Low voltage with high suspicion in athlete's heart

We have read with great interest the manuscript recently published in your journal by Zorzi et al.1 about the prevalence and significance of the presence of isolated low voltages in the electrocardiogram (ECG) of young athletes. About this work, several aspects are of interest, especially the proposal to include this electrocardiographic finding among the infrequent but potentially pathological changes in the athlete's heart. Based on our experience with similar two triathletes with low voltage, a 40-year-old male with syncope and ventricular tachycardia and a 29-year-old female with exertional premature ventricular contractions both with subepicardial inferolateral late gadolinium enhancement (LGE) and negative genetic test that ruled out left ventricle arrhythmogenic cardiomyopathy—according to the Padua criteria—we raised several questions related to the published manuscript.2 In this, not all athletes with low voltage have magnetic resonance imaging (MRI) performed but only those with ventricular tachycardias, it remains in the air therefore if the rest would also have LGE and if this could be the substrate of a low electrocardiographic voltage in the ECGs. On the other hand, once the diagnosis of left-sided dysplasia has been ruled out, it is worth asking whether the LGE present in our patients, in both at the same location and with a similar electrocardiographic expression, could be the result of an excessive training responsible of a non-ischaemic myocardial damage in over-trained susceptible individuals or just the result of a previous myocarditis. This takes us even further: would it be necessary to perform MRI on all the athletes with low voltage or at least a closer periodic follow-up that includes Holter monitoring and exercise stress test? Are we facing a new expression of the heart of a high-performance athlete? The real significance of LGE described in athletes is unclear, as mentioned by Domenech-Ximenos et al.,3 the presence of LGE indicates that the local matrix and fibre structure has changed, similar to what happens in histologic fibrosis and scar, otherwise it has been shown that acute profound exercise-related oxidative stress and inflammation may impair endothelial function and arterial stiffness and this phenomena could be responsible for fibrosis.4,5