Arrhythmias and the athlete: mechanisms and clinical significance

We read with great interest the article by Ector et al.1 reporting ventricular arrhythmias (VA) in highly trained endurance athletes, originating from a mild right ventricular (RV) dysfunction. Of note, the authors conclude that endurance exercise may act as a promoter for RV changes and a resultant trigger for VA. In part, we agree with the authors' findings; however, we have some comments regarding the postulated cause and effect relationship between RV dysfunction and VA. An increased prevalence of arrhythmias in endurance-trained athletes has been noted previously, predominantly in veteran athletes.2 Several forms of idiopathic VA have been identified in athletes, which, by definition, originate in hearts without structural abnormalities.3 Unpublished observations from our laboratory at the CRY Centre for Sport Cardiology support these findings. The differentiation of pathological VA and benign VA originating in the right ventricle is important clinically when discussing prognosis and management options.4 This is of particular importance in the differentiation of right ventricular outflow tract-ventricular tachycardia (RVOT-VT) and arrhythmogenic right ventricular cardiomyopathy (ARVC) given the association of the latter with sudden death in athletes. We concur with hypothesis 1 proposed by Ector et al.1 in the difficulties associated with the differentiation of RVOT-VT and ARVC, particularly when the early concealed phase of ARVC is considered. A recent case in our laboratory highlighted this difficulty; however, the EP study was instrumental in the differential diagnosis, a finding that concurs with previous work in the field.4 The mechanism(s) underlying VA in endurance-trained athletes is unclear. Our group, and others, has demonstrated an elevation in cardiac troponins following endurance exercise5 and a concomitant but unrelated reduction in cardiac function.6 Although the presence of cardiac troponins is pathognemonic of cardiac damage, the rapid return of cardiac troponins to baseline (<24 h) has led to the suggestion that this phenomenon is physiological in nature. The impact of multiple episodes of prolonged exercise as experienced by highly trained and life-long endurance athletes however is not fully understood. Previous studies have reported myocardial fibrosis7 and heart failure8 in highly trained athletes. Our group recently investigated a case of sudden cardiac death in an experienced veteran Marathon runner. Post-mortem examination revealed widespread idiopathic interstitial myocardial fibrosis. In the absence of any other cause, we postulate that life-long, repetitive bouts of arduous physical activity may result in fibrous replacement of the myocardium, resulting in a pathological substrate for the propagation of arrhythmias. This proposed mechanism is supported in studies in non-ischaemic cardiomyopathy where myocardial damage leading to fibrosis has been implicated in myocardial re-entry leading to VA.9 Furthermore, previous studies have supported the view that conduction system abnormalities and arrhythmias in athletes may be associated with myocardial damage.10 Although these findings may be somewhat supportive of hypothesis 2 proposed by Ector et al.,1 we feel some care is warranted in the interpretation of the observed RV dysfunction. Long-standing VA can result in ventricular hypokinesis, leading to dysfunction. Following cardioversion through pharmacological or non-pharmacological means, a normal function is often restored. Ector et al.1 did not report the intervention employed or outcome in those athletes with VA, and this may be informative for the journal readership. In contrast to the conclusion of the authors, we propose a third hypothesis that the burden of long-standing sustained or non-sustained VA may lead to RV dysfunction. Furthermore, the mechanism(s) underlying the increased arrhythmia prevalence observed in endurance-trained athletes remains elusive. Future studies should aim to identify the potential mechanism(s), including interstial myocardial fibrosis.