Characterization of the epicardial substrate for catheter ablation of Brugada syndrome

Background Catheter ablation in the right ventricular outflow tract (RVOT) may modify the electrophysiologic substrate for recurrent ventricular tachycardia/ventricular fibrillation (VT/VF) in patients with Brugada syndrome (BrS). Objective The purpose of this study was to investigate the mechanism and arrhythmogenic substrate of VT/VF and to evaluate the long-term outcomes of catheter ablation in patients with BrS. Methods Eleven consecutive patients with BrS referred to 2 academic medical centers underwent combined epicardial–endocardial electroanatomic mapping. Catheter ablation was performed in regions of localized conduction slowing. Transmural dispersion of late activation was calculated as the difference between the latest activation between epicardium and endocardium, and low-voltage areas were analyzed. Results Eleven patients met diagnostic criteria for BrS (spontaneous type 1, n = 9; Na channel provocation = 2). All patients were found to have a localized region in the anterior epicardial RVOT with conduction slowing evidenced by prolonged electrogram duration (78.79 ± 19.87 ms vs 58.93 ± 10.11 ms in epicardial right ventricle, and 59.87 ± 12.61 ms in endocardial RVOT, P <.005, respectively) with variable low voltage (0.97 ± 0.48 mV; median scar area 19.8 ± 25.9 cm²). Epicardial ablation resulted in normalization of spontaneous type 1 Brugada ECG pattern in all patients, and 73% were free from VT/VF at 25 ± 11 months. Conclusion Prolonged electrograms localized to epicardial RVOT with variable low voltage were identified in all patients with BrS. J-point and ST-segment elevation correlated with greater transmural dispersion of late activation and was independent of total low-voltage area. Despite normalization of spontaneous type 1 pattern in all patients after ablation, recurrence was still observed, suggesting the implantable cardioverter–defibrillator as the cornerstone therapy for BrS.