Author + information
- Received March 13, 2019
- Revision received August 26, 2019
- Accepted August 26, 2019
- Published online January 20, 2020.
- Ramanathan Parameswaran, MBBSa,b,c,
- Christophe P. Teuwen, MDd,
- Troy Watts, BSca,
- Chrishan J. Nalliah, MBBSa,b,
- Alistair Royse, MBBSb,e,
- John Goldblatt, MBBSe,
- Marco Larobina, MBBSe,
- Prashanthan Sanders, MBBS, PhDf,
- Peter Kistler, MBBS, PhDb,c,g,
- Andres Orozco-Duque, PhDh,
- Geoffrey Lee, MBBS, PhDa,b,∗ and
- Jonathan M. Kalman, MBBS, PhDa,b,∗∗ ()
- aDepartment of Cardiology, Royal Melbourne Hospital, Melbourne, Australia
- bDepartment of Medicine, University of Melbourne, Melbourne, Australia
- cHeart Centre, Alfred Hospital, Melbourne, Australia
- dDepartment of Cardiology, Erasmus Medical Center, Rotterdam, the Netherlands
- eDepartment of Cardiothoracic Surgery, Royal Melbourne Hospital, Melbourne, Australia
- fCentre for Heart Rhythm Disorders, South Australian Health and Medical Research Institute, University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia
- gBaker IDI Heart and Diabetes Institute, Melbourne, Australia
- hDepartment of Applied Sciences, Instituto Tecnológico Metropolitano, Medellín, Colombia
- ↵∗Address for correspondence:
Prof. Jonathan M. Kalman, Department of Cardiology, Royal Melbourne Hospital, Level 2, 300 Grattan Street, Parkville, Victoria 3050, Australia.
Objectives 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).
Background SHD commonly predisposes to arrhythmias. Although progressive remodeling is implicated, direct demonstration of FEED in the human atrium has not been reported previously.
Methods 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 (600 ms and 400 ms cycle length), and premature extrastimulation (PES). Unipolar electrograms (EGMs) were exported into custom-made software for activation and phase mapping. Difference of ≥20 ms between paired endocardial and epicardial electrodes defined dissociation. EGMs with ≥3 deflections were classified as fractionated.
Results 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 600 ms and 400 ms (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).
Conclusions 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.
- functional dissociation
- electrogram morphology
- epicardial–endocardial mapping
- structural heart disease
↵∗ Drs. Lee and Kalman contributed equally to this work and are joint senior authors.
Drs. Parameswaran and Nalliah are supported by the National Health and Medical Research Council research scholarship. Drs. Kalman and Sanders are supported by practitioner fellowships from the National Health and Medical Research Council. Dr. Sanders is also supported by a practitioner fellowship from the National Heart Foundation; has served on the advisory board of Biosense Webster, Medtronic, St. Jude Medical, and Boston Scientific; has received lecture and/or consulting fees from Biosense Webster, Medtronic, St. Jude Medical, and Boston Scientific; and has received research funding from Medtronic, St. Jude Medical, Boston Scientific, Biotronik, and Sorin. Dr. Kalman has received research support from Biosense Webster, Boston Scientific, St. Jude Medical, and Medtronic; and has served on the advisory board of Boston Scientific and Biosense Webster. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Francis Marchlinski, MD, served as Guest Editor for this paper.
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Clinical Electrophysiology author instructions page.
- Received March 13, 2019.
- Revision received August 26, 2019.
- Accepted August 26, 2019.
- 2020 American College of Cardiology Foundation
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