Author + information
- Received November 13, 2013
- Revision received January 15, 2014
- Accepted January 20, 2014
- Published online April 29, 2014.
- Barry J. Maron, MD∗ (, )
- Tammy S. Haas, RN,
- Caleb J. Murphy, BS,
- Aneesha Ahluwalia and
- Stephanie Rutten-Ramos, DVM, PhD
- ↵∗Reprint requests and correspondence:
Dr. Barry J. Maron, Hypertrophic Cardiomyopathy Center, Minneapolis Heart Institute Foundation, 920 East 28th Street, Suite 620, Minneapolis, Minnesota 55407.
Objectives The goal of this study was to reliably define the incidence and causes of sudden death in college student-athletes.
Background The frequency with which cardiovascular-related sudden death occurs in competitive athletes importantly influences considerations for pre-participation screening strategies.
Methods We assessed databases (including autopsy reports) from both the U.S. National Registry of Sudden Death in Athletes and the National Collegiate Athletic Association (2002 to 2011).
Results Over the 10-year study period, 182 sudden deaths occurred (age 20 ± 1.7 years; 85% male; 64% white), 52 resulting from suicide (n = 31) or drug abuse (n = 21) and 64 probably or likely attributable to cardiovascular causes (6/year). Of these 64 athletes, 47 had a confirmed post-mortem diagnosis; the most common were hypertrophic cardiomyopathy in 21 and congenital coronary anomalies in 8. The 4,052,369 athlete participations (in 30 sports over 10 years) incurred mortality risks as follows: suicide and drugs combined, 1.3/100,000 athlete participation-years (5 deaths/year); and documented cardiovascular disease, 1.2/100,000 athlete participation-years (4 deaths/year). Notably, cardiovascular deaths were 5-fold more common in African-American athletes than in white athletes (3.8 vs. 0.7/100,000 athlete participation-years; p < 0.01) but did not differ from the general population of the same age and race (p = 0.6).
Conclusions In college student-athletes, risk of sudden death due to cardiovascular disease is relatively low, with mortality rates similar to suicide and drug abuse, but less than expected in the general population, although highest in African-American athletes. A substantial minority of confirmed cardiovascular deaths would not likely have been reliably detected by pre-participation screening with 12-lead electrocardiograms.
Sudden death in young competitive athletes has become a highly visible issue, attracting substantial public interest within communities and in cardiovascular medicine (1–10). Much of the current debate regarding pre-participation screening concerns selection of the most effective and practical strategy for identifying (or raising suspicion of) a diverse array of cardiovascular diseases known to be responsible for sudden death in this population (2–16). A particularly relevant consideration is the magnitude of this public health issue, that is, the incidence of sudden deaths due to unsuspected cardiovascular disease relative to other mortality risks.
Most mortality data in young athletes suggest that these catastrophes occur with relatively low event rates (1,3,6,9,11,15). However, a recent nonforensic-based analysis in college student-athletes reported a relatively high frequency of 2.3/100,000 athlete-years for deaths believed to be of cardiovascular origin (7). Such data have heightened concern in the college sports community that intercollegiate student-athletes have uniquely high (even excessive) risks; this concern has contributed to a promotion of cardiovascular screening with electrocardiograms (ECGs) (2,5–7,10,12–14). We have therefore taken this opportunity to analyze our forensic database for both the causes and incidence of sudden deaths in college student-athletes over the recent decade.
The U.S. National Registry of Sudden Death in Athletes was instituted at the Minneapolis Heart Institute Foundation in 1992 to systematically assemble (prospectively and retrospectively) data on young athletes participating in organized competitive sports. Subjects are considered for inclusion when they are a participant in an organized team or individual sport requiring regular training and competition (15). Deaths occurring in club or intramural sports or from automobile accidents, homicides, cancer, or systemic diseases were not tabulated. This project was approved by the Allina Health System Institutional Review Board.
For the years 2002 to 2011, we used a variety of sources to identify deaths in intercollegiate athletes active in competitive organized programs (but not necessarily occurring on the athletic field) (Table 1). For each case, systematic tracking was established to obtain available clinical data and/or the circumstances of death, as well as complete autopsy reports with gross, histopathological, and toxicological data from the medical examiner of record. Post-mortem findings were adjudicated by 1 senior investigator (B.J.M.) with >30 years experience and expertise in this discipline (1,8,15–17). When necessary, autopsy findings were verified by communication with medical examiners. Detailed information on demographic characteristics, circumstances of death, and pertinent clinical data was assembled, sometimes from written accounts or telephone interviews with family members, witnesses, or coaches.
