- Email: [email protected]
Incidence of cardiovascular sudden deaths in Minnesota high school athletes
Incidence of cardiovascular sudden deaths in Minnesota high school athletes Barry J. Maron, MD, Tammy S. Haas, RN, Aneesha Ahluwalia, Stephanie C. Rutten-Ramos, DVM, PhD From the Hypertrophic Cardiomyopathy Center, Minneapolis Heart Institute Foundation, Minneapolis, Minnesota. BACKGROUND Sudden death (SD) in young competitive athletes due to cardiovascular disease is an important community issue with relevance to designing effective screening initiatives. However, the frequency with which these tragic events occur importantly affects considerations for selecting the most appropriate screening strategy. OBJECTIVE To determine the incidence and causes of cardiovascular SDs in Minnesota high school athletes. METHODS The forensic case records of the US National Registry of Sudden Death in Athletes were interrogated to identify those events judged to be cardiovascular in origin, occurring in organized competitive interscholastic sports participants. RESULTS Over the 26-year period, 1986–2011, 13 SDs occurred in high school student-athletes related to physical exertion, during competition (n ¼ 7) or at practice (n ¼ 6). Ages were 12–18 years (median 16 years); each was a white man. Most common sports involved were basketball, wrestling, or cross-country running. Forensic examination found cardiac causes in 7: hypertrophic cardiomyopathy (in 2), anomalous coronary artery (2), myocarditis (1), aortic stenosis (1), and arrhythmogenic right ventricular cardiomyopathy (1); 4 had structurally normal hearts (with negative toxicity). There were 4,440,161 sports participations,
Introduction Sudden death (SD) in young competitive athletes due to cardiovascular disease has become a highly visible public health issue.1–8 Recent interest in preparticipation screening to identify young at-risk athletes has triggered a robust dialog among concerned parties regarding the most appropriate strategy to detect potentially lethal diseases.9–16 Fundamental to this debate is the true frequency with which these SDs occur, which in turn affects perceptions regarding the priority that should be given these events relative to other risks of living in this age group.5,8,12,17–19 While much of the available data support SDs in young competitive athletes as a low event rate phenomenon, one recent report suggests that these risks may have been significantly underestimated in young athletes.20 Therefore, this is an opportune time to Address reprint requests and correspondence: Dr Barry J. Maron, Hypertrophic Cardiomyopathy Center, Minneapolis Heart Institute Foundation, 920 East 28th St, Suite 620, Minneapolis, MN 55407. E-mail address: [email protected].
1547-5271/$-see front matter B 2013 Heart Rhythm Society. All rights reserved.
including 1,930,504 individual participants among 24 sports. SD risk was 1:341,551 participations and 148,500 participants/academic year (0.7/100,000 person-years). In only 4 (31%) athletes could the responsible cardiovascular diseases have been reliably detected by screening with history/physical examination or 12lead electrocardiogram, equivalent to 1:1,000,000 participations (2:1,000,000 participants/year). CONCLUSIONS In this high school athlete population, risk of cardiovascular SD was small, in the range of 1:150,000 participants/year. Based on autopsy data, only about 30% of the SDs were due to diseases that could be reliably detected by preparticipation screening, even with 12-lead electrocardiograms. KEYWORDS Sudden death; Physical activity; Hypertrophic cardiomyopathy; Athletes; Screening; Electrocardiograms ABBREVIATIONS ARVC ¼ arrhythmogenic right ventricular cardiomyopathy; CI ¼ confidence interval; ECG ¼ electrocardiogram; HCM ¼ hypertrophic cardiomyopathy; SD ¼ sudden death (Heart Rhythm 2013;10:374–377) All rights reserved.
I
2013 Heart Rhythm Society.
revisit and expand our data over a 26-year period with respect to the epidemiology and incidence of SDs in young athletes in the state of Minnesota.
