A prospective study of 106 veteran male endurance athletes found that myocardial fibrosis – heart scarring – was significantly associated with the development of ventricular arrhythmia over a median follow-up of 720 days.
The study enrolled asymptomatic cyclists and triathletes aged 50 years and older who had competed regularly for at least 15 years and trained for a minimum of 10 hours per week. All participants were free of known cardiovascular disease and underwent cardiovascular magnetic resonance (CMR) imaging and implantable loop recorder (ILR) monitoring.
Of the 106 athletes, 50 of 106 (47.2%) had focal myocardial fibrosis identified by late gadolinium enhancement CMR imaging. All fibrosis was nonischemic and primarily affected the basal inferolateral segment of the left ventricle in 44 of 50 (88.0%) athletes. In contrast, 3 of 27 (11.1%) age-matched nonathletic controls had fibrosis (P < .001).
During follow-up, 23 athletes (21.7%) experienced at least one ventricular arrhythmia, including 3 (2.8%) with sustained ventricular tachycardia and 20 athletes (18.9%) with nonsustained ventricular tachycardia. Among those with arrhythmias, 18 of 23 (78.3%) had myocardial fibrosis. All athletes with sustained ventricular tachycardia had fibrosis detected on CMR.
Myocardial fibrosis was independently associated with arrhythmic risk. In univariate Cox regression, fibrosis was linked to ventricular arrhythmia (hazard ratio [HR] = 4.7; 95% confidence interval [CI] = 1.8–12.8; P = .002). This association remained significant after adjusting for left ventricular end-diastolic volume indexed (LVEDVi), with an adjusted HR of 4.7 (95% CI = 1.7–12.7; P = .002). Athletes with arrhythmia had higher mean LVEDVi (113 ± 18 mL/m²) than those without (106 ± 13 mL/m²; P = .04).
Premature ventricular contractions (PVCs) during exercise were more common among athletes with fibrosis (35 of 49 [71.4%]) compared to those without (21 of 50 [42.0%]; P = .003). Atypical PVC features were also more frequent in athletes with fibrosis (23 of 49 [46.9%] vs 9 of 50 [18.0%]; P = .002). PVCs during exercise were associated with future arrhythmia (HR = 3.9; 95% CI, 1.32–11.4; P = .01).
Right ventricular insertion point (RVIP) fibrosis was not significantly associated with arrhythmia. It was found in 19 of 23 (82.6%) athletes with arrhythmia and 60 of 83 (72.3%) without (P = .32).
Participants did not show evidence of inducible ischemia, myocardial infarction, or acute myocarditis. Resting and stress myocardial blood flow, myocardial perfusion reserve, and T2 values were similar across groups.
The findings suggest that myocardial fibrosis in older endurance athletes may be a marker of arrhythmic risk. Further research is needed to determine whether the fibrosis is a direct cause of arrhythmia or a sign of an underlying heart muscle disease.
The authors reported no conflicts of interest.