Author + information
- Received May 27, 2018
- Revision received July 2, 2018
- Accepted August 7, 2018
- Published online December 17, 2018.
- Rajiv Mahajan, MD, PhDa,b,
- Adam Nelson, MBBSa,
- Rajeev K. Pathak, MBBS, PhDa,
- Melissa E. Middeldorpa,
- Christopher X. Wong, MBBS, PhDa,
- Darragh J. Twomey, MBBS, PhDa,
- Angelo Carbone, BSca,
- Karen Teo, MBBS, PhDa,
- Thomas Agbaedeng, BSca,
- Dominik Linz, MD, PhDa,
- Joris R. de Groot, MD, PhDc,
- Jonathan M. Kalman, MBBS, PhDd,e,
- Dennis H. Lau, MBBS, PhDa and
- Prashanthan Sanders, MBBS, PhDa,∗ ()
- aCentre for Heart Rhythm Disorders, South Australian Health and Medical Research Institute, University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia
- bDepartment of Cardiology, Lyell McEwin Hospital, Adelaide, Australia
- cHeart Center, Department of Cardiology, Academic Medical Center, Amsterdam, the Netherlands
- dDepartment of Cardiology, Royal Melbourne Hospital, Melbourne, Australia
- eDepartment of Medicine, University of Melbourne, Melbourne, Australia
- ↵∗Address for correspondence:
Dr. Prashanthan Sanders, Centre for Heart Rhythm Disorders (CHRD), Department of Cardiology, Royal Adelaide Hospital, Port Road, Adelaide, SA 5000, Australia.
Objectives The aims of the study were to characterize: 1) electrical and electroanatomical remodeling in patients with atrial fibrillation (AF) with obesity; and 2) the impact of epicardial fat depots on adjacent atrial tissue.
Background Obesity is associated with an increased risk of AF.
Methods A total of 115 patients with AF who underwent AF ablation were screened. After exclusion, 26 patients were divided into 2 groups (obese: body mass index [BMI] ≥27 kg/m2 and reference: BMI <27 kg/m2). They underwent cardiac magnetic resonance (CMR) imaging and electroanatomic mapping of the left atrium (LA) in sinus rhythm before AF ablation. Atrial and ventricular epicardial adipose tissue (EAT) were assessed by CMR. The following electrophysiological parameters were assessed: global and regional voltage, conduction velocity (CV), electrogram fractionation, and CV heterogeneity. In addition, the regional relationship between LA EAT depots and the electrophysiological substrate was evaluated.
Results The BMIs of the obese and reference groups were 30.2 ± 2.6 and 25.2 ± 1.3 kg/m2, respectively (p < 0.001). There was no difference in the left ventricular ejection fraction and a nonsignificant increase in LA size with obesity. Obesity was associated with increase in all measures of EAT (p < 0.05), with a predominant distribution adjacent to the posterior LA and the atrioventricular groove. Obesity was associated with reduced global CV (0.86 ± 0.31 m/s vs. 1.26 ± 0.29 m/s; p < 0.001), with a nonsignificant increase in conduction heterogeneity (p = 0.10), increased fractionation (54 ± 17% vs. 25 ± 10%; p < 0.001), and regional alteration in voltage (p < 0.001). Although the global LA voltage was preserved, there was greater voltage heterogeneity (p = 0.001) and increased low-voltage areas (13.9% vs. 3.4%; p < 0.001) in the obese group compared with the reference group. The low voltage areas were predominantly seen in the posterior and/or inferior LA, which was similar to location of EAT on CMR imaging. Among various measures of obesity, LA EAT volume correlated best with posterior LA fractionation (r2 = 0.55 for LA EAT volume vs. r2 = 0.36 for BMI) and CV (r2 = 0.31 for LA EAT volume vs. r2 = 0.22 for BMI).
Conclusions Obesity is associated with electroanatomical remodeling of the atria, with areas of low voltage, conduction slowing, and greater fractionation of electrograms. These changes were more pronounced in regions adjacent to epicardial fat depots, which suggested a role for fat depots in the development of the AF substrate.
This study was supported by funds from the Centre of Heart Rhythm Disorders at the University of Adelaide. This study was presented at the Annual Scientific Sessions of the Heart Rhythm Society, May 2015, Boston, Massachusetts and was awarded the Eric Prystowsky Clinical Research Award. Drs. Mahajan, Pathak, and Wong are supported by Early Career Fellowships from the National Health and Medical Research Council (NHMRC). Dr. Mahajan is supported by the National Heart Foundation (NHF) of Australia and by the Leo J. Mahar Lectureship from the University of Adelaide. Ms. Middeldorp is supported by a post-graduate scholarship from the NHMRC and the Robert J. Craig Scholarship from the University of Adelaide. Mr. Agbaedeng is supported by the Leo J. Mahar Scholarship from the University of Adelaide. Dr. Linz is supported by a Beacon Fellowship from the University of Adelaide. Dr. Lau is supported by the Robert J. Craig Lectureship from the University of Adelaide. Dr. Sanders is supported by Practitioner Fellowships from the NHMRC and NHF of Australia. This study was supported by funds from the Centre of Heart Rhythm Disorders at the University of Adelaide. This study was presented at the Annual Scientific Sessions of the Heart Rhythm Society, May 2015, Boston, Massachusetts and was awarded the Eric Prystowsky Clinical Research Award.
Dr. Mahajan reports that the University of Adelaide has received on his behalf lecture and/or consulting fees and research funding from Abbott and Medtronic. Dr. de Groot has been a consultant for Atricure and Daiichi Sankyo; and has received research grants from Boston Scientific, Medtronic, Abbott, and St. Jude Medical. Dr. Lau reports that the University of Adelaide has received on his behalf lecture and/or consulting fees from Abbott, Pfizer, Bayer, and Boehringer Ingelheim; and has received research funding from Abbott. Dr. Sanders has served on the advisory board of Biosense-Webster, Medtronic, Abbott, Boston Scientific, and CathRx; reports that the University of Adelaide has received on his behalf lecture and/or consulting fees from Biosense-Webster, Medtronic, Abbott, and Boston Scientific; and that the University of Adelaide has received on his behalf research funding from Medtronic, Abbott, Boston Scientific, Biotronik, and Liva Nova. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. William Stevenson, MD, served as Guest Editor for this paper.
All 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 May 27, 2018.
- Revision received July 2, 2018.
- Accepted August 7, 2018.
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