Pathogeneses of sudden cardiac death in national collegiate athletic association athletes

Academic Article


  • Background-The pathogenesis of sudden cardiac death in college athletes has not been defined by systematic case identification. Methods and Results-A total of 45 cases of sudden cardiac death were identified in National Collegiate Athletic Association (NCAA) athletes from 2004 to 2008 based on an internal reporting system and review of media reports. Autopsy reports were reviewed and adjudicated by a multidisciplinary panel. Cause of death could be reasonably determined in 36 cases; 3 athletes had no autopsy, 5 autopsy reports could not be obtained, and 1 autopsy had insufficient information to determine cause of death. The most common finding at death was a structurally normal heart or autopsy-negative sudden unexplained death (11, 31%), followed by coronary artery abnormalities (5, 14%), dilated cardiomyopathy (3, 8%), myocarditis related (3, 8%), aortic dissection (3, 8%), and idiopathic left ventricular hypertrophy/possible hypertrophic cardiomyopathy (HCM; 3, 8%). There was 1 case each (3%) of hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, long QT syndrome, commotio cordis, and Kawasaki disease. There was 1 case of death in a sickle cell positive athlete who also had left ventricular hypertrophy. The adjudicated diagnosis agreed with the official pathology report in only 59% of cases. Conclusions-Unexplained death with a structurally normal heart is the most common finding after suspected sudden cardiac death in NCAA athletes. Hypertrophic cardiomyopathy is infrequently seen, and conclusions in autopsy reports may not accurately reflect the pathological findings. Standardized protocols for cardiovascular autopsies in athletes are needed, including postmortem genetic testing, particularly in autopsy-negative cases. © 2014 American Heart Association, Inc.
  • Authors

    Digital Object Identifier (doi)

    Pubmed Id

  • 15085859
  • Author List

  • Harmon KG; Drezner JA; Maleszewski JJ; Lopez-Anderson M; Owens D; Prutkin JM; Asif IM; Klossner D; Ackerman MJ
  • Start Page

  • 198
  • End Page

  • 204
  • Volume

  • 7
  • Issue

  • 2