Purpose of review

This review will summarize the distinction between hypertrophic cardiomyopathy (HCM) and exercise-induced cardiac remodeling (EICR), describe treatments of particular relevance to athletes with HCM, and highlight the evolution of recommendations for exercise and competitive sport participation relevant to individuals with HCM.

Recent findings

Whereas prior guidelines have excluded individuals with HCM from more than mild-intensity exercise, recent data show that moderate-intensity exercise improves functional capacity and indices of cardiac function and continuation of competitive sports may not be associated with worse outcomes. Moreover, recent studies of athletes with implantable cardioverter defibrillators (ICDs) demonstrated a safer profile than previously understood. In this context, the updated American Heart Association/American College of Cardiology (AHA/ACC) and European Society of Cardiology (ESC) HCM guidelines have increased focus on shared decision-making and liberalized restrictions on exercise and sport participation among individuals with HCM.

Summary

New data demonstrating the safety of exercise in individuals with HCM and in athletes with ICDs, in addition to a focus on shared decision-making, have led to the most updated guidelines easing restrictions on exercise and competitive athletics in this population. Further athlete-specific studies of HCM, especially in the context of emerging therapies such as mavacamten, are important to inform accurate risk stratification and eligibility recommendations.

Background Habitual high-intensity endurance exercise is associated with increased atrial fibrillation (AF) risk and impaired cardiac conduction. It is unknown whether these observations extend to prior strength-type sports exposure. The primary aim of this study was to compare AF prevalence in former National Football League (NFL) athletes to population-based controls. The secondary aim was to characterize other conduction system parameters. Methods and Results This cross-sectional study compared former NFL athletes (n=460, age 56±12 years, black 47%) with population-based controls of similar age and racial composition from the cardiovascular cohort Dallas Heart Study-2 (n=925, age 54±9 years, black 53%). AF was present in 28 individuals (n=23 [5%] in the NFL group; n=5 [0.5%] in the control group). After controlling for other cardiovascular risk factors in multivariable regression analysis, former NFL participation remained associated with a 5.7 (95% CI: 2.1-15.9, P<0.001) higher odds ratio of AF. Older age, higher body mass index, and nonblack race were also independently associated with higher odds ratio of AF, while hypertension and diabetes mellitus were not. AF was previously undiagnosed in 15/23 of the former NFL players. Previously undiagnosed NFL players were rate controlled and asymptomatic, but 80% had a CHA₂DS₂-VASc score ≥1. Former NFL players also had an 8-fold higher prevalence of paced cardiac rhythms (2.0% versus 0.25%, P<0.01), compared with controls. Furthermore, former athletes had lower resting heart rates (62±11 versus 66±11 beats per minute, P<0.001), and a higher prevalence of first-degree atrioventricular block (18% versus 9%, P<0.001). Conclusions Former NFL participation was associated with an increased AF prevalence and slowed cardiac conduction when compared with a population-based control group. Former NFL athletes who screened positive for AF were generally rate controlled and asymptomatic, but 80% should have been considered for anticoagulation based on their stroke risk.