National Collegiate Athletic Association participation data
The National Collegiate Athletic Association (NCAA) is a governing body for colleges and universities with organized competitive athletic programs, comprising 1,273 member institutions and representing 85% of students competing in college. For 2001 through 2011, participation data were tabulated from the comprehensive NCAA Sports Sponsorship and Participation Rates Report (18); these findings, however, do not take into account the possibility of multisport participation. Demographic, sex, and race/ethnic information were obtained from the NCAA Student-Athlete Ethnicity Report (19).
Comparison of data sources
The U.S. National Registry of Sudden Death in Athletes (which primarily accesses public domain sources) and the internal NCAA Memorial Resolutions List were compared with respect to identification of sudden cardiovascular deaths in NCAA athletes. Of the 64 total sudden death cases on initial interrogation, the registry method recognized 56 sudden deaths (88%), including 14 not represented on the NCAA list. The NCAA included 50 (78%) of 64 cases, including 8 not recognized by initial registry searches, due to absence within the media reports of key words prospectively established for tracking these events (e.g., “athlete” or “sudden death”).
Mortality rates in NCAA athletes were compared with available data for suicide, drugs, drowning, and cardiovascular causes in the general population: 1) U.S. National Vital Statistics Reports (20) with all causes of death for ages 15 to 24 years during 2006, the most recent year in which causes of mortality were tabulated according to age and race; and 2) data reported for suicide in U.S. college students, ages 18 to 24 years, for 2009 through 2010 (21). The extent of 1 athlete-year was defined as participating in a sport from August to July.
Mortality rates were estimated by using Poisson regression and compared across populations and subpopulations. Mortality rates, incidence, and 95% confidence intervals (CIs) were reported as deaths/100,000 athlete participation-years (or person-years). All analyses were performed using SAS version 9.3 (SAS Institute, Inc., Cary, North Carolina). Statistical significance was defined as p < 0.05.
Over the 10-year study period, the total number of student-athlete participations in 30 intercollegiate sports was 4,052,369, ranging from 367,653 (2001 to 2002) to 449,576 (2010 to 2011) for a mean of 405,237 per year. Age at death ranged from 17 to 26 years (20 ± 1.7 years); 154 (85%) were male; and 116 (64%) were white and 60 (33%) were African American, with 6 (3%) subjects of other races.
Epidemiology of sudden deaths
There were a total of 182 sudden deaths recorded during the 10-year study period (0.004% of 4,052,369) or 18/year (Table 2, Fig. 1). Events occurred at a similar rate over time (p = 0.61) but were highest in 2004 and 2007 (n = 22 each) and lowest in 2006 (n = 11).
Causes of death
A variety of diseases or circumstances were responsible for mortality in this athlete population (Table 2, Fig. 2). In 16 of 182 sudden deaths, cause was unresolved because post-mortem examinations were not performed (n = 2), it was not possible to obtain autopsy findings due to state confidentiality restrictions (n = 6), or the report was ambiguous without sufficient detail to reliably assign the cause of death (n = 8). These 16 deaths occurred while sedentary (or during sleep) and were unrelated to sports or physical exertion.
Noncardiovascular disease–related sudden death
Of the 182 sudden deaths, 118 (65%) were due to causes other than cardiovascular disease (Table 2, Fig. 2). The most common of these was suicide (n = 31 [17%]), including gunshot trauma or hanging (n = 8, each), or were drug related as confirmed by toxicology (n = 21 [12%]); together, drugs and suicide were thus responsible for 29% of all sudden deaths (n = 52). Other noncardiovascular causes of sudden death were blunt trauma (n = 15; including 2 with commotio cordis); sickle cell trait (n = 11) (17); drowning (n = 11); and heat stroke (n = 5).
Cardiovascular disease–related sudden death
In 64 athletes, a cardiovascular abnormality was judged the likely or probable cause of death. Most common sports were basketball (n = 23) and football (n = 16) (Table 2); 29 collapsed with physical exertion during competition (n = 6) or practice (n = 23), 14 others during recreational sports, and 21 while sedentary. Of these, 58% were white and 41% were African American.
