Brugada syndrome is linked to ventricular fibrillation (VF), a precursor to sudden cardiac death. This patient population suffers from electrical abnormalities originating from the right ventricular outflow tract (RVOT). The mechanisms underlying such arrhythmic activity remain unclear, but clinical electrophysiological observations have indicated conduction abnormalities in the RVOT.

To mimic sub-clinical epicardial microstructural defects in the RVOT to provide a substrate for conduction delay as a possible mechanism of BrS.

Dual coronary-perfused left and right ventricular wedge preparations were studied in 20 pigs (35–45kg). Patchy microlesions were created through an array of ablation needles in either the RVOT, right ventricle (RV) or both (DOUBLE ablation) and compared to a control group in the absence of ablation. Paced and arrhythmic activity were assessed by optical mapping of the epicardial surface in the presence and absence of the sodium channel blocker, flecainide.

At baseline, the action potential duration (APD80) is shorter in the RVOT region compared to the RV free wall (209.8ms±26.91 vs. 212.6±37.19, P=0.026). APD80 of the RVOT is prolonged by ablation (228.1ms±23.02 for RVOT ablation and 231.2ms±27.18 for double ablation vs 202.5ms±45.37 for RV ablation and 209.8ms±26.91 for control, P<0.0001). Arrhythmia complexity was greatest in the RVOT ablation group compared to control (dominant frequency 8.016Hz±1.286 vs. 5.834Hz±1.726, P=0.0191). Rotors were preferentially clustered to the ablation area in the RVOT ablation group compared to control.

Microstructural defects in the RVOT provides the substrate for sustained ventricular arrhythmias.