The effects of hypothermia in patients with brugada syndrome: The characteristics of epicardial substrates and ventricular arrhythmogenicity

Background: Hypothermia therapy has been applied to patients with Brugada syndrome (BrS) experiencing sudden cardiac death (SCD). Objective: The study aimed at elucidating the substrate characteristics and ventricular arrhythmogenesis at a hypothermic status. Methods: Six patients with type 1 BrS experiencing VT/VF were studied. Epicardial cold saline infusion (ECSI) was performed (33-34°C). Baseline ECG, repeated electroanatomical mapping, and inducibility by programmed stimulation were compared after ECSI. Results: ECSI attenuated type 1 BrS phenotype in 4 of 6 patients. Epicardial scar/low voltage zone slightly increased from 82.7±49.1 cm2 to 108.2±50.2 cm2 (P=0.03; FigureA) after ECSI, while late potential area increased from 12.7±0.5 cm2 to 22.3±3.7 cm2 (P=0.03; FigureB). ECSI prolonged total RV epicardial activation from 167.6±56.0 ms to 215.7±74.1 (P=0.03), especially changing the activation pattern within anterior free wall of RVOT and resulting a confluent propagation. Inducibility of VT/VF increased from 0% to 83.3% (P=0.02) after ECSI. Ablation by targeting the confluent abnormal substrates rendered noninducibility of VT/VF in all patients. Conclusion: Hypothermia may increase the ventricular tachyarrhythmogenesis owing to the confluent wavelet propagation within the latest conductoin zone inspite of the attenuation of BrS phenotype. (Figure presented).