Methods The US National Registry of Sudden Death in Athletes was instituted at the Minneapolis Heart Institute Foundation for the purpose of prospectively and retrospectively assembling data on the deaths of young athletes participating in organized competitive sports. Over a 26-year period (1986– 2011), 2118 such SDs have been tabulated. This project was reviewed by the Allina Institutional Review Board. The study population was identified by targeted searches that used a variety of sources: (1) LexisNexis archival informational database with searchable access to authoritative news, legal, and public records (n ¼ 5 billion searchable documents from thousands of sources); (2) Minnesota State High School League records, including access to a mandatory insurance plan covering catastrophic injury or death http://dx.doi.org/10.1016/j.hrthm.2012.11.024
Maron et al
Cardiovascular Sudden Deaths in Minnesota High School Athletes
automatically administered to all student athletes (grades 7– 12) engaged in interscholastic sports programs; (3) news media accounts systematically assembled through Burrelle’s Information Services (Livingston, NJ) with access to 18,000 US newspapers and international media sources daily; (4) Internet searches, with online information via World Wide Web-based search engines (eg, Google, Yahoo); (5) reports from the US Consumer Product Safety Commission (Washington, DC); (6) records of the national center for Catastrophic Sports Injury Research (University of North Carolina, Chapel Hill, NC); (7) National Heart, Lung, and Blood Institute Pathology Branch archives, prior to 1990; (8) reports submitted directly to the registry or personal contact from physicians, attorneys, coroners/medical examiners, high school/colleges, and patient advocacy/support organizations. Individual athletes were included in the registry when identified through the aforementioned sources if 2 criteria were met: (1) participation in organized team or individual sports that required regular competition against others as a central component, placed a high premium on excellence and achievement, and required systematic and, in most instances, vigorous training (individuals participating in collegesponsored intramural or club sports were not included); and (2) SD r39 years of age. SD was defined as an unexpected collapse (with or without physical exertion) associated with a previously uneventful clinical course. A systematic tracking process was established to assemble detailed information on each case, which included the autopsy report (with gross anatomic, histological, and toxicological findings) and pertinent clinical and demographic information.
Selected data (eg, circumstances of collapse) were often derived from written accounts or telephone interviews with family members, witnesses, or coaches. When necessary, autopsy findings were verified by direct communication with medical examiners, and primary pathological materials were selectively requested and analyzed.
Results Sports participations Over the 26-year study period, the total number of participations in 24 high school sports was 4,440,161. This number included 2,494,226 (56%) men aged 12–18 years.
Epidemiology of SDs Thirteen SDs, unrelated to trauma (and with negative toxicology) occurred during organized high school sports activities, and were judged as probably owing to cardiovascular causes. Over the most recent 15 years, only 5 deaths occurred and 12 of these 15 years were without an event (Figure 1). At the time of collapse, 7 athletes were engaged in organized competition and 6 in practice or training. Each was a white man, and ages were 12–18 years (median 16 years). Athletes participated in a variety of sports: basketball (n ¼ 4), wrestling (n ¼ 4), cross-country running (n ¼ 3), baseball (n ¼ 1), and football (n ¼ 1) (Table 1).
Causes of death On the basis of autopsy reports, 7 athletes had structural abnormalities likely responsible for SD, that is, congenital
Number of Sudden Deaths
2
1
Year Figure 1
375
Year of occurrence for 13 Non-trauma-related sudden deaths in Minnesota state high school athletes over 26 years, 1986–2011.
376 Table 1
Heart Rhythm, Vol 10, No 3, March 2013 Clinical and morphologic profiles of 13 sudden deaths in Minnesota high school athletes
Age at death (y)
Race/sex
Sport
Circumstance of collapse
Autopsy diagnosis
12 (2002) 14 (1986) 14 (1994) 14 (2005) 14 (2002) 15 (1991) 16 (2008) 16 (1993) 16 (1990) 16 (1987) 17 (1996) 17 (1991) 18 (2005)
W/M W/M W/M W/M W/M W/M W/M W/M W/M W/M W/M W/M W/M
Cross-country Wrestling Basketball Wrestling Wrestling Basketball Wrestling Cross-country Cross-country Football Basketball Baseball Basketball
After running 1 mile at practice During match During practice End of practice session During match During game After practice Early in 5K race During warmup calisthenics at practice During game On bench during game Running during practice During game
Normal heart Normal heart Anomalous LMCA Bridging of LAD Normal heart* HCM† Normal heart Possible myocarditis Anomalous LMCA No autopsy Aortic stenosis HCM† ARVC‡
ARVC ¼ arrthymogenic right ventricular cardiomyopathy; HCM ¼ hypertrophic cardiomyopathy; LAD ¼ left anterior descending; LMCA ¼ left main coronary artery; M ¼ male; W ¼ white. * Serial sectioning of the conduction system was also normal. †No known family history of HCM. ‡Known family history of ARVC in a sister.
