and the incidence of sudden coronary death with and without coronary thrombosis in blacks. Circulation. 2002;105:419–424[Abstract/Free Full Text]

37. Lewis JF, Maron BJ. Diversity of patterns of hypertrophy in patients with systemic hypertension and marked left ventricular wall thickening. Am J Cardiol. 1990;65:874–881[CrossRef][Medline]

38. Glover DW, Maron BJ. Profile of preparticipation cardiovascular screening for high school athletes. JAMA. 1998;279:1817–1819[Abstract/Free Full Text]

39. Pfister GC, Puffer JC, Maron BJ. Preparticipation cardiovascular screening for US collegiate student-athletes. JAMA. 2000;283:1597–1599[Abstract/Free Full Text]

40. Pelliccia A, Maron BJ. Preparticipation cardiovascular evaluation of the competitive athlete: perspectives from the 30-year Italian experience. Am J Cardiol. 1995;75:827–828[CrossRef][Medline]

41. Corrado D, Basso C, Schiavon M, et al. Screening for hypertrophic cardiomyopathy in young athletes. N Engl J Med. 1998;339:364–369[Abstract/Free Full Text]

42. Schwartz K, Carrier L, Guicheney P, et al. Molecular basis of familial cardiomyopathies. Circulation. 1995;91:532–540[Free Full Text]

43. Maron BJ, Moller JH, Seidman CE, et al. Impact of laboratory molecular diagnosis on contemporary diagnostic criteria for genetically transmitted cardiovascular diseases: hypertrophic cardiomyopathy, long-QT syndrome, and Marfan syndrome. Circulation. 1998;98:1460–1471[Free Full Text]

44. Maron BJ, Isner JM, McKenna WJ. 26th Bethesda conference: recommendations for determining eligibility for competition in athletes with cardiovascular abnormalities. Task Force 3: hypertrophic cardiomyopathy, myocarditis and other myopericardial diseases and mitral valve prolapse. J Am Coll Cardiol. 1994;24:880–885[Medline]

45. Maron BJ, Shen W-K, Link MS, et al. Efficacy of implantable cardioverter-defibrillators for the prevention of sudden death in patients with hypertrophic cardiomyopathy. N Engl J Med. 2000;342:365–373[Abstract/Free Full Text]

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				S. Nazarian and J. A.C. Lima Cardiovascular Magnetic Resonance for Risk Stratification of Arrhythmia in Hypertrophic Cardiomyopathy J. Am. Coll. Cardiol., April 8, 2008; 51(14): 1375 - 1376. [Full Text] [PDF]

				B. R. Chaitman An Electrocardiogram Should Not Be Included in Routine Preparticipation Screening of Young Athletes Circulation, November 27, 2007; 116(22): 2610 - 2615. [Full Text] [PDF]

				B. J. Maron, P. D. Thompson, M. J. Ackerman, G. Balady, S. Berger, D. Cohen, R. Dimeff, P. S. Douglas, D. W. Glover, A. M. Hutter Jr, et al. Recommendations and Considerations Related to Preparticipation Screening for Cardiovascular Abnormalities in Competitive Athletes: 2007 Update: A Scientific Statement From the American Heart Association Council on Nutrition, Physical Activity, and Metabolism: Endorsed by the American College of Cardiology Foundation Circulation, March 27, 2007; 115(12): 1643 - 1655. [Full Text] [PDF]

				B. J. Maron and A. Pelliccia The Heart of Trained Athletes: Cardiac Remodeling and the Risks of Sports, Including Sudden Death Circulation, October 10, 2006; 114(15): 1633 - 1644. [Full Text] [PDF]

				K. M. Harris, A. Sponsel, A. M. Hutter Jr., and B. J. Maron Brief communication: Cardiovascular screening practices of major North American professional sports teams. Ann Intern Med, October 3, 2006; 145(7): 507 - 511. [Abstract] [Full Text] [PDF]

				Developed in Collaboration With the European Heart, D. P. Zipes, A. J. Camm, M. Borggrefe, A. E. Buxton, B. Chaitman, M. Fromer, G. Gregoratos, G. Klein, A. J. Moss, et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) J. Am. Coll. Cardiol., September 5, 2006; 48(5): e247 - e346. [Full Text] [PDF]

