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The timing and relationship of ventricular arrhythmia with exercise patterns in veteran male endurance athletes
Wasim Javed1, Benjamin Brown1, Bradley Chambers1
1Multidisciplinary Cardiovascular Research Centre and Department of Biomedical Imaging Science, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds/Leeds Teaching Hospitals National Health Service Trust, Clarendon Way, Leeds LS2 9JT, UK.
Aims:
The aim of this study was to determine whether exercise training patterns were associated with the incidence and timing of ventricular arrhythmia in veteran male endurance athletes.
Methods And Results:
One-hundred and six healthy male endurance athletes (cyclists/triathletes) aged ≥50 y undertaking ≥10 h/week of exercise for ≥15 y underwent clinical assessment, cardiac magnetic resonance (CMR), and implantable loop recorder (ILR) implantation. Daily exercise was tracked with computerized exercise tracking devices. Athletes were followed up for ventricular arrhythmia on ILR, ventricular tachycardia (VT), and non-sustained VT (NSVT). Fifty-five ventricular arrhythmia events occurred (median follow-up 796 days): 3 (5.5%) VT and 52 (94.5%) NSVT in 25 (23.5%) athletes. Myocardial fibrosis was significantly more prevalent in athletes with ventricular arrhythmia than those without ventricular arrhythmia [19 (76.0%) vs. 31 (38.3%), P < 001]. The incidence of exercise-related ventricular arrhythmia was 0.4/1000 h of exercise vs. non-exercise-related ventricular arrhythmia incidence of 0.01/1000 h of non-exercise. All three sustained VT cases occurred during exercise in athletes with fibrosis and were preceded by NSVT. There were no training differences between athletes with and without ventricular arrhythmia over 2 years and in the month prior to each arrhythmic event.
Conclusion:
A significant proportion of highly trained male veteran athletes developed ventricular arrhythmia which was predominantly NSVT and was strongly associated with myocardial fibrosis. Acute exercise exposure was associated with an increased risk of developing ventricular arrhythmia, but chronic exercise load was not. Our findings therefore highlight myocardial fibrosis as a potential pro-arrhythmic substrate upon which intense exercise may trigger arrhythmogenesis in certain male veteran athletes.
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