Does Ventricular Tachycardia Ablation Targeting Local Abnormal Ventricular Activity Elimination Reduce Ventricular Fibrillation Incidence?

BACKGROUND Various strategies for ablation of ventricular tachycardia (VT) have been described, but their impact on ventricular fibrillation (VF) is largely unknown. The aim of our study was to assess the effect of substrate-based VT ablation targeting local abnormal ventricular activity (LAVA) on recurrent VF events in patients with structural heart disease. METHODS A retrospective 2-center study was performed on patients with structural heart disease and both VT and VF, with incident VT ablation procedures targeting LAVAs. Generalized estimating equations with a Poisson loglinear model were used to assess the impact of catheter ablation on VF episodes. The change in VF events before and after catheter ablation was compared with matched controls without ablation. RESULTS From a total of 686 patients with an incident VT ablation procedure targeting LAVAs, 21 patients (age, 57±14 years; left ventricular ejection fraction, 30±10%) had both VT and VF and met inclusion criteria. A total of 80 VF events were recorded in the implantable cardioverter-defibrillator logs the 6 months preceding ablation. Complete and partial LAVA elimination was achieved in 11 (52%) and 10 (48%) patients, respectively. Catheter ablation was associated with a highly significant reduction in VF recurrences (P<0.0001), which were limited to 3 (14%) patients at 6 months. The total number of VF events thereby decreased from 80 to 3, from a median of 1.0 (range, 1-29) to 0.0 (range, 0-1) in the 6 months before and after ablation, respectively. The reduction in VF events was significantly greater in patients with catheter ablation compared with 21 matched controls during 6-month periods following and preceding a baseline assessment (Poisson β-coefficient, 1.39; P=0.0003). CONCLUSIONS Substrate-guided VT ablation targeting LAVAs may be associated with a significant reduction in recurrent VF, suggesting that VT and VF share overlapping arrhythmogenic substrates in patients with structural heart disease.