Trigger- vs Substrate-Based Purkinje De-Networking for Ventricular Fibrillation: Insights From a Multicenter Study.

BACKGROUND

Purkinje-mediated ventricular fibrillation (VF) may arise from discrete fascicular triggers or diffuse abnormal Purkinje substrate. The relative performance of trigger-based vs substrate-based de-networking remains uncertain.

OBJECTIVES

The goal of this study was to compare outcomes of trigger-focused and substrate-based Purkinje de-networking for VF.

METHODS

In this retrospective multicenter cohort, 43 patients underwent Purkinje-targeted VF ablation using high-power, short-duration radiofrequency energy (90 W for 4 seconds or 50 W for 10 seconds). Patients were grouped according to ablation strategy: 1) trigger group (n = 19), ablation of the culprit premature ventricular complex-triggering fascicle; or 2) substrate group (n = 24), elimination of all abnormal Purkinje-like potentials. The primary endpoint was recurrence of polymorphic ventricular tachycardia/VF; secondary endpoints included conduction system complications. Median follow-up was 12.2 months (Q1-Q3: 8.8-18.8 months).

RESULTS

Baseline characteristics were similar between groups. Freedom from polymorphic ventricular tachycardia/VF was higher with substrate modification (22 of 24 [91.7%]; 95% CI: 73.0%-98.9%) than with trigger-based ablation (12 of 19 [63.2%]; 95% CI: 38.4%-83.7%; HR: 0.20 [95% CI: 0.05-0.76]; log-rank test; P = 0.026). Both approaches significantly reduced arrhythmic burden (trigger group: 3.9 ± 0.8 episodes to 0.4 ± 0.2 episodes [P < 0.001]; substrate group: 4.8 ± 1.2 episodes to 0.1 ± 0.1 episodes [P < 0.001]). Conduction complications differed: new left bundle branch block occurred in 5 of 24 substrate patients (20.8%), whereas one posterior fascicular block occurred in the trigger group (1 of 19 [5.3%]; P < 0.001).

CONCLUSIONS

Substrate-based de-networking was associated with greater freedom from ventricular tachycardia/VF but a higher rate of conduction system injury. Trigger-focused ablation may serve as an initial strategy in patients with identifiable premature ventricular complex triggers, with substrate modification reserved for refractory or nontriggered VF.