				N. M. Panhuyzen-Goedkoop and F. W.A. Verheugt Sudden cardiac death due to hypertrophic cardiomyopathy can be reduced by pre-participation cardiovascular screening in young athletes Eur. Heart J., September 2, 2006; 27(18): 2152 - 2153. [Full Text] [PDF]

				Writing Committee Members, D. P. Zipes, A. J. Camm, M. Borggrefe, A. E. Buxton, B. Chaitman, M. Fromer, G. Gregoratos, G. Klein, A. J. Moss, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society Europace, September 1, 2006; 8(9): 746 - 837. [Full Text] [PDF]

				T. E. Paterick, T. J. Paterick, G. F. Fletcher, and B. J. Maron Medical and Legal Issues in the Cardiovascular Evaluation of Competitive Athletes JAMA, December 21, 2005; 294(23): 3011 - 3018. [Abstract] [Full Text] [PDF]

				B J Maron Distinguishing hypertrophic cardiomyopathy from athlete's heart: a clinical problem of increasing magnitude and significance Heart, November 1, 2005; 91(11): 1380 - 1382. [Abstract] [Full Text] [PDF]

				W. D. Binder, M. A. Fifer, M. E. King, and J. R. Stone Case 26-2005 - A 48-Year-Old Man with Sudden Loss of Consciousness while Jogging N. Engl. J. Med., August 25, 2005; 353(8): 824 - 832. [Full Text] [PDF]

				B. J. Maron and D. P. Zipes Introduction: Eligibility recommendations for competitive athletes with cardiovascular abnormalities--general considerations J. Am. Coll. Cardiol., April 19, 2005; 45(8): 1318 - 1321. [Full Text] [PDF]

				S. L. Van Driest, M. A. Jaeger, S. R. Ommen, M. L. Will, B. J. Gersh, A. J. Tajik, and M. J. Ackerman Comprehensive analysis of the beta-myosin heavy chain gene in 389 unrelated patients with hypertrophic cardiomyopathy J. Am. Coll. Cardiol., August 4, 2004; 44(3): 602 - 610. [Abstract] [Full Text] [PDF]

				B. J. Maron, B. R. Chaitman, M. J. Ackerman, A. Bayes de Luna, D. Corrado, J. E. Crosson, B. J. Deal, D. J. Driscoll, N.A. M. Estes III, C. G. S. Araujo, et al. Recommendations for Physical Activity and Recreational Sports Participation for Young Patients With Genetic Cardiovascular Diseases Circulation, June 8, 2004; 109(22): 2807 - 2816. [Abstract] [Full Text] [PDF]

				R. G. Williams and A. Y. Chen Identifying athletes at risk for sudden death J. Am. Coll. Cardiol., December 3, 2003; 42(11): 1964 - 1966. [Full Text] [PDF]

				B. J. Maron, W. J. McKenna, G. K. Danielson, L. J. Kappenberger, H. J. Kuhn, C. E. Seidman, P. M. Shah, W. H. Spencer III, P. Spirito, F. J. Ten Cate, et al. American College of Cardiology/European Society of Cardiology Clinical Expert Consensus Document on Hypertrophic Cardiomyopathy: a report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines J. Am. Coll. Cardiol., November 5, 2003; 42(9): 1687 - 1713. [Full Text] [PDF]

				Writing Committee Members, B. J. Maron, W. J. McKenna, G. K. Danielson, L. J. Kappenberger, H. J. Kuhn, C. E. Seidman, P. M. Shah, W. H. Spencer III, P. Spirito, et al. American College of Cardiology/European Society of Cardiology Clinical Expert Consensus Document on Hypertrophic Cardiomyopathy: A report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines Eur. Heart J., November 1, 2003; 24(21): 1965 - 1991. [Full Text] [PDF]

				B. J. Maron Sudden Death in Young Athletes N. Engl. J. Med., September 11, 2003; 349(11): 1064 - 1075. [Full Text] [PDF]

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