Exercise-induced right ventricular dysfunction is associated with ventricular arrhythmias in endurance athletes.
Andre La Gerche, Guido Claessen, Steven Dymarkowski, Jens-Uwe Voigt, Frederik De Buck, Luc Vanhees, Walter Droogne, Johan Van Cleemput, Piet Claus, Hein Heidbuchel
Author Information
Andre La Gerche: Department of Cardiovascular Medicine, University Hospitals Leuven, Leuven, Belgium Sports Cardiology, Baker IDI Heart and Diabetes Institute, 75 Commercial Road, Melbourne, VIC 3004, Australia St. Vincent's Hospital Melbourne, Fitzroy, Australia andre.lagerche@bakeridi.edu.au.
Guido Claessen: Department of Cardiovascular Medicine, University Hospitals Leuven, Leuven, Belgium.
Steven Dymarkowski: Department of Radiology, University Hospitals Leuven, Leuven, Belgium.
Jens-Uwe Voigt: Department of Cardiovascular Medicine, University Hospitals Leuven, Leuven, Belgium.
Frederik De Buck: Department of Anesthesiology, University Hospitals Leuven, Leuven, Belgium.
Luc Vanhees: Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium.
Walter Droogne: Department of Cardiovascular Medicine, University Hospitals Leuven, Leuven, Belgium.
Johan Van Cleemput: Department of Cardiovascular Medicine, University Hospitals Leuven, Leuven, Belgium.
Piet Claus: Department of Cardiovascular Imaging and Dynamics, KU Leuven, Leuven, Belgium.
Hein Heidbuchel: Hasselt University and Heart Center, Jessa Hospital, Hasselt, Belgium.
AIMS: Intense exercise places disproportionate strain on the right ventricle (RV) which may promote pro-arrhythmic remodelling in some athletes. RV exercise imaging may enable early identification of athletes at risk of arrhythmias. METHODS AND RESULTS: Exercise imaging was performed in 17 athletes with RV ventricular arrhythmias (EA-VAs), of which eight (47%) had an implantable cardiac defibrillator (ICD), 10 healthy endurance athletes (EAs), and seven non-athletes (NAs). Echocardiographic measures included the RV end-systolic pressure-area ratio (ESPAR), RV fractional area change (RVFAC), and systolic tricuspid annular velocity (RV S'). Cardiac magnetic resonance (CMR) measures combined with invasive measurements of pulmonary and systemic artery pressures provided left-ventricular (LV) and RV end-systolic pressure-volume ratios (SP/ESV), biventricular volumes, and ejection fraction (EF) at rest and during intense exercise. Resting measures of cardiac function were similar in all groups, as was LV function during exercise. In contrast, exercise-induced increases in RVFAC, RV S', and RVESPAR were attenuated in EA-VAs during exercise when compared with EAs and NAs (P < 0.0001 for interaction group × workload). During exercise-CMR, decreases in RVESV and augmentation of both RVEF and RV SP/ESV were significantly less in EA-VAs relative to EAs and NAs (P < 0.01 for the respective interactions). Receiver-operator characteristic curves demonstrated that RV exercise measures could accurately differentiate EA-VAs from subjects without arrhythmias [AUC for ΔRVESPAR = 0.96 (0.89-1.00), P < 0.0001]. CONCLUSION: Among athletes with normal cardiac function at rest, exercise testing reveals RV contractile dysfunction among athletes with RV arrhythmias. RV stress testing shows promise as a non-invasive means of risk-stratifying athletes.
