Andre La Gerche1, Guido Claessen2, Steven Dymarkowski3, Jens-Uwe Voigt2, Frederik De Buck4, Luc Vanhees5, Walter Droogne2, Johan Van Cleemput2, Piet Claus6, Hein Heidbuchel7. 1. 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. 2. Department of Cardiovascular Medicine, University Hospitals Leuven, Leuven, Belgium. 3. Department of Radiology, University Hospitals Leuven, Leuven, Belgium. 4. Department of Anesthesiology, University Hospitals Leuven, Leuven, Belgium. 5. Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium. 6. Department of Cardiovascular Imaging and Dynamics, KU Leuven, Leuven, Belgium. 7. Hasselt University and Heart Center, Jessa Hospital, Hasselt, Belgium.
Abstract
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. Published on behalf of the European Society of Cardiology. All rights reserved.
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. Published on behalf of the European Society of Cardiology. All rights reserved.
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