Ventricular Arrhythmias in Athletes: Most Often a Right Ventricular Origin

Athletic performance tests the limits of the human body and mind. Awe-inspiring achievements is what makes sports so fascinating. It is well appreciated however that top-level sports may sometimes overtax the body, and can lead to injuries, most notably of musculo-skeletal nature. This paper defends the thesis that the heart can also develop sports injuries at the ventricular level. We will elaborate on our hypothesis, originally put forward in 2003, that intense endurance activities put a particularly high strain on the right ventricle (RV), which over time, may lead to a proarrhythmic state resembling right (or less often) left ventricular cardiomyopathy. This can develop even in the absence of underlying demonstrable genetic abnormalities, probably just as a result of excessive RV wall stress during exercise. The syndrome of ‘exercise-induced arrhythmogenic RV cardiomyopathy’ may easily be overlooked. Sports cardiologists, like orthopaedic specialists, should be prepared to realise that excessive sports activity can lead to cardiac sports injuries in some, which will help to council on safe participation in all. INTRODUCTION Ventricular arrhythmias in athletes are rare, but by nature they may be life threatening. Physical activity is associated by a 2.5 times increased risk for sudden death.1 The classical concept is that arrhythmic events are due to underlying (structural or electrical) heart disease, on which physical activity acts as a trigger for initiation of arrhythmias. Indeed, many autonomic and metabolic modulators are infl uenced by exercise, and may create the milieu for initiation and maintenance of ventricular arrhythmias. A multitude of underlying cardiovascular conditions have been shown to predispose an athlete to exercise-related sudden death in multiple registries.1 2 We presented a second, additional, hypothesis in 2003, postulating that intense endurance activities may lead to cardiac alterations due to a particularly high strain on the right ventricle (RV).3 Excessive RV strain may lead to minor cell damage after an endurance event, as evidenced by cardiac enzyme elevations that are very commonly observed after endurance competition. Over time, repetitive injury may lead to changes that resemble right (or less often) left ventricular (LV) cardiomyopathy, even in the absence of underlying demonstrable genetic abnormalities. The syndrome of ‘exercise-induced arrhythmogenic RV cardiomyopathy’ may have been overlooked and under-recognised in prior series. The aim of this article is to describe the pathophysiological fi ndings that support the hypothesis of ‘exerciseinduced arrhythmogenic right ventricular cardiomyopathy (ARVC)’. VENTRICULAR ARRHYTHMIAS IN ATHLETES: MOST OFTEN A RIGHT VENTRICULAR ORIGIN Sudden death in athletes usually is the result of ventricular tachy-arrhythmias. The most common underlying cardiovascular abnormalities that have been identifi ed in younger athletes (<35 year) are hypertrophic cardiomyopathy, coronary anomalies, ARVC, myocarditis and channelopathies, while silent coronary artery disease is the main cause in athletes over 35 years.1 2 Given this distribution of underlying disease, we were puzzled by fi ndings in 46 high-level endurance athletes (performing ≥3×2 h of sports per week for more than 5 years; 80% competitive; 80% cyclists) that were referred to us for evaluation in the context of aspecifi c symptoms like palpitations and dizziness, but that could later be attributed through work-up to ventricular arrhythmias.3 The great majority of those ventricular arrhythmias (86%) had a RV origin (ie, with left bundle branch block morphology in the right precordial leads), which would not be expected based on the mentioned underlying pathologies, which statistically would have a much higher probability of inducing arrhythmias of LV origin. Nevertheless, the arrhythmic outcome, although clinically mild at presentation, proved to have an ominous course: after a medium follow-up of 4.7 years, 18 out of 46 had a major rhythm disorder, of which 9 were (aborted) sudden deaths (all cyclists; a mean of 3 years after presentation). Only an electrophysiological study inducing re-entrant arrhythmias was predictive for later arrhythmic events outcome (RR 3.4; p=0.02), pointing to an underlying structural substrate. Although the athletes presented with RV arrhythmias, overt structural fi ndings of ARVC were less frequently present than seen in familial forms. Only 1/46 had a familial history. Nevertheless, many of them showed other electrical signs of right ventricular changes like deep negative T-waves in the right precordial leads up to or even beyond V3, or the presence of late potentials on the signal averaged ECG (each about 40%).3 Combining major and minor criteria of the (original) ARVC diagnostic framework, 59% had manifest ARVC and an additional 30% had probable ARVC.4 It is of interest that others have also noted that asymptomatic athletes, and especially endurance athletes, develop changes on 1Department of Cardiovascular Sciences, University Hospital Leuven, Leuven, Belgium 2Department of Medicine, University of Melbourne, Melbourne, Australia Correspondence to Hein Heidbuchel, Department of Cardiovascular Sciences – Arrhythmology, University Hospital Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium; Hein.Heidbuchel@ uz.kuleuven.ac.be Received 9 March 2012 Accepted 21 May 2012 Ventricular arrhythmias associated with long-term endurance sports: what is the evidence? Hein Heidbuchel,1 David L Prior,2 André La Gerche1,2 bjsports-2012-091162.indd 1 9/27/2012 9:18:40 PM i44 Br J Sports Med 2012;46(Suppl I):i44–i50. doi:10.1136/bjsports-2012-091162 Current updates OPEN ACCESS group.bmj.com on April 28, 2017 Published by http://bjsm.bmj.com/ Downloaded from