Skip main navigation

Sudden Death in Female Athletes: Insights From a Large Regional Registry in the United Kingdom

Originally publishedhttps://doi.org/10.1161/CIRCULATIONAHA.121.055535Circulation. 2021;144:1827–1829

    Sudden cardiac death (SCD) in sport often affects apparently healthy individuals.1 There is consistency among studies that women are less prone to exercise-related SCD than men,2,3 but knowledge pertaining to the specific cause and precipitating circumstance is sparse. The increase in the number of women who participate in various sports, including disciplines historically dominated by men, calls for a more focused perspective surrounding exercise-related SCDs in female athletes. We investigated the causes and circumstances of SCD in a large cohort of female athletes in whom cardiac autopsy was conducted by an expert cardiac pathologist.

    We reviewed a database of 6847 cases of SCD that were referred to the Cardiac Risk in the Young, a center for cardiac pathology at St George’s, University of London, between 1994 and 2020. SCD was defined as death occurring within 12 hours of apparent well-being. We retrieved a subgroup of 748 (10.9%) decedents who engaged in sport activities, defined as >3 hours of organized physical training per week. Clinical information was obtained from referring coroners. All cases underwent detailed autopsy evaluation of the heart, including histologic analysis, by expert cardiac pathologists. A minimum of 10 blocks of tissue were taken for histologic analysis as reported previously.4 Results are expressed as mean±SD for continuous variables or as number of cases and percentage for categorical variables. Ethical and research governance approval has been granted for this study (10/H0724/38).

    Women constituted 98 (13%) of the 748 SCDs among individuals who engage in regular sports activities. There were no differences in the mean age at death between women and men (31±15 vs 32±14 years; P=0.573). The heart weight was lower in women (333±89 vs 433±122 g; P<0.001). A total of 41 (42%) female decedents were competitive athletes who participated in team (n=20) or individual (n=21) sports. The remainder (n=57 [58%]) participated in recreational sport. Sporting disciplines included running (n=16 [16%]), gym activities (n=14 [14%]), regular physical exercise/athletics (n=13 [13%]), and swimming (n=10 [10%]). The majority were asymptomatic (n=85 [87%]); 13 (13%) were symptomatic (5 had syncope, 4 had palpitations, 3 had chest pain, and 1 complained of decreased exercise tolerance). Cardiac investigations in these athletes did not lead to a diagnosis of potentially fatal cardiac disease. Four athletes had a preexisting cardiac diagnosis (dilated cardiomyopathy, hypertrophic cardiomyopathy, mitral valve prolapse, and complete heart block treated with a permanent pacemaker). All 4 of these individuals engaged in recreational sport.

    A normal autopsy indicative of sudden arrhythmic death syndrome (SADS) was the most common finding and accounted for 56 (57%) deaths (Figure). Myocardial disease was present in 23 (23%) cases: arrhythmogenic right ventricular cardiomyopathy accounted for 7 (7%) deaths, followed by idiopathic fibrosis (n=6 [6%]), hypertrophic cardiomyopathy (n=4 [4%]), dilated cardiomyopathy (n=4 [4%]), and idiopathic left ventricular hypertrophy (n=2 [4%]). Sex comparisons revealed that although SADS was the most prevalent cause of death in both sexes, it was more common in women (57% vs 43%; P=0.008). In contrast, myocardial disease was a less common cause of SCD in women compared with men (23% vs 37%; P=0.006).

    Figure.

    Figure. Causes of sudden cardiac death in male and female athletes. In the female athletes population, the subgroup classified as “other” (n=6) comprised cardiac tumor (n=1), Kawasaki syndrome (n=1), microinfarcts of unknown origin (n=1), and hypertensive disease (n=3). ARVC indicates arrhythmogenic right ventricular cardiomyopathy; CAA, coronary artery anomaly; CAD, coronary artery disease; CHD, coronary heart disease; DCM, dilated cardiomyopathy; HCM, hypertrophic cardiomyopathy; ILVF, idiopathic left ventricular fibrosis; ILVH, idiopathic left ventricular hypertrophy; SADS, sudden arrhythmic death syndrome; and VHD, valvular heart disease.

