Abstract
It has been more than a decade since the 35th Bethesda Conference published guidelines recommending against competitive sports participation for individuals with hypertrophic cardiomyopathy (HCM).1 These recommendations are predicated on the view that vigorous physical exertion creates an unstable substrate that increases susceptibility to sudden cardiac death (SCD). But what precisely is the risk of SCD, and is it really higher in athletic compared with nonathletic patients with HCM? The overall incidence of SCD in young athletic cohorts is exceedingly low, ≈1 to 3:100 000 person years, and is similar to the frequency of SCD in the young general population. Despite this finding, HCM has been thought to convey a disproportionately high risk because of early registry reports that HCM was the most common cause of SCD in young athletes. However, several subsequent studies have challenged this statistic. In the US National Collegiate Athletic Association, HCM accounted for only 8% of all sudden deaths. In a meta-analysis of retrospective cohort studies, registries, and autopsy series (1990–2014), structurally normal hearts were the most common finding on autopsies of young victims of SCD (26.7%; 95% confidence interval [CI], 21.0–32.3), with HCM attributed to a much smaller proportion (10.3%; 95% CI, 8.0–12.6).2 A structurally normal heart similarly represented the largest cohort (40%) of SCD in children and young adults in a prospective population study in Australia and New Zealand, even …
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