Abstract
Brugada syndrome is characterized by right bundle branch block pattern with ST-segment elevation in leads V(1) to V(3) and a propensity for sudden cardiac death due to ventricular arrhythmias. The arrhythmogenic substrate in Brugada syndrome may not be restricted to the ventricles, and atrial arrhythmias are being increasingly reported. Incidences of spontaneous atrial arrhythmias vary from 6% to 38% and those of inducible atrial arrhythmias from 3% to 100%. Atrial fibrillation (AF) is the most common atrial arrhythmia found in Brugada syndrome. Enhanced duration of atrial action potential and increased intra-atrial conduction time may contribute to the genesis of atrial arrhythmias in Brugada syndrome. Atrial arrhythmias are an important cause of inappropriate discharge of implantable defibrillators in patients with Brugada syndrome. Hence, implantation of dual-chamber defibrillators and careful programming of single-chamber devices have been recommended. Atrial fibrillation has been associated with mutations in both the sodium and calcium channels of the heart, as well as with cases of Brugada syndrome that could not genotyped to any of the known genes associated with the disease. This observation suggests that the substrate responsible for the development of ventricular arrhythmias also may contribute to arrhythmogenesis in the atria of the heart. The presence of a prominent transient outward current in atria and the observation that episodes of AF are triggered by closely coupled atrial extrasystoles point to the possibility that a substrate similar to that responsible for ventricular arrhythmogenesis underlies the development of AF in patients with Brugada syndrome.