Brugada syndrome (BrS) is an inherited channelopathy linked to an increased risk of developing malignant ventricular arrhythmias and sudden cardiac death in otherwise healthy individuals.1 Currently, implantable cardioverter-defibrillator (ICD) is still the mainstay of treatment for BrS,1 but for patients experiencing recurrent ICD shocks despite optimal medical therapy, radiofrequency (RF) transcatheter ablation of the arrhythmogenic substrate is an available option with promising results.2–5 Although there is a generalized consensus in considering the right ventricular outflow tract (RVOT) epicardium as the locus harboring the pathologic substrate, the exact pathogenesis of BrS is still a matter of debate.