coronary anomaly of wrong sinus origin with left main coronary artery origin from right aortic sinus (n ¼ 2), hypertrophic cardiomyopathy (HCM) (n ¼ 2), myocarditis (n ¼ 1), valvular aortic stenosis (n ¼ 1), and arrhythmogenic right ventricular cardiomyopathy (ARVC) (n ¼ 1); one other had the isolated finding of myocardial bridging of the left anterior descending coronary artery. Of the remaining 5 athletes, autopsy failed to identify significant structural cardiac abnormalities in 4 (each with normal toxicology examination) and one did not have postmortem examination. Each of these 13 athletes had standard preparticipation history and physical examination screening, customarily administered to all student athletes in Minnesota high schools.
Incidence of SD Participations Given the 4,440,161 sports participations and 13 SDs, the calculated risk was 1:341,551 (0.3/100,000 participations; 95% CI; 0.2–0.5). For men, the risk of SD was 1:191,864 (0.5/100,000 participations; 95% CI: 0.3–0.9). The risk for female athletes was zero. Participants Using a calculation correction factor of 2.3 (ie, average number of sports participated in by individual high school student athletes),17,18 the estimated number of individual participants was 1,930,504. Therefore, given the 13 deaths, the calculated risk was 1:148,500 participants/academic year (0.7/100,000 person-years; 95% CI: 0.4–1.2). When considering only those athletes with diseases regarded as reliably detectable by screening with 12-lead electrocardiogram (ECG) and history/physical examination (n ¼ 4: HCM [2], ARVC [1], and aortic stenosis [1]), the incidence of SD was 1:1,000,000 participations, or
2:1,000,000 participants (0.2/100,000 person-years; 95% CI: 0.1–0.6).
Discussion The incidence of SDs in young trained athletes is a central element in the evolving debate regarding the most appropriate preparticipation screening strategy to detect cardiovascular disease and ultimately prevent these tragic events.5,11–13,17–20 Italian investigators have promoted systematic mass ie., national athlete screening with routine 12-lead ECGs (in addition to history and physical examination).2,3,5,6,10 However, obstacles to this strategy include the extensive resources required for such massive programs, limitations posed by false-positive and negative-test results, competing health-care priorities, and recognition that no particular screening approach can reliably identify all athletes with these complex cardiovascular diseases.4,12,21–23 Within our Minnesota cohort of athletes competing in organized high school sports, SD events were particularly uncommon, in the range of 1:150,000 participants/year. A number of other surveys of athletic field deaths in different populations have also reported a similar low event frequency in the range of 1:100,000 or higher.5,17–19,24 Indeed, in placing the frequency of our high school athlete deaths in perspective, the rate of (0.5) deaths/ academic year reported here is identical to that of lightningrelated fatalities (at all ages) in Minnesota during the last 22 years (ie, also 0.5).25,26 Therefore, a high school student in Minnesota has the same statistical likelihood of dying suddenly on the athletic field as incurring a fatal lightning strike. At such rates, it becomes exceedingly difficult to justify a large-scale regional or national screening program within the US health-care system to detect cardiovascular disease confined to young athletes.4,9,12,15 One recent report in young college athletes differs distinctly from our data (and virtually all other reports) by presenting much higher mortality rates thought to be due to cardiovascular causes—that is, 43,770 participants/academic year.20 However, those data possibly overestimate the incidence of SD,
Maron et al
Cardiovascular Sudden Deaths in Minnesota High School Athletes
