Methods

The registry is a forensic database 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 31-year period (1980 to 2010), 2,462 such sudden deaths (and survivors of cardiac arrest) have been tabulated.

The registry population was identified by targeted searches using a variety of sources at the time each of these strategies became available during the duration of the study, including LexisNexis archival database. Athletes were included in the registry if 2 criteria were met: (1) participation in organized team or individual sports requiring regular competition, and placing a premium on excellence and achievement, and (2) sudden death at ≤39 years of age. A systematic tracking process was established to assemble detailed information on each case, including the complete autopsy report and pertinent clinical and demographic information.

Data are expressed as mean ± SD. Proportions were compared using chi-square or Fisher’s exact tests. Continuous variables were compared using unpaired Student’s t tests or Mann-Whitney rank-sum tests.

Results

There were 2,462 athlete deaths recorded in the registry as of December 2010. Ages ranged from 8 to 39 years (mean 18.7 ± 6); 1,459 patients were white (59%), 34 (1.4%) Asian, and 699 (28%) African American. The most common causes of death were blunt trauma (n = 476), commotio cordis (n = 98), and a variety of cardiovascular diseases (n = 1,396). The latter were most frequently hypertrophic cardiomyopathy (n = 375) and congenital coronary artery anomalies of wrong sinus origin (n = 131).

Notably, 23 of the deaths (0.9%) were in athletes with SCT, documented by testing during life or at autopsy; each of these athletes was African American ( Table 1 ). Ages ranged from 12 to 22 years (mean 18.6 ± 2.6); 21 (91%) were male. At the time of their deaths, these athletes were competing in organized college (n = 17), high school (n = 5), or junior high school (n = 1) sports.

The 23 athletes with SCT-related death represent 3.3% of 699 African American athletes in the registry. SCT diagnosis was made by solubility testing alone (n = 7, including 3 by newborn or university screening), hemoglobin electrophoresis alone (n = 10, 5 antemortem), or both (n = 6).

All athletes died under similar distinctive circumstances: noninstantaneous collapse with gradual but rapid deterioration (i.e., dyspnea, fatigue, weakness, and muscle cramping) over an estimated 10 to 45 minutes, associated with exertional rhabdomyolysis in 11. Each event occurred during vigorous or exhaustive maximal physical exertion, usually during training and conditioning (n = 22), or competition (n = 1), and often after brief sustained effort such as repetitive short-distance sprints or endurance running. SCT events were most common early in the conditioning season and in 6 cases were documented on the first day of practice.

Notably, SCT-deaths occurred predominately in football players (n = 19 of 23 [83%]), constituting 2.6% of all 723 deaths occurring in that sport and 7.0% of deaths in the 271 African American football players (i.e., 1 of 14). Other SCT-deaths occurred in basketball (n = 3) and track sprinting (n = 1).

SCT deaths were similar to other cardiovascular deaths in the registry with respect to age (mean 18.6 ± 2.6 vs 17.6 ± 5.0 years, p = 0.092) and gender (91% vs 88% male, p = 1.00) but were more common in African Americans (100% vs 37%, p <0.001). Deaths were most frequent in the summer and early autumn months of June to October (17 of 23 [74%]). Twenty of the 23 deaths (87%) occurred in southern or border states, most commonly Florida (n = 5), Texas (n = 4), Mississippi, North Carolina, and Ohio (n = 2 each).

Potential associated triggers for SCT collapse were environmental temperature (≥80°F) in 20 (87%) and high altitude in 2 (Albuquerque, New Mexico, and Tucson, Arizona), as well as maximum intensity of exercise. Four of the 23 athletes had associated structural cardiac abnormalities identified at autopsy: 2 with tunneled coronary arteries (1 left anterior descending and 1 right coronary), 1 with redundant mitral valve and features consistent with hypertrophic cardiomyopathy, and 1 with 80% right coronary artery narrowing by atherosclerosis. Heart weights ranged from 225 to 640 g (mean 423); 5 were >500 g. Largely on the basis of the circumstances of collapse, these features are unlikely to be the primary or a major cause of death.