Author + information
- Received May 29, 2014
- Revision received August 17, 2014
- Accepted September 8, 2014
- Published online December 2, 2014.
- Rajeev K. Pathak, MBBS∗,
- Melissa E. Middeldorp∗,
- Dennis H. Lau, MBBS, PhD∗,
- Abhinav B. Mehta, MActSt†,
- Rajiv Mahajan, MD∗,
- Darragh Twomey, MBBS∗,
- Muayad Alasady, MBBS∗,†,
- Lorraine Hanley, BSc∗,
- Nicholas A. Antic, MBBS, PhD‡,
- R. Doug McEvoy, MBBS, MD‡,
- Jonathan M. Kalman, MBBS, PhD§,
- Walter P. Abhayaratna, MBBS, PhD‖ and
- Prashanthan Sanders, MBBS, PhD∗∗ ()
- ∗Centre for Heart Rhythm Disorders, South Australian Health and Medical Research Institute, University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia
- †Research School of Finance, Actuarial Studies and Applied Statistics, Australian National University, Canberra, Australia
- ‡Adelaide Institute for Sleep Health, Repatriation General Hospital and Department of Medicine, Flinders University, Adelaide, Australia
- §Department of Cardiology, Royal Melbourne Hospital and the Department of Medicine, University of Melbourne, Melbourne, Australia
- ‖College of Medicine, Biology and Environment, Australian National University and Canberra Hospital, Canberra, Australia
- ↵∗Reprint requests and correspondence:
Dr. Prashanthan Sanders, Centre for Heart Rhythm Disorders, Department of Cardiology, Royal Adelaide Hospital, L5 McEwin Building, North Terrace, Adelaide 5000, Australia.
Background The long-term outcome of atrial fibrillation (AF) ablation demonstrates attrition. This outcome may be due to failure to attenuate the progressive substrate promoted by cardiovascular risk factors.
Objectives The goal of this study was to evaluate the impact of risk factor and weight management on AF ablation outcomes.
Methods Of 281 consecutive patients undergoing AF ablation, 149 with a body mass index ≥27 kg/m2 and ≥1 cardiac risk factor were offered risk factor management (RFM) according to American Heart Association/American College of Cardiology guidelines. After AF ablation, all 61 patients who opted for RFM and 88 control subjects were assessed every 3 to 6 months by clinic review and 7-day Holter monitoring. Changes in the Atrial Fibrillation Severity Scale scores were determined.
Results There were no differences in baseline characteristics, number of procedures, or follow-up duration between the groups (p = NS). RFM resulted in greater reductions in weight (p = 0.002) and blood pressure (p = 0.006), and better glycemic control (p = 0.001) and lipid profiles (p = 0.01). At follow-up, AF frequency, duration, symptoms, and symptom severity decreased more in the RFM group compared with the control group (all p < 0.001). Single-procedure drug-unassisted arrhythmia-free survival was greater in RFM patients compared with control subjects (p < 0.001). Multiple-procedure arrhythmia-free survival was markedly better in RFM patients compared with control subjects (p < 0.001), with 16% and 42.4%, respectively, using antiarrhythmic drugs (p = 0.004). On multivariate analysis, type of AF (p < 0.001) and RFM (hazard ratio 4.8 [95% confidence interval: 2.04 to 11.4]; p < 0.001) were independent predictors of arrhythmia-free survival.
Conclusions Aggressive RFM improved the long-term success of AF ablation. This study underscores the importance of therapy directed at the primary promoters of the AF substrate to facilitate rhythm control strategies.
Dr. Antic has received lecture fees from ResMed and GlaxoSmithKline; and research grants from Philips Respironics, ResMed, Fisher & Paykel, Compumedics, and SomnoMed. Dr. McEvoy has received lecture fees from Philips Respironics; and research funding from Philips Respironics and ResMed. Dr. Kalman has received lecture fees from Bard Electrophysiology and Biotronik; research support from Medtronic, St. Jude Medical, and Biosense Webster; and travel support from Medtronic and St. Jude Medical. Dr. Sanders has served on the advisory board of Biosense Webster, Medtronic, St. Jude Medical, Sanofi, and Merck Sharp & Dohme; has received lecture fees from Biosense Webster, Medtronic, St. Jude Medical, Boston Scientific, Merck Sharp & Dohme, Biotronik, and Sanofi; and has received research funding from Medtronic, St. Jude Medical, Boston Scientific, Biotronik, and Sorin. Dr. Pathak is supported by a Postgraduate Scholarship from the Lion’s Medical Research Foundation and an Australian Postgraduate Award from the University of Adelaide. Drs. Pathak and Twomey are supported by Leo J. Mahar Electrophysiology Scholarships from the University of Adelaide. Dr. Lau is supported by a Postdoctoral Fellowship from the National Health and Medical Research Council of Australia. Dr. Mahajan is supported by the Leo J. Mahar Lectureship from the University of Adelaide. Dr. Alasady is supported by a Postgraduate Scholarship from the National Health and Medical Research Council of Australia. Drs. McEvoy, Kalman, and Sanders are supported by Practitioner Fellowships from the National Health and Medical Research Council of Australia. Drs. Abhayaratna and Sanders are supported by the National Heart Foundation of Australia. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. This research was originally presented by Dr. Pathak and was awarded the Eric Prystowsky Clinical Research Award at the 2014 Heart Rhythm Society Annual Scientific Sessions, San Francisco, California, and was published in abstract form (Heart Rhythm 2014;11:S75).
- Received May 29, 2014.
- Revision received August 17, 2014.
- Accepted September 8, 2014.
- American College of Cardiology Foundation