Mechanistic Insights Into Reduced Arrhythmia Prevalence in Female Endurance Athletes

Female athletes exhibit lower rates of atrial fibrillation (AF) and sudden cardiac death compared with male athletes, but the mechanisms behind this sex disparity in arrhythmia risk remain unclear.

This study analyzed findings from Holter monitors, echocardiograms, and cardiac magnetic resonance imaging in a cohort of 397 endurance athletes enriched with prevalent AF. Athletes with cardiomyopathies, channelopathies, pre-excitation, and/or myocardial infarction were excluded.

Female athletes (n = 125; age 27 [18-47] years) had a lower prevalence of AF (6% vs 31%; P < 0.001) and nonsustained ventricular tachycardia (2% vs 11%; P = 0.004) than male athletes (n = 272; age 44 [22-61] years). Despite comparable exercise volume and sports duration, female athletes had lower maximal oxygen consumption. Female athletes had smaller age-adjusted left atrial volume (40 [34-47] mL/m² vs 44 [37-52] mL/m²; P = 0.007) and ventricular volume (indexed left ventricular end-diastolic volume: 98 ± 16 mL/m² vs 109 ± 21 mL/m²; P < 0.001; indexed right ventricular end-diastolic volume: 109 ± 20 mL/m² vs 123 ± 23 mL/m²; P < 0.001). Age-adjusted hinge (13% vs 24%; P = 0.120) and non-hinge-point (12% vs 20%; P = 0.875) fibrosis were equally prevalent between the sexes. Lower left ventricular mass, similar native T1 times, and higher extracellular volume in female athletes suggested less cardiomyocyte hypertrophy than in male athletes. Compared with a subset of 125 age-matched male athletes, female athletes had a similar prevalence of atrial and ventricular ectopy. Less bradycardia and lower resting and peak exercise blood pressure in female athletes suggested additional modulating factors.

Lower rates of AF and nonsustained ventricular tachycardia in female athletes may be attributed to smaller atrial and ventricular volumes and reduced cardiomyocyte hypertrophy, although there are likely additional modulating factors. A comparable prevalence of ectopy suggests that the disparity in arrhythmia risk may be more attributable to differences in underlying substrate than arrhythmogenic triggers.