Author + information
- Received February 9, 2015
- Revision received February 26, 2015
- Accepted March 1, 2015
- Published online May 26, 2015.
- Rajeev K. Pathak, MBBS∗,
- Melissa E. Middeldorp∗,
- Megan Meredith∗,
- Abhinav B. Mehta, MActSt†,
- Rajiv Mahajan, MD, PhD∗,
- Christopher X. Wong, MBBS, PhD∗,‡,
- Darragh Twomey, MBBS∗,
- Adrian D. Elliott, PhD∗,§,
- Jonathan M. Kalman, MBBS, PhD¶,
- Walter P. Abhayaratna, MBBS, PhD#,
- Dennis H. Lau, MBBS, PhD∗ and
- Prashanthan Sanders, MBBS, PhD∗∗ ()
- ∗Centre for Heart Rhythm Disorders (CHRD), South Australian Health and Medical Research Institute (SAHMRI), University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia
- †Research School of Finance, Actuarial Studies and Applied Statistics, Australian National University, Canberra, Australia
- ‡Clinical Trial Service Unit and Epidemiological Studies Unit, University of Oxford, Oxford, United Kingdom
- §School of Medical Sciences, University of Adelaide, 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, University of Adelaide and Royal Adelaide Hospital, Department of Cardiology, Royal Adelaide Hospital, North Terrace, Adelaide, South Australia 5000, Australia.
Background Obesity and atrial fibrillation (AF) frequently coexist. Weight loss reduces the burden of AF, but whether this is sustained, has a dose effect, or is influenced by weight fluctuation is unknown.
Objectives This study sought to evaluate the long-term impact of weight loss and weight fluctuation on rhythm control in obese individuals with AF.
Methods Of 1,415 consecutive patients with AF, 825 had a body mass index ≥27 kg/m2 and were offered weight management. After screening for exclusion criteria, 355 were included in this analysis. Weight loss was categorized as group 1 (≥10%), group 2 (3% to 9%), and group 3 (<3%). Weight trend and/or fluctuation was determined by yearly follow-up. We determined the impact on the AF severity scale and 7-day ambulatory monitoring.
Results There were no differences in baseline characteristics or follow-up among the groups. AF burden and symptom severity decreased more in group 1 compared with groups 2 and 3 (p < 0.001 for all). Arrhythmia-free survival with and without rhythm control strategies was greatest in group 1 compared with groups 2 and 3 (p < 0.001 for both). In multivariate analyses, weight loss and weight fluctuation were independent predictors of outcomes (p < 0.001 for both). Weight loss ≥10% resulted in a 6-fold (95% confidence interval: 3.4 to 10.3; p < 0.001) greater probability of arrhythmia-free survival compared with the other 2 groups. Weight fluctuation >5% partially offset this benefit, with a 2-fold (95% confidence interval: 1.0 to 4.3; p = 0.02) increased risk of arrhythmia recurrence.
Conclusions Long-term sustained weight loss is associated with significant reduction of AF burden and maintenance of sinus rhythm. (Long-Term Effect of Goal directed weight management on Atrial Fibrillation Cohort: A 5 Year follow-up study [LEGACY Study]; ACTRN12614001123639)
This study was supported by the Centre for Heart Rhythm Disorders at the University of Adelaide, Adelaide, Australia. The sponsor has had no direct involvement in the design and conduct of the study, collection, management, analysis and interpretation of the data, preparation, review or approval of the paper, or the decision to submit the paper for publication. 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. Wong is supported by a Rhodes scholarship and a Postgraduate Medical Scholarship 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. Drs. 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. Dr. Lau is supported by a Postdoctoral Fellowship from the National Health and Medical Research Council of Australia.
Dr. Kalman has received research funding from St. Jude Medical, Biosense-Webster, Medtronic, and Boston Scientific. Dr. Sanders has served on the advisory board of Biosense-Webster, Medtronic, St. Jude Medical, Sanofi, and Merck, Sharpe and Dohme; has received lecture and/or consulting fees from Biosense-Webster, Medtronic, St. Jude Medical, Boston Scientific, Merck, Sharpe and Dohme, Biotronik, and Sanofi; and has received research funding from Medtronic, St. Jude Medical, Boston Scientific, Biotronik, and Sorin. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received February 9, 2015.
- Revision received February 26, 2015.
- Accepted March 1, 2015.
- American College of Cardiology Foundation