LAUSR

T wenty-five years ago, Josep and Pedro Brugada first identified a small group of patients with no structural heart disease and characteristic electrocardiogram (ECG) findings of right bundle branch block morphology with persistent STsegment elevation in the right-sided precordial leads, who experienced recurrent episodes of aborted sudden death with no clear medical explanation (1). The initial cohort of patients with Brugada syndrome were characterized by a dismal prognosis, with recurrent sustained ventricular arrhythmias in 62% of patients who presented with sudden cardiac death and a first sustained ventricular arrhythmia in 14% of asymptomatic patients after a 2-year follow-up (2). Since the original description, there has been a dramatic evolution in our understanding of the basic cellular mechanisms and clinical treatment of Brugada syndrome, but important gaps remain. Perhaps the most pressing is how to best identify asymptomatic patients who are at high risk for sustained ventricular arrhythmias and could benefit from prophylactic implantable cardioverter-defibrillator (ICD) implant.