Prevention of Ventricular Fibrillation Episodes in Brugada Syndrome by Catheter Ablation Over the Anterior Right Ventricular Outflow Tract Epicardium

TLDR

Brugada syndrome’s ventricular tachycardia and ventricular fibrillation arise from an as‑yet‑unelucidated electrophysiological substrate, with evidence pointing to the right ventricular outflow tract. The study aimed to determine whether recurrent ventricular fibrillation in Brugada patients originates from the RVOT, either epicardially or endocardially, and to test whether catheter ablation of abnormal electrograms at this site can prevent arrhythmia. Electroanatomic mapping of the right ventricle (endocardial and epicardial) and left‑ventricular epicardium was performed in nine symptomatic Brugada patients during sinus rhythm. Ablation of low‑voltage, prolonged, fractionated potentials confined to the anterior RVOT epicardium rendered ventricular tachycardia/fibrillation non‑inducible in 78 % of patients, normalized the Brugada ECG pattern in 89 %, and yielded no recurrences over a 20‑month follow‑up, confirming delayed depolarization in this region as the underlying mechanism.

Abstract

The underlying electrophysiological mechanism that causes an abnormal ECG pattern and ventricular tachycardia/ventricular fibrillation (Vt/VF) in patients with the Brugada syndrome (BrS) remains unelucidated. However, several studies have indicated that the right ventricular outflow tract (RVOT) is likely to be the site of electrophysiological substrate. We hypothesized that in patients with BrS who have frequent recurrent VF episodes, the substrate site is the RVOT, either over the epicardium or endocardium; abnormal electrograms would be identified at this location, which would serve as the target site for catheter ablation.We studied 9 symptomatic patients with the BrS (all men; median age 38 years) who had recurrent VF episodes (median 4 episodes) per month, necessitating implantable cardioverter defibrillator discharge. Electroanatomic mapping of the right ventricle, both endocardially and epicardially, and epicardial mapping of the left ventricle were performed in all patients during sinus rhythm. All patients had typical type 1 Brugada ECG pattern and inducible Vt/VF; they were found to have unique abnormal low voltage (0.94±0.79 mV), prolonged duration (132±48 ms), and fractionated late potentials (96±47 ms beyond QRS complex) clustering exclusively in the anterior aspect of the RVOT epicardium. Ablation at these sites rendered Vt/VF noninducible (7 of 9 patients [78%]; 95% confidence interval, 0.40 to 0.97, P=0.015) and normalization of the Brugada ECG pattern in 89% (95% confidence interval, 0.52 to 0.99; P=0.008). Long-term outcomes (20±6 months) were excellent, with no recurrent Vt/VF in all patients off medication (except 1 patient on amiodarone).The underlying electrophysiological mechanism in patients with BrS is delayed depolarization over the anterior aspect of the RVOT epicardium. Catheter ablation over this abnormal area results in normalization of the Brugada ECG pattern and prevents Vt/VF, both during electrophysiological studies as well as spontaneous recurrent Vt/VF episodes in patients with BrS.