Cardiac Phenotypes and Risk Markers of Elite Athletes With Ventricular Arrhythmias
- The heart can physiologically adapt to exercise, but pathophysiologic adaptation may result in a dose-dependent manner.
- Using a multimodality approach, this study reports on cardiac phenotypes that overlap with characteristics of arrhythmogenic cardiomyopathy.
Can cardiac phenotypes and risk markers of life-threatening arrhythmic events be identified in athletes with ventricular arrhythmia?
This study enrolled consecutive competitive athletes referred for symptomatic ventricular arrhythmias and compared them to healthy controls using clinical data and cardiac imaging. Only the study group athletes were deconditioned for ≥6 weeks prior to imaging. No patients had family or genetic history of any discernable etiology of ventricular arrhythmia. Biventricular function was assessed by echocardiography. Cardiac magnetic resonance imaging (CMR) was used for right ventricular (RV) ejection fraction assessment and screening for inflammatory heart disease.
The authors included 43 athletes (16% female) with ventricular arrhythmias and 30 healthy control athletes (7% female). Athletes with ventricular arrhythmias had significantly worse RV function and increased late gadolinium enhancement (though not statistically significant). In the 23 (53%) athletes with ventricular arrhythmias who had had a history of life-threatening arrhythmic events (e.g., aborted cardiac arrest, sustained ventricular tachycardia, or appropriate implantable cardioverter-defibrillator therapy), worse left ventricular (LV) mechanical dispersion (defined as the standard deviation of time to peak strain in 16 LV segments) was an independent risk factor. Impaired LV function, abnormal electrocardiogram, and impaired RV function were also associated with increased risk. Having an abnormal LV by mechanical dispersion identified athletes at high risk for life-threatening events with a 74% sensitivity and 80% specificity.
In competitive athletes, 1) life-threatening ventricular arrhythmias can occur even if the only known exposure is exercise-induced remodeling, 2) impaired RV function is associated with higher risk of ventricular arrhythmias, and 3) LV dysfunction is significantly associated with life-threatening events.
This was a relatively large single-center controlled cohort study of competitive athletes with ventricular arrhythmias. Without a control group of nonathletes matched for similar ventricular arrhythmias, causal inference is limited. But the authors identified screenable cardiac phenotypes that mimic arrhythmogenic cardiomyopathy phenotypes. Exercise was the only discernable etiology. By asking subjects to detrain for ≥6 weeks, the authors were able to reveal residual structural adaptations. The RV outflow tract (RVOT) is a common source for ventricular arrhythmias, and interestingly, increased RVOT diameter correlated with increased lifetime exercise duration, consistent with a dose-dependent response.
Clinical Topics: Arrhythmias and Clinical EP, Diabetes and Cardiometabolic Disease, Heart Failure and Cardiomyopathies, Noninvasive Imaging, Prevention, Sports and Exercise Cardiology, Implantable Devices, SCD/Ventricular Arrhythmias, Atrial Fibrillation/Supraventricular Arrhythmias, Echocardiography/Ultrasound, Magnetic Resonance Imaging, Exercise, Sports and Exercise and Imaging
Keywords: Adaptation, Physiological, Arrhythmias, Cardiac, Athletes, Cardiomyopathies, Defibrillators, Implantable, Diagnostic Imaging, Echocardiography, Electrocardiography, Exercise, Gadolinium, Heart Arrest, Magnetic Resonance Imaging, Phenotype, Risk Factors, Tachycardia, Ventricular
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