Tailored Atrial Substrate Modification Based on Low-Voltage Areas in Catheter Ablation of Atrial Fibrillation

医学 心房颤动 心脏病学 导管消融 内科学 烧蚀 导管 外科
作者
Sascha Rolf,Simon Kircher,Arash Arya,Charlotte Eitel,Philipp Sommer,Sergio Richter,Thomas Gaspar,Andreas Bollmann,David Altmann,Carlos Piedra,Gerhard Hindricks,Christopher Piorkowski
出处
期刊:Circulation-arrhythmia and Electrophysiology [Lippincott Williams & Wilkins]
卷期号:7 (5): 825-833 被引量:508
标识
DOI:10.1161/circep.113.001251
摘要

Reduced electrogram amplitude has been shown to correlate with diseased myocardium. We describe a novel individualized approach for catheter ablation of atrial fibrillation (AF) based on low-voltage areas (LVAs) in the left atrium (LA). We sought to assess (1) the incidence of LVAs in patients undergoing AF catheter ablation, (2) the distribution of LVAs within the LA, and (3) the effect of an individualized ablation strategy on long-term rhythm outcomes.In 178 patients with paroxysmal or persistent AF, LA voltage maps were created during sinus rhythm after circumferential pulmonary vein isolation. Subsequent substrate modification was confined to the presence of LVA (<0.5 mV) and inducible regular atrial tachycardias. LVAs were identified in 35% and 10% of patients with persistent and paroxysmal AF, respectively. The LA roof and the anterior, septal, and posterior wall LA were most often affected. The 12-month atrial tachycardias/AF-free survival was 62% for patients without LVAs and 70% for patients with LVAs and tailored substrate modification (P=0.3). Success rate in a comparison group of 26 LVA patients without further substrate modification was 27%.LVAs can be found at preferred sites in 10% of patients with paroxysmal AF and in 35% of patients with persistent AF. This is the first clinical report describing a consistent voltage-based approach for substrate modification in addition to circumferential pulmonary vein isolation irrespective of AF type. Application of this limited individualized approach may have the potential to compensate for the impaired 12-month outcome of patients with endocardial structural defects.
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