given the lack of autopsy reports to confirm a cardiovascular cause of death, as is otherwise the convention.2,5,8,17,18 In 1998, we reported the frequency of SDs in Minnesota high school athletes (up to 1996) to be 1:217,000 participants.18 This analysis was confined to deaths occurring specifically during in-season interscholastic high school competition and practice. In the present study, we expanded our analysis of this cohort, both with respect to the length of observation (ie, by 15 additional years) and by including all deaths not necessarily limited to those occurring in season for a particular sport. Consequently, the total number of deaths reported here (n ¼ 13) exceeds by 4-fold that in the initial report, and the present study also includes an at-risk population that is 3-fold larger. Each of the 13 SDs in this study were related to physical activity and witnessed under circumstances that strongly suggested cardiovascular collapse. However, in only about 65% of these cases was a cardiac abnormality identified at autopsy that could be considered as the probable or possible cause of death, including 2 athletes each with HCM (the most common cause of SD in US athletes)8 and anomalous left main coronary artery (the second leading cause of SD in US athletes),8 as well as one each with ARVC (most common in Italy),27 aortic valvular stenosis, and myocarditis. One athlete had isolated myocardial bridging of the left anterior descending coronary artery, considered here as only a possible cause of death.28 Notably, in 4 athletes, the cause of death could not be resolved, even after autopsy examination, given that the heart (and other organs) were structurally normal. Whether any of these 4 deaths were due to ion channelopathies is unresolved, given the absence of cardiovascular testing during life. Furthermore, based on our forensic data, only 30% of athletes who died suddenly (n ¼ 4) had structural cardiac diseases for which there is a reasonable expectation of detection with ECG-based preparticipation screening (as dictated by the Italian model) that is, 2 athletes with HCM and one each with ARVC and aortic stenosis. The other athletes (including 2 with congenital coronary anomalies of wrong sinus origin) would probably not have been suspected by ECG screening.29 In terms of incidence, the present findings translate to an expectation that only 2 athletes with cardiovascular disease would likely have been detected by screening (including 12lead ECGs) among 1 million participants per year. These data underscore an important limitation to mass screening: false-negative screening test results are not inconsequential,21 and all at-risk athletes are not potentially detectable by screening with the 12-lead ECG. Our findings also argue against the prudence and effectiveness of national mandatory 12-lead ECG screening to detect cardiovascular disease in US competitive athletes.
References 1. Maron BJ. Sudden death in young athletes. N Engl J Med 2003;349:1064–1075. 2. Corrado D, Basso C, Schiavon M, Thiene G. Screening for hypertrophic cardiomyopathy in young athletes. N Engl J Med 1998;339:364–369. 3. Corrado D, Pelliccia A, Bjørnstad HH, et al. Cardiovascular pre-participation screening of young competitive athletes for prevention of sudden death: proposal for a common European protocol. Consensus Statement of the Study Group of
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Sport Cardiology of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of Myocardial and Pericardial Diseases of the European Society of Cardiology. Eur Heart J 2005;26:516–524. Maron BJ, Thompson PD, Ackerman MJ, et al. Recommendations and considerations related to preparticipation screening for cardiovascular abnormalities in competitive athletes: Update 2007. A Scientific Statement from the American Heart Association, Nutrition, Physical Activity, and Metabolism Council. Circulation 2007;115:1643–1655. Corrado D, Basso C, Pavei A, Michieli P, Schiavon M, Thiene G. Trends in sudden cardiovascular death in young competitive athletes after implementation of a preparticipation screening program. JAMA 2006;296:1593–1601. Pelliccia A, DiPaolo FM, Quattrini FM, et al. Outcomes in athletes with marked ECG repolarization abnormalities. N Engl J Med 2008;358:152–161. Maron BJ, Zipes DP. 36th Bethesda Conference: Eligibility Recommendations for Competitive Athletes with Cardiovascular Abnormalities. J Am Coll Cardiol 2005;45:1312–1375. Maron BJ, Doerer JJ, Haas TS, Tierney DM, Mueller FO. Sudden deaths in young competitive athletes: analysis of 1866 deaths in the U.S., 1980–2006. Circulation 2009;119:1085–1092. Maron BJ. National electrocardiogram screening for competitive athletes: feasible in the United States?. Ann Intern Med 2010;152:324–326. Corrado D, Pelliccia A, Heidbuchel H, et al. