ArticlePacing and clinical electrophysiology : PACE2022
Bi-atrial characterization of the electrical substrate in patients with atrial fibrillation.
Article in Pacing and clinical electrophysiology : PACE, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Pro- and Anti-Inflammatory Cytokines' Implication in Right Heart Disease, Arrhythmogenesis, and Atrial Fibrillation.Biomolecules · 2026Review
- Polygenic risk scores are associated with atrial electrophysiologic substrate abnormalities and outcomes after atrial fibrillation catheter ablation.Heart rhythm · 2023Article
- Bi-atrial characterization of the electrical substrate in patients with atrial fibrillation.Pacing and clinical electrophysiology : PACE · 2022Article
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20 authors.
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Abstract
backgroundLittle is known regarding the characterization of electrical substrate in both atria in patients with atrial fibrillation (AF).
methodsEight consecutive patients undergoing AF ablation (five paroxysmal, three persistent) underwent electrical substrate characterization during sinus rhythm. Mapping of the left (LA) and right atrium (RA) was performed with the use of the HD Grid catheter (Abbott). Bipolar voltage maps were analyzed to search for low voltage areas (LVA), the following electrophysiological phenomena were assessed: (1) slow conduction corridors, and (2) lines of block. EGMs were characterized to search for fractionation. Electrical characteristics were compared between atria and between paroxysmal versus persistent AF patients.
resultsIn the RA, LVAs were present in 60% of patients with paroxysmal AF and 100% of patients with persistent AF. In the LA, LVAs were present in 40% of patients with paroxysmal AF and 66% of patients with persistent AF. The areas of LVA in the RA and LA were 4.8±7.3 cm
conclusionBi-atrial involvement is present in patients with paroxysmal and persistent AF. This is expressed by low voltage areas and slow conduction corridors whose extension progresses as the arrhythmia becomes persistent. This electrophysiological substrate demonstrates the important interplay with the pulmonary vein triggers to constitute the substrate for persistent arrhythmia.
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