In 47 of 64 athletes, a post-mortem examination documented a cardiovascular abnormality considered responsible for the sudden death. Most common were: hypertrophic cardiomyopathy (n = 21 [12 African American, 9 white]); mean heart weight 563 ± 70 g; mean maximum left ventricular wall thickness 22 ± 4 mm (range 17 to 31 mm); myocyte disarray (n = 10); anomalous coronary artery of wrong sinus origin (n = 8); atherosclerotic coronary artery disease (n = 5); aortic dissection and rupture (n = 3 [including 2 positive for a fibrillin-1 gene mutation]); arrhythmogenic right ventricular cardiomyopathy with right ventricular enlargement and extensive fatty infiltration (n = 3); healed myocarditis with patchy myocardial fibrosis (n = 2); dilated cardiomyopathy with 4-chamber enlargement (n = 2); myxomatous mitral valve (n = 1); myocardial infarction (n = 1 [Kawasaki syndrome]); and 1 athlete with a structurally normal heart and family history of sudden death due to long QT syndrome (LQTS), which strongly suggested LQTS as the cause of death (Table 2, Fig. 2).
In 17 of 64 athletes, collapse occurred virtually instantaneously after physical activity during competition or practice, suggesting that underlying cardiovascular disease was responsible (“presumed cardiovascular”) (Table 2, Fig. 2). However, the precise cause of death could not be established, either because a post-mortem examination was not performed (n = 3), the autopsy report was inconclusive (i.e., judged inadequate to reliably assign the specific cause of SD [n = 12]), or because confidentiality considerations restricted access to the report (n = 2). Also included in this group were 3 athletes in whom the sole pathologic abnormality was myocardial bridging of left anterior descending coronary artery (22).
Sudden death incidence
Given that there were 4,052,369 NCAA athlete participations/year over the 10-year study period, calculated mortality rates were: 1) suicide, 3/year (0.8/100,000 athlete participation-years) and drug-related, 2/year (0.5/100,000 athlete participation-years); 2) suicide and drugs combined, 5/year (1.3/100,000 athlete participation-years); 3) confirmed cardiovascular disease (n = 47), 4/year (1.2/100,000 athlete participation-years); and 4) combined confirmed or presumed cardiovascular disease (n = 64), 6/year (1.6/100,000 athlete participation-years).
Mortality from suicide and drugs combined did not differ from the 47 confirmed cardiovascular causes (p = 0.39) but was less than confirmed/presumed cardiovascular disease (p < 0.0006). Deaths due to confirmed cardiovascular disease were 2.5-fold more common in athletes competing in Division I compared with Division III sports (1.5 vs. 0.6/100,000 participation-years; p = 0.012). Mortality from any cause did not increase significantly over the 10-year observation period (p = 0.06 to 0.9) (Fig. 1).
NCAA and general population mortality
NCAA athletes had significantly lower cardiovascular mortality rates than expected in the general population of similar age, either for the 47 athletes with confirmed diagnoses (p < 0.0001) or the 64 athletes with combined confirmed/presumed cardiovascular diseases (p < 0.0007) (Tables 3 and 4).
Suicide rates in the general population were significantly higher than in NCAA athletes (p < 0.0001); however, suicide was less common in college student-athletes than in other college students (p < 0.0001). Drug-related deaths occurred with similar frequency in NCAA athletes and in the general population of comparable age and sex (p = 0.32).
Impact of race and sex
Cardiovascular deaths were 5-fold more common in African-American subjects than in white subjects (3.8 vs. 0.7/100,000 athlete participation-years; p < 0.01) but were similar to that in a general black population of the same age (4.3/100,000 athlete participation-years; p = 0.6) (Table 4).
In contrast, the suicide rate was similar in African-American and white athletes (1.0 vs. 0.8/100,000 athlete participation-years; p = 0.7), but in both instances, it was significantly less common than in the general population (p < 0.0001). Drug-related death rates also were similar in African-American athletes (0.6/100,000 athlete participation-years) and white athletes (0.5/100,000 athlete participation-years; p = 0.75) but were not significantly different from the general population (p > 0.2).
Cardiovascular deaths were 6-fold more common in male athletes than in female athletes (1.8/100,000 athlete participation-years [95% CI: 0.3 to 9.3/100,000 athlete participation-years] vs. 0.3/100,000 athlete participation-years [95% CI: 0.2 to 0.8/100,000 athlete participation-years]; p < 0.0001) but lower than the general male population of the same age (2.8/100,000 athlete participation-years [95% CI: 0.6 to 14/100,000 athlete participation-years]; p < 0.001).
The suicide rate was 3-fold higher in male subjects than in female subjects (1.1/100,000 athlete participation-years [95% CI: 0.2 to 5.8/100,000 athlete participation-years] vs. 0.3/100,000 athlete participation-years [95% CI: 0.2 to 0.8/100,000 athlete participation-years]; p < 0.01) but was much lower than in the general male population of the same age (16/100,000 athlete participation-years; p < 0.0001).
