European Heart Journal Advance Access originally published online on May 4, 2007
European Heart Journal 2007 28(11):1401; doi:10.1093/eurheartj/ehm122
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Arrhythmias and the athlete: mechanisms and clinical significance: reply
Department of Cardiology
University Hospital Gasthuisberg
University of Leuven
Leuven
Belgium
Department of Cardiology
University Hospital Gasthuisberg
University of Leuven
Herestraat 49
B-3000 Leuven
Belgium
Tel: +32 16 34 34 69, Fax: +32 16 34 42 40, E-mail address: hein.heidbuchel{at}uz.kuleuven.ac.be
We would like to thank Dr Whyte and his coworkers for their interest in our study1 and their critical reflection on the cause and effect relationship between right ventricular (RV) dysfunction and ventricular arrhythmias (VA).
Tachycardia-induced cardiomyopathy is indeed a well-known entity, mainly as the result of incessant supraventricular tachyarrhythmias. A few reports have described reversible cardiomyopathy related to repetitive or persistent VA or very frequent ventricular ectopy.2–4 It is important to note, however, that these reversible cardiomyopathies were invariably associated with left ventricular dysfunction, whereas athletes with VA in our study had a normal left ventricular ejection fraction, which was comparable with athletes without VA. Moreover, all athletes in our study had paroxysmal and symptomatic episodes of VA. None had incessant VT or very frequent ventricular ectopy, which could explain a tachycardia-induced cardiomyopathy. Therefore, we think that the third hypothesis that Whyte and coworkers present for our findings is unlikely.
We concur that the mechanism of complex VA in endurance athletes is not yet elucidated and that it is always ambiguous to conclude that RV outflow tract ectopy is ‘idiopathic’ and benign. We previously highlighted the role of an electrophysiological study for risk stratification in athletes with VA, with induction of sustained ventricular tachycardia or ventricular fibrillation and a re-entry mechanism implicating a worse prognosis.5 On the basis of the current study, RV ejection fraction could be used as an additional and early risk stratification tool. The outcome of endurance athletes with complex VA was not the object of the present study, but our previous data5 noted the development of a major arrhythmic event in 18 of 46 high-level endurance athletes (sudden death in nine) presenting with complex VA after a median follow-up of 4.7 years. On the basis of these data and derived risk-stratification tools, 11 of 22 athletes with VA in the current study were treated with an implantable cardioverter-defibrillator, five of whom received at least one appropriate shock since implantation.
Concerning the possible mechanisms underlying RV dysfunction and/or arrhythmias, recent data have shown increased pulmonary artery pressures, increased RV dimensions, and decreased RV function (correlating with the release of cardiac troponin T) in recreational athletes completing the Boston marathon.6 The hypothesis that such life-long, repetitive bouts of physical activity could lead to myocardial fibrosis, cardiac dysfunction, and arrhythmias remains certainly to be proven. The finding of myocardial fibrosis as described in the case of a marathon runner by Whyte and coworkers can be non-specific, possibly due to other causes (like the late stage of myocarditis). The observation of acute RV dysfunction and the release of cardiac troponins after endurance-athletic events are nevertheless intriguing in the light of our findings and will definitely stimulate further research in this area.
References
- Ector J, Ganame J, Van der Merwe N, Adriaenssens B, Pison L, Willems R, Gewillig M, Heidbuchel H. Reduced right ventricular ejection fraction in endurance athletes presenting with ventricular arrhythmias: a quantitative angiographic assessment. Eur Heart J (2007) 28:345–353.
[Abstract/Free Full Text] - Grimm W, Menz V, Hoffmann J, Maisch B. Reversal of tachycardia induced cardiomyopathy following ablation of repetitive monomorphic right ventricular outflow tract tachycardia. Pacing Clin Electrophysiol (2001) 24:166–171.[CrossRef][Medline]
- Singh B, Kaul U, Talwar KK, Wasir HS. Reversibility of ‘tachycardia induced cardiomyopathy’ following the cure of idiopathic left ventricular tachycardia using radiofrequency energy. Pacing Clin Electrophysiol (1996) 19:1391–1392.[CrossRef][Medline]
- Vijgen J, Hill P, Biblo LA, Carlson MD. Tachycardia-induced cardiomyopathy secondary to right ventricular outflow tract ventricular tachycardia: improvement of left ventricular systolic function after radiofrequency catheter ablation of the arrhythmia. J Cardiovasc Electrophysiol (1997) 8:445–450.[ISI][Medline]
- Heidbuchel H, Hoogsteen J, Fagard R, Vanhees L, Ector H, Willems R, Van LJ. High prevalence of right ventricular involvement in endurance athletes with ventricular arrhythmias. Role of an electrophysiologic study in risk stratification. Eur Heart J (2003) 24:1473–1480.
[Abstract/Free Full Text] - Neilan TG, Januzzi JL, Lee-Lewandrowski E, Ton-Nu TT, Yoerger DM, Jassal DS, Lewandrowski KB, Siegel AJ, Marshall JE, Douglas PS, Lawlor D, Picard MH, Wood MJ. Myocardial injury and ventricular dysfunction related to training levels among nonelite participants in the Boston marathon. Circulation (2006) 114:2325–2333.
[Abstract/Free Full Text]
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