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. Eur Heart J 2010;31:243–259. Eur Heart J 2010;31:379. Maron BJ, Haas TS, Doerer JJ, Thompson PD, Hodges JS. Comparison of U.S. and Italian experiences with sudden cardiac deaths in young competitive athletes and implications for preparticipation screening strategies. Am J Cardiol 2009;104:276–280. Maron BJ. Counterpoint. Mandatory screening of young competitive athletes. Heart Rhythm 2012;9:1646–9. Steinvil A, Chundadze T, Zeltser D, et al. Mandatory electrocardiographic screening of athletes to reduce their risk for sudden death proven fact or wishful thinking? J Am Coll Cardiol 2011;57:1291–1296. Myerburg RJ, Vetter VL. Electrocardiograms should be included in preparticipation screening of athletes. Circulation 2007;116:2616–2626. Chaitman BR. An electrocardiogram should not be included in routine preparticipation screening of young athletes. Circulation 2007;116:2610–2614. Drezner JA. ECG screening in athletes: time to develop infrastructure. Heart Rhythm 2011;8:1560–1561. Van Camp SP, Bloor CM, Mueller FO, Cantu RC, Olson HG. Non-traumatic sports death in high school and college athletes. Med Sci Sports Exerc 1995;27:641–647. Maron BJ, Gohman TE, Aeppli D. Prevalence of sudden cardiac death during competitive sports activities in Minnesota high school athletes. J Am Coll Cardiol 1998;32:1881–1884. Driscoll DJ, Edward WD. Sudden unexpected death in children and adolescents. J Am Coll Cardiol 1985;5:118B–121B. Harmon KG, Asif IM, Klossner D, Drezner JA. Incidence of sudden cardiac death in National Collegiate Athletic Association athletes. Circulation 2011;123:1594–1600. Rowin EJ, Maron BJ, Appelbaum E, et al. Significance of false negative electrocardiograms in preparticipation screening of athletes for hypertrophic cardiomyopathy. Am J Cardiol 2012;110:1027–1032. Link MS, Estes NAM. Sudden death in the athlete: bridging the gaps between evidence, policy and practice. Circulation 2012;125:2511–2516. Maron BJ, Bodison SA, Wesley YE, Tucker E, Green KJ. Results of screening a large group of intercollegiate competitive athletes for cardiovascular disease. J Am Coll Cardiol 1987;10:1214–1221. Holst AG, Winkel BG, Theilade J, et al. Incidence and etiology of sports related sudden cardiac death in Denmark—implications for preparticipation. Heart Rhythm 2010;7:1365–1371. National Lightning Safety Institute. Lightning Fatalities, Injuries, and Damage Reports in the United States/Number of Lightning Deaths in the United States 1990–2003. Available from: http://www.lightningsafety.com/nlsi_lls_fatalities_us.html. Accessed April 13, 2006. National Weather Service. Lightning Fatalities by State, 2002–2011. Available from: http://www.lightningsafety.noaa.gov/stats/02-11_deaths_by_state.pdf. Accessed October 17, 2012. Thiene G, Nava A, Corrado D, Rossi L, Pennelli N. Right ventricular cardiomyopathy and sudden death in young people. N Engl J Med 1988;318:129–133. Basso C, Thiene G, Mackey-Bojack S, Frigo AC, Corrado D, Maron BJ. Myocardial bridging: a frequent component of the hypertrophic cardiomyopathy phenotype lacks systematic association with sudden cardiac death. Eur Heart J 2009;30:1627–1634. 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.
Introduction Sudden death (SD) in young competitive athletes due to cardiovascular disease has become a highly visible public health issue.1–8 Recent interest in preparticipation screening to identify young at-risk athletes has triggered a robust dialog among concerned parties regarding the most appropriate strategy to detect potentially lethal diseases.9–16 Fundamental to this debate is the true frequency with which these SDs occur, which in turn affects perceptions regarding the priority that should be given these events relative to other risks of living in this age group.5,8,12,17–19 While much of the available data support SDs in young competitive athletes as a low event rate phenomenon, one recent report suggests that these risks may have been significantly underestimated in young athletes.20 Therefore, this is an opportune time to Address reprint requests and correspondence: Dr Barry J. Maron, Hypertrophic Cardiomyopathy Center, Minneapolis Heart Institute Foundation, 920 East 28th St, Suite 620, Minneapolis, MN 55407. E-mail address: [email protected].
