Myocardial mitochondrial proliferation and arrhythmias in a cyclist: the role of erythropoietin

Ventricular arrhythmias (VAs) in competitive athletes are a challenging problem. They may be linked to structural or functional cardiomyopathies, but the role of banned drugs utilization must always be considered. We report the case of a young asymptomatic professional cyclist with frequent and repetitive VAs, an apparently normal heart at imaging and history of erythropoietin (EPO) use. At the electroanatomical mapping during the electrophysiological study, a low-voltage area in the right ventricular outflow tract was documented. At biopsy, we unexpectedly found mitochondrial proliferation into myocardiocytes. As mitochondrial myopathies/cardiomyopathies were ruled out, we considered the possibility of a link between EPO assumption and this mitochondrial proliferation. In this case, moreover, the artificial and inappropriate stimulus for mitochondrial proliferation induced by EPO has the potential to explain the new occurrence of VAs.