Extensive ablation strategies with vein of Marshall ethanol infusion were associated with higher odds of PVC incidence compared to ablation without it (OR 5.2; 95% CI: 2.4-12.1; P<0.001).
Cohort (n=502)
No
Does extensive ablation strategy with vein of Marshall ethanol infusion increase the incidence of premature ventricular complexes in patients undergoing atrial fibrillation ablation?
Extensive ablation strategies including vein of Marshall ethanol infusion for AF are associated with a significantly higher incidence of premature ventricular complexes, particularly originating from papillary muscles.
Effect estimate: OR 5.2 (95% CI 2.4-12.1)
Absolute Event Rate: 27.9% vs 6%
p-value: p=<0.001
BACKGROUND: Premature ventricular complexes (PVCs) may occur after ablation of atrial fibrillation (AF). Extensive ablation strategies (EAS), including vein of Marshall ethanol infusion (VOMEI), may affect ventricular innervation, increasing PVC risk. OBJECTIVES: This aim of this study was to evaluate the frequency, anatomical origin, and burden of PVCs after AF ablation, and the impact of EAS with VOMEI (EAS-VOMEI). METHODS: A retrospective, single-center cohort study was conducted, including 502 patients after AF ablation with and without EAS-VOMEI (251 each). EAS included VOMEI and ablation of the posterior wall, mitral isthmus, coronary sinus, and others. PVC burden >5% was considered relevant. PVC origin was determined using electrocardiography or from intraoperative mapping. Innervation around the vein of Marshall and basal ventricles was studied using acetylcholinesterase staining in human hearts. RESULTS: PVC incidence was higher after EAS-VOMEI (70 of 251 vs 15 of 251; P < 0.001). Papillary muscle PVCs occurred more frequently after EAS-VOMEI (47 of 70 vs 5 of 15; P < 0.001). More bigeminy (24 of 70 vs 3 of 15; P < 0.001) and multifocal PVCs (33 of 70 vs 6 of 15; P < 0.001) were observed after EAS-VOMEI. Firth penalized logistic regression demonstrated that VOMEI was associated with 5.2 (95% CI: 2.4-12.1; P < 0.001) higher odds of PVC incidence, and a time-to-event analysis over 12 months showed an adjusted HR of 4.6 (95% CI: 1.5-13.7; P = 0.005). PVCs were mostly transient, and only a minority in each group required PVC ablation (20 post-EAS-VOMEI vs 7; P = 0.01). Innervation around the vein of Marshall and coronary sinus reached the basal left ventricle. CONCLUSIONS: EAS-VOMEI was associated with a higher occurrence of PVCs, which more commonly originated from the papillary muscles. EAS-VOMEI may affect ventricular innervation. Future studies are warranted to investigate the ventricular neuromodulatory impact of VOMEI.
A Sun, study conducted a cohort in Atrial fibrillation (n=502). Extensive ablation strategies with vein of Marshall ethanol infusion (EAS-VOMEI) vs. Atrial fibrillation ablation without EAS-VOMEI was evaluated on Premature ventricular complex (PVC) incidence (OR 5.2, 95% CI 2.4-12.1, p=<0.001). Extensive ablation strategies with vein of Marshall ethanol infusion were associated with higher odds of PVC incidence compared to ablation without it (OR 5.2; 95% CI: 2.4-12.1; P<0.001).