LAUSR

It has been postulated that increasing exercise volumes beyond an optimal dose may lead to cardiac maladaptation, including phenotype expression of arrhythmogenic cardiomyopathy. Complex ventricular arrhythmias (VA) and premature ventricular beats (PVB) of uncommon morphologies may signify underlying cardiac pathology in athletes. Cardiac dysfunction in the form of abnormal myocardial strain and prolonged mechanical dispersion (MD) has been demonstrated in symptomatic veteran athletes with VA as well as several cardiac pathologies. This study sought to investigate myocardial strain and left ventricular mechanical dispersion (LVMD) in veteran asymptomatic athletes with complex VA on ambulatory electrocardiogram (ECG), and in veteran athletes demonstrating uncommon morphology PVB on exercise testing. 44 male veteran endurance athletes (55± 7 years, 19±12 years of training) with complex VA on ambulatory ECG and 44 age matched male veteran athletes (53±6 years, 20±13 years of training) without complex VA had echocardiographic assessment including comprehensive layer specific LV circumferential, radial and longitudinal myocardial strain. Subjects also underwent cardiac magnetic resonance imaging (CMR) to assess the presence of myocardial fibrosis, and cardiopulmonary exercise testing (CPET). Exercise induced PVB on CPET ECG traces were divided by morphology into common PVB and uncommon PVB. There was no difference in left ventricular ejection fraction (LVEF) on echocardiography and CMR. Athletes with complex VA had significantly reduced global mid and endocardial longitudinal strain, and endocardial circumferential strain compared with athletes without complex VA. There was no difference in LVMD, radial strain and epicardial longitudinal strain. Exercise induced PVB were more frequent in athletes with complex VA, and a greater proportion of athletes in this group demonstrated uncommon PVB. Athletes with PVB of uncommon morphology had significantly lower global mid and endocardial longitudinal strain than athletes without exercise induced PVB. Proportionately more athletes with complex VA had pathological fibrosis on CMR. Pathological fibrosis on CMR was the only independent predictor of exercise induced PVB. Veteran endurance athletes with complex VA on ambulatory ECG had reduced global longitudinal strain and endocardial circumferential strain compared to veteran athletes without complex VA. This was not explained by a difference in training volume, experience or a difference in LVEF. Additionally, veteran athletes with exercise induced uncommon PVB had lower global longitudinal strain and endocardial longitudinal strain than athletes without exercise induced PVB. These differences may represent subclinical cardiac dysfunction. However, it is not possible to attribute them to an exercise induced cardiomyopathy and longitudinal studies incorporating detraining protocols are required.