Vein of Marshall chemical ablation decreases atrial fibrillation drivers detected by CARTOFINDER

Author:

Hasebe Hideyuki12ORCID,Furuyashiki Yoshitaka2,Yoshida Kentaro13

Affiliation:

1. Department of Cardiology Institute of Medicine, University of Tsukuba Tsukuba Japan

2. Department of Arrhythmology Shizuoka Saiseikai General Hospital Shizuoka Japan

3. Department of Cardiology Ibaraki Prefectural Central Hospital Kasama Japan

Abstract

AbstractIntroductionThis study sought to elucidate the impact of vein of Marshall (VOM) chemical ablation on atrial fibrillation (AF) drivers by investigating the changes in CARTOFINDER mappings before and after VOM chemical ablation in patients with persistent AF.MethodsThis study included 23 consecutive patients undergoing catheter ablation for long‐persistent AF (>18 months). VOM chemical ablation was performed following pulmonary vein isolation. CARTOFINDER and AF cycle length (AFCL) maps were created in the left atrium (LA) before and after VOM chemical ablation. The LA was divided into 8 segments, and the number of focal activation points with 6 or more repetitions was counted in each segment.ResultsThe number of focal activation points was largest in the LA appendage (LAA). After VOM chemical ablation, the number of focal activation points in the LA decreased significantly (37 [interquartile range, IQR: 19–55] vs. 15 [IQR: 7–21], p < .001), and median AFCL was significantly prolonged (159 [147–168] vs. 164 [150–173] ms, p < .001). In the assessment of each segment, significant decreases in focal activation points were observed in the inferior, lateral, and anterior segments and LAA. Among the focal activation points disappearing after chemical ablation, the number in the non‐ethanol‐affected area was significantly larger than that in the affected area (13 [8–25] vs. 4 [1–10], p < .001).ConclusionsVOM chemical ablation decreases AF drivers detected by CARTOFINDER. Mechanisms other than direct myocardial damage are considered to contribute the attenuation of AF drivers.

Publisher

Wiley

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