Drug deaths were more common in male subjects than in female subjects (0.9/100,000 athlete participation-years [95% CI: 0.6 to 1.4/100,000 athlete participation-years] vs. zero; p < 0.0001) but were similar to the general male population of the same age (1.0/100,000 athlete participation-years; p = 0.7).
Reliability of screening for cardiovascular causes of sudden death
We estimated reliability of the 12-lead ECG for diagnosis of specific cardiac causes of sudden death. Of 47 diagnoses confirmed at autopsy, 28 (60%) would most likely have been identified or suspected of being cardiac related according to the ECG findings: hypertrophic cardiomyopathy (n = 19 of 21) (30); arrhythmogenic right ventricular cardiomyopathy (n = 3); aortic rupture (n = 2 with Marfan syndrome); dilated cardiomyopathy (n = 2); LQTS (n = 1); and mitral valve prolapse (n = 1).
Considerable discussion has emerged over the last several years regarding the impact on the general public health of sudden deaths tragically occurring in young competitive athletes (1–16) and the most effective screening strategy to detect the responsible causes in this population (2–7,9–14). Indeed, the justification for broad-based (even national) screening initiatives would seem to rest importantly on the frequency with which cardiovascular catastrophes do occur in trained athletes (3,9,11,15,16,23). For example, in Denmark, systematic screening of athletes (and others) is not performed by any method because the sudden death rate is considered particularly low (11).
In a previous survey of NCAA athletes without forensic (autopsy) confirmation of causes of death, Harmon et al. (7) reported 9 athlete deaths/year (over a 5-year period) among 400,000 participations, which these investigators believed were cardiovascular based, but without diagnostic anatomic substantiation. The present data essentially target the same population (albeit with a 2-fold longer study period) and have identified a significantly lower event rate of 4 to 6 deaths/year, aided by access to documented causes of death by virtue of post-mortem examinations. Perhaps not unexpectedly, the 2 studies in the literature that report the highest cardiovascular sudden death rate in athletes of >2 per 100,000 do not include diagnostic autopsy or clinical data (i.e., Steinvil et al.  from Israel and the Harmon et al.  study of U.S. college athletes).
However, we wish to underscore that the differences in incidence of athletic field deaths between Harmon et al. (7) and the present study are nevertheless relatively small when compared with the more compelling rates of sudden death due to the many other risks to living in the general population of the same age group (Fig. 3). Indeed, an important aspect of the present investigation is the placing of cardiovascular sudden deaths in college athletes within a broader context.
Our analysis underscores the principle that NCAA athlete sudden deaths represent a numerically low event rate phenomenon (1,3,6,9,11,15,23); for example, by comparison, annual automobile fatalities in the same age group are >2,500-fold more common. Furthermore, cardiovascular deaths in NCAA athletes are significantly less common than those in the general population, but similar to the unexpectedly high combined suicide and drug-related mortality rates identified in these college athletes.
Notably, the cardiovascular sudden death rate in our college athletes is higher than that previously reported in a cohort of high school athletes (1.2 vs. 0.7/100,000) (9). Although the determinants are uncertain, these differences are potentially attributable to the longer exposure by college student-athletes to rigid and rigorous training regimens extended over more substantial periods of life. Sudden deaths were, in fact, most common in Division I (scholarship) athletes for whom training and competition are most demanding. In addition, susceptibility to cardiovascular events could conceivably be influenced by risk factors associated with the initial experience of independent living at college (e.g., failure to adhere to healthy lifestyle practices with proper rest and nutrition, increased exposure to alcohol and drugs).
In a sizeable minority of athlete sudden deaths, it was not possible to conclusively determine the cause of death, even after considering the submitted autopsy findings. This circumstance largely reflects the current state-of-the-art in the medical examiner community regarding post-mortem diagnoses in sudden deaths due to genetic heart diseases (24,25). Indeed, a minority of our sudden death events (n = 17) were considered likely of cardiovascular origin, given the instantaneous collapse linked to physical exertion, even though a precise cause of death could not be assigned due to ambiguous (or absent) autopsy findings. Nevertheless, some of these latter deaths could have been due to noncardiac causes, a potential source for overestimating our sudden death rates. Alternatively, the small subset of athletes for whom diagnosis remained unresolved (n = 16) could possibly have included cardiovascular disease–related deaths and in this way underestimated the incidence of sudden deaths.
