Why the study?
When refractory ventricular fibrillation is accompanied by infrequent and multifocal premature ventricular complexes, the optimal treatment strategy is uncertain.
Does ventricular fibrillation electrical substrate ablation reduce the composite of implantable cardioverter-defibrillator shock, electrical storm, or all-cause mortality in patients with refractory ventricular fibrillation and infrequent, multifocal premature ventricular complexes?
Does ventricular fibrillation electrical substrate ablation reduce the composite of implantable cardioverter-defibrillator shock, electrical storm, or all-cause mortality in patients with refractory ventricular fibrillation and infrequent, multifocal premature ventricular complexes?
Electrical substrate ablation of ventricular fibrillation may significantly reduce the risk of ICD shocks, electrical storm, and mortality in patients with refractory VF and infrequent, multifocal PVCs.
Answers are grounded in this paper and cite their sources.
May support VF ablation in refractory VF; hypothesis-generating from small cohort, needs randomized confirmation.
Background: Refractory ventricular fibrillation (VF) is a challenging clinical entity, for which ablation of triggering premature ventricular complexes is described. When premature ventricular complexes are infrequent and multifocal, the optimal treatment strategy is uncertain. Methods: We prospectively enrolled consecutive patients presenting with multiple implantable cardioverter-defibrillator shocks for VF refractory to antiarrhythmic drug therapy, exhibiting infrequent (≤3%), multifocal premature ventricular complexes (≥3 morphologies). Procedurally, VF was induced with rapid pacing and mapped, identifying sites of conduction slowing and rotation or rapid focal activation. VF electrical substrate ablation was then performed. Outcomes were compared against reference patients with VF who were unable or unwilling to undergo catheter ablation. The primary outcome was a composite of implantable cardioverter-defibrillator shock, electrical storm, or all-cause mortality. Results: VF was induced and mapped in 6 patients (60±10 years; left ventricular ejection fraction, 46±19%) with ischemic (n=3) and nonischemic cardiomyopathy. An average of 3.3±0.5 sites of localized reentry during VF were targeted for radiofrequency ablation (38.3±10.9 minutes) during sinus rhythm, rendering VF noninducible with pacing. Freedom from the primary outcome was 83% in the VF ablation group versus 17% in 6 nonablation reference patients at a median of 1.0 years (interquartile range, 0.5–1.5 years; P =0.046) of follow-up. Conclusions: VF electrical substrate ablation is associated with a reduction in the combined end point compared with the nonablation reference group. Additional work is required to understand the precise pathophysiologic changes that promote VF to improve preventative and therapeutic strategies.
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Krummen et al. (2021) studied this question.
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