1547-5271/$-see front matter B 2013 Heart Rhythm Society. All rights reserved.
including 1,930,504 individual participants among 24 sports. SD risk was 1:341,551 participations and 148,500 participants/academic year (0.7/100,000 person-years). In only 4 (31%) athletes could the responsible cardiovascular diseases have been reliably detected by screening with history/physical examination or 12lead electrocardiogram, equivalent to 1:1,000,000 participations (2:1,000,000 participants/year). CONCLUSIONS In this high school athlete population, risk of cardiovascular SD was small, in the range of 1:150,000 participants/year. Based on autopsy data, only about 30% of the SDs were due to diseases that could be reliably detected by preparticipation screening, even with 12-lead electrocardiograms. KEYWORDS Sudden death; Physical activity; Hypertrophic cardiomyopathy; Athletes; Screening; Electrocardiograms ABBREVIATIONS ARVC ¼ arrhythmogenic right ventricular cardiomyopathy; CI ¼ confidence interval; ECG ¼ electrocardiogram; HCM ¼ hypertrophic cardiomyopathy; SD ¼ sudden death (Heart Rhythm 2013;10:374–377) All rights reserved.
I
2013 Heart Rhythm Society.
revisit and expand our data over a 26-year period with respect to the epidemiology and incidence of SDs in young athletes in the state of Minnesota.
Methods The US National Registry of Sudden Death in Athletes was instituted at the Minneapolis Heart Institute Foundation for the purpose of prospectively and retrospectively assembling data on the deaths of young athletes participating in organized competitive sports. Over a 26-year period (1986– 2011), 2118 such SDs have been tabulated. This project was reviewed by the Allina Institutional Review Board. The study population was identified by targeted searches that used a variety of sources: (1) LexisNexis archival informational database with searchable access to authoritative news, legal, and public records (n ¼ 5 billion searchable documents from thousands of sources); (2) Minnesota State High School League records, including access to a mandatory insurance plan covering catastrophic injury or death http://dx.doi.org/10.1016/j.hrthm.2012.11.024
Maron et al
Cardiovascular Sudden Deaths in Minnesota High School Athletes
automatically administered to all student athletes (grades 7– 12) engaged in interscholastic sports programs; (3) news media accounts systematically assembled through Burrelle’s Information Services (Livingston, NJ) with access to 18,000 US newspapers and international media sources daily; (4) Internet searches, with online information via World Wide Web-based search engines (eg, Google, Yahoo); (5) reports from the US Consumer Product Safety Commission (Washington, DC); (6) records of the national center for Catastrophic Sports Injury Research (University of North Carolina, Chapel Hill, NC); (7) National Heart, Lung, and Blood Institute Pathology Branch archives, prior to 1990; (8) reports submitted directly to the registry or personal contact from physicians, attorneys, coroners/medical examiners, high school/colleges, and patient advocacy/support organizations. Individual athletes were included in the registry when identified through the aforementioned sources if 2 criteria were met: (1) participation in organized team or individual sports that required regular competition against others as a central component, placed a high premium on excellence and achievement, and required systematic and, in most instances, vigorous training (individuals participating in collegesponsored intramural or club sports were not included); and (2) SD r39 years of age. SD was defined as an unexpected collapse (with or without physical exertion) associated with a previously uneventful clinical course. A systematic tracking process was established to assemble detailed information on each case, which included the autopsy report (with gross anatomic, histological, and toxicological findings) and pertinent clinical and demographic information.
Selected data (eg, circumstances of collapse) were often derived from written accounts or telephone interviews with family members, witnesses, or coaches. When necessary, autopsy findings were verified by direct communication with medical examiners, and primary pathological materials were selectively requested and analyzed.
Results Sports participations Over the 26-year study period, the total number of participations in 24 high school sports was 4,440,161. This number included 2,494,226 (56%) men aged 12–18 years.
