Abstract

Rapid PV activity is critical in initiating and maintaining AF. The underlying substrate responsible for this remains uncertain. We sought to identify if patients with paroxysmal (PAF) and persistent atrial fibrillation (PeAF) have an abnormal substrate within the pulmonary veins (PVs). Thirty-nine patients with AF (21 PAF, 18 PeAF) were compared with 15 age-matched controls with left-sided accessory pathways (AVRT). High-density 3D electroanatomic maps of the PVs were created. PV voltage, conduction, PV muscle sleeve length, effective refractory periods (ERPs) of the PVs, posterior left atrium (PLA), left atrial appendage (LAA) and distal coronary sinus (CSd), and signal complexity were assessed. Compared with controls, the PVs of AF patients had (1) lower mean-voltage and a higher % low-voltage; (2) shorter PV muscle sleeves; (3) slower conduction; (4) shorter ERP; and (5) more prevalent complex signals. Compared with the PAF group, the PeAF group had (1) higher % low voltage; (2) slower conduction; and (3) more complex signals. In PAF patients, the PLA and LAA ERPs were longer than controls and the PV ERP was shorter than controls; in PeAF patients PLA and LAA ERPs were reduced, but to a lesser extent than in the PVs. AF induction occurred during PV ERP testing in both AF groups, but not controls. PAF and PeAF patients demonstrate electrical and electroanatomic remodeling of the PVs compared to control patients without prior AF. Some of these changes were more marked in PeAF.

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