Abstract 13822: Comparison of Produced Potential Delay in Superior Vena Cava During Right Pulmonary Vein Isolation Between High-power Short-duration and Conventional Settings

Abstract

Background: Recently, a high-power short-duration (HP-SD) setting has been introduced in atrial fibrillation (AF) ablation. Ablation using this setting reduces collateral tissue damage by shortening the conductive heating phase compared to conventional setting. However, the lesion characteristics have not been rigorously evaluated during ablation procedure. We hypothesized that superior vena cava (SVC) potential could be affected by excessive transmural lesions in anterior-superior right pulmonary vein isolation (PVI), adjacent to posterior aspect of SVC. Therefore, we compared the produced potential delay in SVC between HP-SD and conventional settings. Methods and Results: The consecutive 42 patients (61±10 years, 32 men) who underwent PVI for drug refractory AF were analyzed. Before introduction of HP-SD setting to AF ablation in November 2018, 14 patients underwent right PVI with conventional setting with output of 20-30 W (Conventional group). In the remaining 28 patients after then, right PVI was performed using HP-SD setting with output of 45-50 W (HP-SD group). We compared total radiofrequency energy and mean contact force along the anterior superior right PVI line between the 2 groups. Moreover, the produced SVC potential delay was calculated after anterior superior right PVI and compared between the 2 groups. Total radiofrequency energy delivered (6138 J vs. 6139 J, P = 0.999) and the mean contact force (17.2 g vs. 20.2 g, P = 0.100) in the anterior superior right PV did not differ between the HP-SD and Conventional groups. However, the produced SVC potential conduction delay after anterior superior right PVI was significantly longer in Conventional group compared to HP-SD group (6.2 ms vs. 0.5 ms, P < 0.001). Conclusions: Our data suggest that HP-SD setting caused less collateral tissue damage than conventional setting during PVI. The significant produced SVC potential delay might be a surrogate marker of collateral tissue damage by conductive heating phase in PVI.