Catheter ablation over the anterior RVOT epicardium rendered Vt/VF noninducible in 78% of patients (95% CI 0.40-0.97; P=0.015) and normalized the Brugada ECG pattern in 89%.
Observational (n=9)
Does catheter ablation over the anterior RVOT epicardium prevent ventricular fibrillation episodes and normalize the ECG pattern in patients with Brugada syndrome?
Epicardial catheter ablation of the anterior RVOT substrate in Brugada syndrome normalizes the ECG pattern and prevents recurrent ventricular fibrillation.
p-value: p=0.015
Background— The underlying electrophysiological mechanism that causes an abnormal ECG pattern and ventricular tachycardia/ventricular fibrillation (V t /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. Methods and Results— 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 V t /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 V t /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 V t /VF in all patients off medication (except 1 patient on amiodarone). Conclusions— 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 V t /VF, both during electrophysiological studies as well as spontaneous recurrent V t /VF episodes in patients with BrS.
Nademanee et al. (2011) conducted an observational in Brugada syndrome with recurrent VF episodes (n=9). Catheter ablation over the anterior right ventricular outflow tract epicardium was evaluated on Noninducibility of Vt/VF (95% CI 0.40-0.97, p=0.015). Catheter ablation over the anterior RVOT epicardium rendered Vt/VF noninducible in 78% of patients (95% CI 0.40-0.97; P=0.015) and normalized the Brugada ECG pattern in 89%.