    Death during intense exertion occurred less frequently in women compared with men (57 [58%] vs 538 [83%]; P<0.001). In women, SCD during exercise most commonly occurred during swimming (n=14).

    The data that support the findings of this study are available from the corresponding author on reasonable request.

    Whereas previous studies on SCD in sports have focused on male athletes, this study reports on SCD in young (≤35 years old) female athletes in the United Kingdom. In agreement with previous studies,2,3 SCD was less prevalent in female athletes than in male athletes. A structurally normal heart (suggestive of SADS) was the most common autopsy finding in female decedents and accounted for more than half of all deaths. In our experience, a high proportion of all SADS deaths can be attributable to primary arrhythmia syndromes.5 Deaths from myocardial disease were less common in women. There was a striking lower prevalence of specific conditions such as hypertrophic cardiomyopathy, myocarditis, and idiopathic left ventricular hypertrophy in female decedents. Whether a higher concentration of circulating anabolic hormones potentiate pathologic hypertrophy in predisposed individuals or exacerbate myocardial inflammation after infection requires further exploration. Because our center is more likely to receive hearts from decedents where the clinical history is suggestive of an inherited cardiac disease, it is possible that pathologies such as coronary artery atherosclerosis may be underestimated in our cohort. A limitation of our study is the absence of genetic testing (molecular autopsy) in our cohort and the lack of premortem ECGs.

    More than 40% of female athletes die at rest or during daily activities. This finding combined with the high prevalence of SADS among SCD cases underscores the role of preventative strategies aimed at the early diagnosis of individuals at risk.

    Article Information

    Nonstandard Abbreviations and Acronyms

    SADS

    sudden arrhythmic death syndrome

    SCD

    sudden cardiac death

    Footnotes

    *M.N. Sheppard and S. Sharma contributed equally.

    For Sources of Funding and Disclosures, see page 1829.

    Circulation is available at www.ahajournals.org/journal/circ

    Correspondence to: Dr Mary N. Sheppard, Professor of Cardiovascular Pathology, St George’s University of London, Cardiovascular Sciences, Cranmer Terrace, London, SW17 0RE, United Kingdom. Email

    References

    • 1. Chandra N, Bastiaenen R, Papadakis M, Sharma S . Sudden cardiac death in young athletes: practical challenges and diagnostic dilemmas.J Am Coll Cardiol. 2013; 61:1027–1040. doi: 10.1016/j.jacc.2012.08.1032CrossrefMedlineGoogle Scholar
    • 2. Maron BJ, Doerer JJ, Haas TS, Tierney DM, Mueller FO . Sudden deaths in young competitive athletes: analysis of 1866 deaths in the United States, 1980–2006.Circulation. 2009; 119:1085–1092. doi: 10.1161/CIRCULATIONAHA.108.804617LinkGoogle Scholar
    • 3. Corrado D, Basso C, Rizzoli G, Schiavon M, Thiene G . Does sports activity enhance the risk of sudden death in adolescents and young adults?J Am Coll Cardiol. 2003; 42:1959–1963. doi: 10.1016/j.jacc.2003.03.002CrossrefMedlineGoogle Scholar
    • 4. Finocchiaro G, Papadakis M, Robertus JL, Dhutia H, Steriotis AK, Tome M, Mellor G, Merghani A, Malhotra A, Behr E, et al . Etiology of sudden death in sports: insights from a United Kingdom regional registry.J Am Coll Cardiol. 2016; 67:2108–2115. doi: 10.1016/j.jacc.2016.02.062CrossrefMedlineGoogle Scholar
    • 5. Papadakis M, Papatheodorou E, Mellor G, Raju H, Bastiaenen R, Wijeyeratne Y, Wasim S, Ensam B, Finocchiaro G, Gray B, et al . The diagnostic yield of Brugada syndrome after sudden death with normal autopsy.J Am Coll Cardiol. 2018; 71:1204–1214. doi: 10.1016/j.jacc.2018.01.031CrossrefMedlineGoogle Scholar

    eLetters(0)

    eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.

    Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.