Epidemiology of SDs Thirteen SDs, unrelated to trauma (and with negative toxicology) occurred during organized high school sports activities, and were judged as probably owing to cardiovascular causes. Over the most recent 15 years, only 5 deaths occurred and 12 of these 15 years were without an event (Figure 1). At the time of collapse, 7 athletes were engaged in organized competition and 6 in practice or training. Each was a white man, and ages were 12–18 years (median 16 years). Athletes participated in a variety of sports: basketball (n ¼ 4), wrestling (n ¼ 4), cross-country running (n ¼ 3), baseball (n ¼ 1), and football (n ¼ 1) (Table 1).
Causes of death On the basis of autopsy reports, 7 athletes had structural abnormalities likely responsible for SD, that is, congenital
Number of Sudden Deaths
2
1
Year Figure 1
375
Year of occurrence for 13 Non-trauma-related sudden deaths in Minnesota state high school athletes over 26 years, 1986–2011.
376 Table 1
Heart Rhythm, Vol 10, No 3, March 2013 Clinical and morphologic profiles of 13 sudden deaths in Minnesota high school athletes
Age at death (y)
Race/sex
Sport
Circumstance of collapse
Autopsy diagnosis
12 (2002) 14 (1986) 14 (1994) 14 (2005) 14 (2002) 15 (1991) 16 (2008) 16 (1993) 16 (1990) 16 (1987) 17 (1996) 17 (1991) 18 (2005)
W/M W/M W/M W/M W/M W/M W/M W/M W/M W/M W/M W/M W/M
Cross-country Wrestling Basketball Wrestling Wrestling Basketball Wrestling Cross-country Cross-country Football Basketball Baseball Basketball
After running 1 mile at practice During match During practice End of practice session During match During game After practice Early in 5K race During warmup calisthenics at practice During game On bench during game Running during practice During game
Normal heart Normal heart Anomalous LMCA Bridging of LAD Normal heart* HCM† Normal heart Possible myocarditis Anomalous LMCA No autopsy Aortic stenosis HCM† ARVC‡
ARVC ¼ arrthymogenic right ventricular cardiomyopathy; HCM ¼ hypertrophic cardiomyopathy; LAD ¼ left anterior descending; LMCA ¼ left main coronary artery; M ¼ male; W ¼ white. * Serial sectioning of the conduction system was also normal. †No known family history of HCM. ‡Known family history of ARVC in a sister.
coronary anomaly of wrong sinus origin with left main coronary artery origin from right aortic sinus (n ¼ 2), hypertrophic cardiomyopathy (HCM) (n ¼ 2), myocarditis (n ¼ 1), valvular aortic stenosis (n ¼ 1), and arrhythmogenic right ventricular cardiomyopathy (ARVC) (n ¼ 1); one other had the isolated finding of myocardial bridging of the left anterior descending coronary artery. Of the remaining 5 athletes, autopsy failed to identify significant structural cardiac abnormalities in 4 (each with normal toxicology examination) and one did not have postmortem examination. Each of these 13 athletes had standard preparticipation history and physical examination screening, customarily administered to all student athletes in Minnesota high schools.
Incidence of SD Participations Given the 4,440,161 sports participations and 13 SDs, the calculated risk was 1:341,551 (0.3/100,000 participations; 95% CI; 0.2–0.5). For men, the risk of SD was 1:191,864 (0.5/100,000 participations; 95% CI: 0.3–0.9). The risk for female athletes was zero. Participants Using a calculation correction factor of 2.3 (ie, average number of sports participated in by individual high school student athletes),17,18 the estimated number of individual participants was 1,930,504. Therefore, given the 13 deaths, the calculated risk was 1:148,500 participants/academic year (0.7/100,000 person-years; 95% CI: 0.4–1.2). When considering only those athletes with diseases regarded as reliably detectable by screening with 12-lead electrocardiogram (ECG) and history/physical examination (n ¼ 4: HCM [2], ARVC [1], and aortic stenosis [1]), the incidence of SD was 1:1,000,000 participations, or
2:1,000,000 participants (0.2/100,000 person-years; 95% CI: 0.1–0.6).