Available estimates of the at-risk athlete population (i.e., the denominator) have limitations, given that we and other investigators (7) are obligated to use NCAA data expressed as participations, rather than for individual participants. With the possibility of multisport involvement by a small minority of athletes, there is the potential for overestimating the at-risk population and thereby underestimating the incidence of sudden death. In addition, ion channelopathies (e.g., LQTS, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia), which are important but uncommon causes of sudden death, are unlikely to be identified within a forensic-based registry such as ours due to the characteristic absence of structural cardiac abnormalities. This issue underscores the advantage of expert cardiac pathologist assessment of autopsy findings in sudden deaths of young athletes (25). The general level of expertise for cardiovascular pathology in the U.S. medical examiner community has been questioned (24).
African-American college athletes were at 5-fold greater risk for cardiovascular sudden death than white athletes (16). However, this sudden death rate in African-American athletes did not differ from the general population of the same age and race. For male athletes, mortality rates for cardiovascular disease, as well as suicide and drugs, exceeded that in female athletes (3- to 6-fold), consistent with reports in other athlete populations (1,3,8,9,15,16). Determinants of such racial and sex differences remain unresolved.
Our data do not focus primarily on the current controversy regarding the most effective pre-participation screening strategy for detection of cardiovascular disease (2–7,10–15). However, certain inferences are unavoidable. In particular, our findings underscore the frequency and importance of false-negative results, whether screening is limited to history taking and physical examination or includes a 12-lead ECG (i.e., the principle that not all at-risk athletes are detectable by screening) (1,3,4,9,26). Based on autopsy confirmation of cause of death, approximately 60% of the athletes in our study cohort would probably have been identified by a screening 12-lead ECG. However, we also estimate that at least 40% would likely have been “false-negative” findings, not reliably suspected by 12-lead ECGs (26).
NCAA student-athletes do not seem to be at unique or particularly high risk for sudden death due to unsuspected cardiovascular disease. Furthermore, the relative importance of suicide and drug deaths reported here with respect to the health and safety of college athletes suggests that there may be a disproportionate focus on cardiovascular disease in this population. These observations support the principle of enhanced resources and energy for suicide prevention and control of drug use, as well as wider dissemination of automatic external defibrillators for secondary prevention of cardiovascular sudden death. Such initiatives may best serve the overall public health of college student-athletes.
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Abbreviations and Acronyms
- confidence interval
- long QT syndrome
- National Collegiate Athletic Association
- Received November 13, 2013.
- Revision received January 15, 2014.
- Accepted January 20, 2014.
- American College of Cardiology Foundation
- Maron B.J.,
- Thompson P.D.,
- Ackerman M.J.,
- et al.
- Chaitman B.R.
- Myerburg R.J.,
- Vetter V.L.
- Steinvil A.,
- Chundadze T.,
- Zeltser D.,
- et al.
- Harmon K.G.,
- Asif I.M.,
- Klossner D.,
- Drezner J.A.
- Corrado D.,
- Pelliccia A.,
- Bjørnstad H.H.,
- et al.
- Holst A.G.,
- Winkel B.G.,
- Theilade J.,
- et al.
- Thiene G.,
- Corrado D.,
- Schiavon M.,
- Basso C.
- Corrado D.,
- Pelliccia A.,
- Heidbuchel H.,
- et al.
- Maron B.J.,
- Doerer J.J.,
- Haas T.S.,
- Tierney D.M.,
- Mueller F.O.
- Maron B.J.,
- Carney K.P.,
- Lever H.M.,
- et al.
- DeHass D.M.
- Zgonc E.
- Turner J.C.,
- Leno E.C.,
- Keller A.
- Basso C.,
- Thiene G.,
- Mackey-Bojack S.,
- et al.
- Maron B.J.,
- Gohman T.E.,
- Aeppli D.
- Papadakis M.,
- Ragu H.,
- Behr E.R.,
- et al.
- ↵National Weather Service. Lightning fatalities by state, 2002-2011. Available at: http://www.lightningsafety.noaa.gov/stats/02-11_deaths_by_state.pdf. Accessed May 6, 2013.
- ↵Centers for Disease Control and Prevention, National Center for Health Statistics. Multiple cause of death 2005-2006 on CDC WONDER on-line database, released February 2010. Data are from the Multiple Cause of Death Files, 2005-2006, as compiled from data provided by the 57 vital statistics jurisdictions through the Vital Statistic Cooperative Program. Available at: http://wonder.cdc.gov/mcd-icd10-archive2006.html. Accessed January 20, 2014.
- ↵Colorado Avalanche Information Center. Fatalities by age, 1996-2006. Available at: http://avalanche.state.co.us/wp-content/uploads/2013/09/Slide10.jpg. Accessed January 9, 2014.