Clinical and Electrophysiological Characteristics of Ventricular Tachycardias From the Basal Septum in Structural Heart Disease

OBJECTIVES This study describes the clinical and electrophysiological characteristics of basal-septat ventricular tachycardias (VTs) in patients with structural heart disease (SHD). BACKGROUND The basal septum is a common source of VT in patients with SHD. METHODS Data from 312 consecutive patients with SHD undergoing catheter ablation of ventricular arrhythmias were reviewed. RESULTS Thirty-three basal-septat VTs in 31 patients (mean age 674 +/- 14.2 years, mean left ventricular ejection fraction [LVEF] 42% +/- 15%) were identified. Patients with VTs with left ventricular basal-septat breakthrough were more likely to have ischemic cardiomyopathy and tower LVEF; patients with right ventricular basal-septat VT were more likely to have sarcoidosis or right ventricular cardiornyopathy of unknown significance, with higher LVEF. Atrioventricular block was present in 45% of patients and intraventricular block including persistent biventricular pacing in 77%. Unipotar scar was larger than bipolar scar (area 18.8% +/- 19.4% vs 12.7% +/- 14.6%; P < 0.001). VTs with right bundle branch block configuration and S wave in lead V-6 with positive V-3/V-4 polarity consistently indicated left ventricular basal-septal breakthrough. Inferior limb-lead discordance with right bundle branch block configuration and "reverse pattern break in lead V-2" were identified in left ventricular basal inferior-septat origin in 3 patients. VT noninducibility was achieved in 55%, and VT recurred in 42% of patients after a single procedure, but VT burden was significantly reduced after ablation (59 episodes before vs 2 episodes after ablation; P = 0.02). CONCLUSIONS Basal-septal VTs in patients with SHD have a distinct clinical, electrocardiographic, and electrophysiological profile depending on the breakthrough site, accompanied by a deep intramural septal substrate that limits procedural success after catheter ablation. Crown Copyright (C) 2021 Published by Elsevier on behalf of the American College of Cardiology Foundation. Alt rights reserved.