Junaid A B Zaman1, William H Sauer1, Mahmood I Alhusseini1, Tina Baykaner1, Ryan T Borne1, Christopher A B Kowalewski1, Sonia Busch1, Paul C Zei1, Shirley Park1, Mohan N Viswanathan1, Paul J Wang1, Johannes Brachmann1, David E Krummen1, John M Miller1, Wouter Jan Rappel1, Sanjiv M Narayan2, Nicholas S Peters1. 1. From the Department of Cardiovascular Medicine, Stanford University, Palo Alto, CA (J.A.B.Z., M.I.A., T.B., C.A.B.K., P.C.Z., S.P., M.N.V., P.J.W., S.M.N.); Imperial Centre for Cardiac Engineering, Imperial College London, United Kingdom (J.A.B.Z., N.S.P.); Cardiac Electrophysiology, Cedars Sinai Heart Institute, Los Angeles, CA (J.A.B.Z.); Department of Cardiology, University of Colorado, Aurora (W.H.S., R.T.B.); Departments of Medicine (T.B., D.E.K.) and Physics (W.J.R.), University of California San Diego; Faculty of Medicine, Friedrich-Alexander-Universität Erlangen-Nürnberg, Germany (C.A.B.K.); Department of Cardiology, Klinikum Coburg, Germany (S.B., J.B.); and Department of Medicine, Indiana University, Bloomington (J.M.M.). 2. From the Department of Cardiovascular Medicine, Stanford University, Palo Alto, CA (J.A.B.Z., M.I.A., T.B., C.A.B.K., P.C.Z., S.P., M.N.V., P.J.W., S.M.N.); Imperial Centre for Cardiac Engineering, Imperial College London, United Kingdom (J.A.B.Z., N.S.P.); Cardiac Electrophysiology, Cedars Sinai Heart Institute, Los Angeles, CA (J.A.B.Z.); Department of Cardiology, University of Colorado, Aurora (W.H.S., R.T.B.); Departments of Medicine (T.B., D.E.K.) and Physics (W.J.R.), University of California San Diego; Faculty of Medicine, Friedrich-Alexander-Universität Erlangen-Nürnberg, Germany (C.A.B.K.); Department of Cardiology, Klinikum Coburg, Germany (S.B., J.B.); and Department of Medicine, Indiana University, Bloomington (J.M.M.). sanjiv1@stanford.edu.
Abstract
BACKGROUND: The mechanisms by which persistent atrial fibrillation (AF) terminates via localized ablation are not well understood. To address the hypothesis that sites where localized ablation terminates persistent AF have characteristics identifiable with activation mapping during AF, we systematically examined activation patterns acquired only in cases of unequivocal termination by ablation. METHODS AND RESULTS: We recruited 57 patients with persistent AF undergoing ablation, in whom localized ablation terminated AF to sinus rhythm or organized tachycardia. For each site, we performed an offline analysis of unprocessed unipolar electrograms collected during AF from multipolar basket catheters using the maximum -dV/dt assignment to construct isochronal activation maps for multiple cycles. Additional computational modeling and phase analysis were used to study mechanisms of map variability. At all sites of AF termination, localized repetitive activation patterns were observed. Partial rotational circuits were observed in 26 of 57 (46%) cases, focal patterns in 19 of 57 (33%), and complete rotational activity in 12 of 57 (21%) cases. In computer simulations, incomplete segments of partial rotations coincided with areas of slow conduction characterized by complex, multicomponent electrograms, and variations in assigning activation times at such sites substantially altered mapped mechanisms. CONCLUSIONS: Local activation mapping at sites of termination of persistent AF showed repetitive patterns of rotational or focal activity. In computer simulations, complete rotational activation sequence was observed but was sensitive to assignment of activation timing particularly in segments of slow conduction. The observed phenomena of repetitive localized activation and the mechanism by which local ablation terminates putative AF drivers require further investigation.
BACKGROUND: The mechanisms by which persistent atrial fibrillation (AF) terminates via localized ablation are not well understood. To address the hypothesis that sites where localized ablation terminates persistent AF have characteristics identifiable with activation mapping during AF, we systematically examined activation patterns acquired only in cases of unequivocal termination by ablation. METHODS AND RESULTS: We recruited 57 patients with persistent AF undergoing ablation, in whom localized ablation terminated AF to sinus rhythm or organized tachycardia. For each site, we performed an offline analysis of unprocessed unipolar electrograms collected during AF from multipolar basket catheters using the maximum -dV/dt assignment to construct isochronal activation maps for multiple cycles. Additional computational modeling and phase analysis were used to study mechanisms of map variability. At all sites of AF termination, localized repetitive activation patterns were observed. Partial rotational circuits were observed in 26 of 57 (46%) cases, focal patterns in 19 of 57 (33%), and complete rotational activity in 12 of 57 (21%) cases. In computer simulations, incomplete segments of partial rotations coincided with areas of slow conduction characterized by complex, multicomponent electrograms, and variations in assigning activation times at such sites substantially altered mapped mechanisms. CONCLUSIONS: Local activation mapping at sites of termination of persistent AF showed repetitive patterns of rotational or focal activity. In computer simulations, complete rotational activation sequence was observed but was sensitive to assignment of activation timing particularly in segments of slow conduction. The observed phenomena of repetitive localized activation and the mechanism by which local ablation terminates putative AF drivers require further investigation.
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