Functional Atrial Endocardial–Epicardial Dissociation in Patients With Structural Heart Disease Undergoing Cardiac Surgery

Abstract

The goal of this study was to describe functional endocardial-epicardial dissociation (FEED), signal complexities, and three-dimensional activation dynamics of the human atrium with structural heart disease (SHD). SHD commonly predisposes to arrhythmias. Although progressive remodeling is implicated, direct demonstration of FEED in the human atrium has not been reported previously. Simultaneous intraoperative mapping of the endocardial and epicardial lateral right atrial wall was performed by using 2 high-density grid catheters during sinus rhythm, pacing drive (600ms and 400ms cycle length), and premature extrastimulation (PES). Unipolar electrograms (EGMs) were exported into custom-made software for activation and phase mapping. Difference of≥20ms between paired endocardial and epicardial electrodes defined dissociation. EGMs with≥3 deflections were classified as fractionated. Sixteen patients (mean age 60.5 ± 4.1 years; 18.7% with a history of atrial fibrillation) with SHD (43%ischemia, 57% valvular disease) were included. A total of 9,218 EGMs were analyzed. Compared with sinus rhythm, phase and activation analyses showed significant FEED during pacing at 600ms and 400ms (phase mapping 22.4% vs. 10% [p<0.0001] and 25.8% vs. 10% [p<0.0001], respectively; activation mapping 25.4% vs. 7.8% [p<0.0001] and 27.7% vs. 7.8% [p<0.0001]) and PES (phase mapping 34% vs. 10% [p<0.0001]; activation mapping 29.5% vs. 7.8% [p<0.0001]). Fractionated EGMs occurred significantly more during PES compared with sinus rhythm (50.2% vs. 39.5%; p<0.0001). Activation patterns differed significantly during pacing drive and PES, with preferential epicardial exit during the latter (15.9% vs. 13.8%; p=0.046). Simultaneous endocardial-epicardial mapping revealed significant FEED with signal fractionation and preferential epicardial breakthroughs with PES. Such complex three-dimensional interaction in electrical activation provides mechanistic insights into atrial arrhythmogenesis with SHD.