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The right heart in athletes

Evidence for exercise-induced arrhythmogenic right ventricular cardiomyopathy

Das rechte Herz beim Sportler

Hinweise auf sportinduzierte arrhythmogene rechtsventrikuläre Kardiomyopathie

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Abstract

Although ‘athlete’s heart’ usually constitutes a balanced dilation and hypertrophy of all four chambers, there is increasing evidence that intense endurance activity may particularly tax the right ventricle (RV), both acutely and chronically. We review the evidence that the high wall stress of the RV during intense sports may explain observed B-type natriuretic peptide (BNP) elevations immediately after a race, may lead to cellular disruption and leaking of cardiac enzymes, and may even result in transient RV dilatation and dysfunction. Over time, this could lead to chronic remodelling and a pro-arrhythmic state resembling arrhythmogenic RV cardiomyopathy (ARVC) in some cases. ARVC in high-endurance athletes most often develops in the absence of underlying desmosomal abnormalities, probably only as a result of excessive RV wall stress during exercise. Therefore, we have labelled this syndrome ‘exercise-induced ARVC’. Sports cardiologists should be aware that excessive sports activity can lead to cardiac sports injuries in some individuals, just like orthopaedic specialists are familiar with musculoskeletal sports injuries. This does not negate the fact that moderate exercise has positive cardiovascular effects and should be encouraged.

Zusammenfassung

Das „Sportlerherz” weist zwar normalerweise eine ausgewogene Dilatation und Hypertrophie aller 4 Kammern auf, aber es gibt zunehmend Belege dafür, dass starke Ausdaueraktivität vor allem den rechten Ventrikel (RV) sowohl akut als auch chronisch strapazieren kann. Hier werden Hinweise darauf diskutiert, dass die hohe Wandbelastung des RV während starker sportlicher Aktivität Erhöhungen des natriuretischen Peptids vom B-Typ (BNP) unmittelbar nach einem Wettkampf erklären, zur Zerstörung der Zellhüllen sowie Freisetzung von Herzenzymen und selbst zur transienten RV-Dilatation und -funktionsstörung führen kann. Mit der Zeit kann dies sogar zum chronischen Remodelling und einer proarrhythmischen Situation führen, die bei manchen einer arrhythmogenen RV-Kardiomyopathie (ARVC) ähnelt. Zumeist entsteht dies ohne zugrunde liegende Desmosomenanomalitäten, wahrscheinlich einfach als Ergebnis ausgeprägter RV-Wandbelastung während des Sports. Daher haben wir dieses Syndrom „sportinduzierte ARVC“ genannt. Sportkardiologen sollten vor Augen haben, dass übermäßige sportliche Aktivität bei manchen zu kardialen Sportverletzungen führen kann, genauso wie Orthopäden mit muskuloskelettalen Sportverletzungen vertraut sind. Dies spricht nicht gegen die Tatsache, dass mäßige sportliche Aktivität nur positive kardiovaskuläre Auswirkungen hat und jeder dazu ermutigt werden sollte.

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Funding and potential conflicts of interest

Publication of this article was not funded.

H.H. is holder of the AstraZeneca Chair in Cardiac Electrophysiology, University of Leuven. H.H. received research funding through the University of Leuven from Siemens Medical Solutions. H.H. is Coordinating Clinical Investigator for the Biotronik-sponsored EuroEco study on health economics of remote device monitoring. H.H. is a member of the scientific advisory board of Biosense Webster, Inc., St Jude Medical, Inc., Siemens Medical Solutions, Boehringer-Ingelheim, Bayer and Sanofi-Aventis, and receives unconditional research grants through the University of Leuven from St Jude Medical, Medtronic, Biotronik and Boston Scientific Inc.

A.L.G. receives a post-doctoral research scholarship from the Australian National Health and Medical Research Council.

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  1. Department of Cardiovascular Medicine, Cardiology – Electrophysiology, University Hospital Gasthuisberg, University of Leuven, Herestraat 49, 3000, Leuven, Belgium

    H. Heidbüchel M.D., Ph.D. & A. La Gerche

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  1. H. Heidbüchel M.D., Ph.D.
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  2. A. La Gerche
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Correspondence to H. Heidbüchel M.D., Ph.D..

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Heidbüchel, H., La Gerche, A. The right heart in athletes. Herzschr. Elektrophys. 23, 82–86 (2012). https://doi.org/10.1007/s00399-012-0180-3

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