Low‐voltage areas detected by high‐density electroanatomical mapping predict recurrence after ablation for paroxysmal atrial fibrillation

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Catheter ablation is an established treatment for patients with atrial fibrillation (AF). Trigger elimination by pulmonary vein antral isolation (PVAI) is the cornerstone of AF ablation.1 Fibrotic and inflammatory infiltration of the right and left atrium are major determinants of the pathogenesis and progression of AF.2 Interestingly, abnormal atrial histology with fibrosis has been found in multiple biopsy specimens in patients with lone AF.3 The DECAAF study, a multicenter, prospective, observational cohort study of patients with AF undergoing catheter ablation, showed that atrial tissue fibrosis estimated by delayed enhancement magnetic resonance imaging (DE‐MRI) was independently associated with arrhythmia recurrence.4 Furthermore, two studies showed that DE‐MRI scar areas exhibit low‐voltage signals (0.39 ± 0.61 mV and 0.38 ± 0.28 mV) compared with healthy atrial tissue (1.38 ± 1.23 mV).5 However, both DE‐MRI and low‐density electroanatomic substrate mapping have important limitations in left atrium (LA) imaging. Previous studies reported electroanatomical mapping of the left atrium using 54–158 points.5 We hypothesized that high‐density electroanatomic mapping using > 2,000 points may allow detailed LA substrate characterization. The aim of our study was to investigate the impact of LA fibrosis, detected through meticulous electroanatomical mapping, in ablation outcomes following PVAI for paroxysmal AF.
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