Abstract
Recurrence rates following ablation for persistent AF (psAF) remain high with the underlying mechanisms complex and poorly understood. Asynchronous activation of the endocardial and epicardial surfaces during AF, defined as endo-epicardial dissociation (EED) may be a driver for AF. We aim to investigate whether using the novel vector mapping approach, Stochastic Trajectory Analysis of Ranked (STAR) signals, endo- epicardial dissociation and early sites of activation (ESA) can be identified. Six (6) patients underwent endo-epicardial AF ablation utilizing the pericardial percutaneous CO2 insufflation technique. Two AdvisorTM HD Grid mapping catheters were placed in corresponding endocardial and epicardial positions in the left atrium. During AF, 30 second segments were recorded at the base of the left atrial appendage, anterior, inferior, left lateral and posterior LA wall. Fifteen (15) corresponding endo-epicardial segments were analysed using STAR maps and assessed for ESA and variation in direction of activation wavefront between the endocardium and epicardium. Activation wavefront direction was defined as dissociated if there was >40-degree difference between activation direction of simultaneous endo-epicardial wavefronts on STAR mapping. For each 30 second recording if there was more than 1 dominant wavefront direction, the 2 most common were used and an average taken. The overall mean difference in angulation of wavefront between the endocardium and epicardium was 71 ± 55 degrees. Nine (9) of 15 STAR maps (53%) showed activation angulation difference of >40 degrees between the endocardial and epicardial wavefront activation. Of these 9, 3 were on the posterior wall, 3 were at the base of the appendage, 2 were on the left lateral wall and 1 was on the anterior wall. ESA was identified in 6 STAR mapped endo and epicardial segments of AF, with 4 of these 6 (67%) ESAs in the epicardium. STAR mapping identifies activation wavefront discrepancy showing EED in multiple sites of the atrium with the majority of ESAs in the epicardial atrial surface.
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