Discussion The incidence of SDs in young trained athletes is a central element in the evolving debate regarding the most appropriate preparticipation screening strategy to detect cardiovascular disease and ultimately prevent these tragic events.5,11–13,17–20 Italian investigators have promoted systematic mass ie., national athlete screening with routine 12-lead ECGs (in addition to history and physical examination).2,3,5,6,10 However, obstacles to this strategy include the extensive resources required for such massive programs, limitations posed by false-positive and negative-test results, competing health-care priorities, and recognition that no particular screening approach can reliably identify all athletes with these complex cardiovascular diseases.4,12,21–23 Within our Minnesota cohort of athletes competing in organized high school sports, SD events were particularly uncommon, in the range of 1:150,000 participants/year. A number of other surveys of athletic field deaths in different populations have also reported a similar low event frequency in the range of 1:100,000 or higher.5,17–19,24 Indeed, in placing the frequency of our high school athlete deaths in perspective, the rate of (0.5) deaths/ academic year reported here is identical to that of lightningrelated fatalities (at all ages) in Minnesota during the last 22 years (ie, also 0.5).25,26 Therefore, a high school student in Minnesota has the same statistical likelihood of dying suddenly on the athletic field as incurring a fatal lightning strike. At such rates, it becomes exceedingly difficult to justify a large-scale regional or national screening program within the US health-care system to detect cardiovascular disease confined to young athletes.4,9,12,15 One recent report in young college athletes differs distinctly from our data (and virtually all other reports) by presenting much higher mortality rates thought to be due to cardiovascular causes—that is, 43,770 participants/academic year.20 However, those data possibly overestimate the incidence of SD,
Maron et al
Cardiovascular Sudden Deaths in Minnesota High School Athletes
given the lack of autopsy reports to confirm a cardiovascular cause of death, as is otherwise the convention.2,5,8,17,18 In 1998, we reported the frequency of SDs in Minnesota high school athletes (up to 1996) to be 1:217,000 participants.18 This analysis was confined to deaths occurring specifically during in-season interscholastic high school competition and practice. In the present study, we expanded our analysis of this cohort, both with respect to the length of observation (ie, by 15 additional years) and by including all deaths not necessarily limited to those occurring in season for a particular sport. Consequently, the total number of deaths reported here (n ¼ 13) exceeds by 4-fold that in the initial report, and the present study also includes an at-risk population that is 3-fold larger. Each of the 13 SDs in this study were related to physical activity and witnessed under circumstances that strongly suggested cardiovascular collapse. However, in only about 65% of these cases was a cardiac abnormality identified at autopsy that could be considered as the probable or possible cause of death, including 2 athletes each with HCM (the most common cause of SD in US athletes)8 and anomalous left main coronary artery (the second leading cause of SD in US athletes),8 as well as one each with ARVC (most common in Italy),27 aortic valvular stenosis, and myocarditis. One athlete had isolated myocardial bridging of the left anterior descending coronary artery, considered here as only a possible cause of death.28 Notably, in 4 athletes, the cause of death could not be resolved, even after autopsy examination, given that the heart (and other organs) were structurally normal. Whether any of these 4 deaths were due to ion channelopathies is unresolved, given the absence of cardiovascular testing during life. Furthermore, based on our forensic data, only 30% of athletes who died suddenly (n ¼ 4) had structural cardiac diseases for which there is a reasonable expectation of detection with ECG-based preparticipation screening (as dictated by the Italian model) that is, 2 athletes with HCM and one each with ARVC and aortic stenosis. The other athletes (including 2 with congenital coronary anomalies of wrong sinus origin) would probably not have been suspected by ECG screening.29 In terms of incidence, the present findings translate to an expectation that only 2 athletes with cardiovascular disease would likely have been detected by screening (including 12lead ECGs) among 1 million participants per year. These data underscore an important limitation to mass screening: false-negative screening test results are not inconsequential,21 and all at-risk athletes are not potentially detectable by screening with the 12-lead ECG. Our findings also argue against the prudence and effectiveness of national mandatory 12-lead ECG screening to detect cardiovascular disease in US competitive athletes.
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