Special Article - Exercise-induced right ventricular injury or arrhythmogenic cardiomyopathy (ACM): The bright side and the dark side of the moon.


Por: Leischik R, Dworrak B, Strauss M, Horlitz M, Pareja-Galeano H, de la Guía-Galipienso F, Lippi G, Lavie CJ, Perez MV and Sanchis-Gomar F

Publicada: 1 sep 2020 Ahead of Print: 26 mar 2020
Categoría: Cardiology and cardiovascular medicine

Resumen:
There is still debate on the range of normal physiologic changes of the right ventricle or ventricular (RV) function in athletes. Genetic links to arrhythmogenic cardiomyopathy (ACM) are well-established. There is no current consensus on the importance of extensive exercise and exercise-induced injury to the RV. During the intensive exercise of endurance sports, the cardiac structures adapt to athletic load over time. Some athletes develop RV cardiomyopathy possibly caused by genetic predisposition, whilst others develop arrhythmias from the RV. Endurance sports lead to increased volume and pressure load in both ventricles and increased myocardial mass. The extent of volume increase and changes in myocardial structure contribute to impairment of RV function and pose a challenge in cardiovascular sports medicine. Genetic predisposition to ACM may play an important role in the risk of sudden cardiac death of athletes. In this review, we discuss and evaluate existing results and opinions. Intensive training in competitive dynamic/power and endurance sports leads to specific RV adaptation, but physiological adaptation without genetic predisposition does not necessarily lead to severe complications in endurance sports. Discriminating between physiological adaptation and pathological form of ACM or RV impairment provoked by reinforced exercise presents a challenge to clinical sports cardiologists.

Filiaciones:
Leischik R:
 Department of Cardiology, Section Prevention and Sports Medicine, School of Medicine, Faculty of Health, Witten/Herdecke University, 58095 Witten, Germany

Dworrak B:
 Department of Cardiology, Section Prevention and Sports Medicine, School of Medicine, Faculty of Health, Witten/Herdecke University, 58095 Witten, Germany

Strauss M:
 Department of Cardiology I - Coronary and Peripheral Vascular Disease, Heart Failure Medicine, University Hospital Muenster, Cardiol, 48149 Muenster, Germany

Horlitz M:
 Department of Cardiology, Section Prevention and Sports Medicine, School of Medicine, Faculty of Health, Witten/Herdecke University, 58095 Witten, Germany

Pareja-Galeano H:
 Facultad de Ciencias del Deporte y Fisioterapia, Universidad Europea, 28670 Madrid, Spain

:
 Cardiology Service of Marina Baixa Hospital, Alicante, Spain

 REMA Sports Cardiology Clinic, 03700 Denia, Alicante, Spain

Lippi G:
 Section of Clinical Biochemistry, University of Verona, 37134 Verona, Italy

Lavie CJ:
 John Ochsner Heart and Vascular Institute, Ochsner Clinical School, The University of Queensland School of Medicine, 70121 New Orleans, LA, USA

Perez MV:
 Division of Cardiovascular Medicine, Stanford University School of Medicine, 94305-5110 Stanford, CA, USA

Sanchis-Gomar F:
 Division of Cardiovascular Medicine, Stanford University School of Medicine, 94305-5110 Stanford, CA, USA

 Department of Physiology, Faculty of Medicine, University of Valencia and INCLIVA Biomedical Research Institute, 46010 Valencia, Spain
ISSN: 00330620





PROGRESS IN CARDIOVASCULAR DISEASES
Editorial
W. B. Saunders Co., Ltd., United States, Estados Unidos America
Tipo de documento: Article
Volumen: 63 Número: 5
Páginas: 671-681
WOS Id: 000594976100016
ID de PubMed: 32224113
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