Brugada syndrome: Cellular mechanisms and approaches to therapy

Nearly 15 years have passed since Pedro and Josep Brugada introduced the syndrome of ST-segment elevation and right bundle branch block (RBBB) associated with a high incidence of ventricular tachycardia/ventricular fibrillation (VT/VF) as a new clinical entity.1 Over 16 years have transpired since the introduction of the concept of phase 2 reentry (induced by sodium channel block), the mechanism believed to underlie the development of arrhythmogenesis in this clinical syndrome.2,3 Thus, the entity, which in 1996 came to be known as the Brugada syndrome,4,5 evolved in the experimental laboratory and in the clinic along parallel but separate tracks until the late 1990s.6