Abstract
The pathophysiological basis of Brugada syndrome (BrS) remains controversial. We attempted to isolate the origin of provoked ventricular tachycardia/ventricular fibrillation (VT/VF) associated with BrS through noncontact mapping of the right ventricle (RV). Programmed ventricular stimulation was performed in 3 patients with BrS. Rapid VT of a similar morphology that degenerated into VF was induced from the RV apex (n = 2) or RV outflow tract (RVOT, n = 1). These VTs arose from the RVOT wall or the RV free wall. The RV as the primary origin of VT may be a key target for BrS therapies.
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