Abstract

Competitive athletes are widely regarded as a special group of healthy individuals with a unique lifestyle who are seemingly invulnerable and often capable of extraordinary physical achievement.
Athlete’s heart is generally regarded as a benign increase in cardiac mass, with specific circulatory and cardiac morphological alterations, that represents a physiological adaptation to systematic training. However, the clinical profile of athlete’s heart has expanded considerably over the last several years as a result of greater accessibility to large populations of trained athletes studied systematically with, ECG, ambulatory Holter ECG monitoring, stress test,  echocardiography and cardiac magnetic resonance. As a consequence, there is increasing recognition of the impact that prolonged conditioning has on cardiac remodeling, which may eventually mimic certain pathological conditions, such as Brugada syndrome,  with the potential for sudden death or disease progression.
These findings indicate that atrioventricular conduction system abnormalities may play a fatal arrhythmogenic role and raise questions regarding the prevention of electrical instability in young people engaged in active sports. At last many drugs have been associated with adverse events in Brugada syndrome patients and  have been indicated to provoke the characteristic Brugada syndrome-linked ECG abnormalities and/or (fatal) ventricular tachyarrhythmias.