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Original research article
Complex interaction of obesity, intentional weight loss and heart failure: a systematic review and meta-analysis
  1. Rajiv Mahajan1,2,
  2. Michael Stokes1,3,
  3. Adrian Elliott1,3,
  4. Dian A Munawar1,3,
  5. Kashif B Khokhar1,3,
  6. Anand Thiyagarajah1,3,
  7. Jeroen Hendriks1,3,
  8. Dominik Linz1,3,
  9. Celine Gallagher1,3,
  10. David Kaye4,5,
  11. Dennis Lau1,3,
  12. Prashanthan Sanders1,3
  1. 1 Centre for Heart Rhythm Disorders, University of Adelaide, Adelaide, South Australia, Australia
  2. 2 Department of Cardiology, Lyell McEwin Hospital, Elizabeth Vale, South Australia, Australia
  3. 3 Department of Cardiology, Royal Adelaide Hospital, Adelaide, South Australia, Australia
  4. 4 Department of Cardiology, Alfred Hospital, Melbourne, Victoria, Australia
  5. 5 Heart Research, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia
  1. Correspondence to Professor Prashanthan Sanders, Centre for Heart Rhythm Disorders, University of Adelaide, Adelaide; prash.sanders{at}adelaide.edu.au

Abstract

Objective The aim of the meta-analysis was to determine the association of obesity and heart failure (HF) and the cardiac impact of intentional weight loss following bariatric surgery on cardiac structure and myocardial function in obese subjects.

Methods MEDLINE, Embase and Web of Science were searched up to 3 April 2018. Studies reporting association and prognostic impact of obesity in HF and the impact of intentional weight loss following bariatric surgery on cardiac structure and myocardial function in obesity were included in the meta-analysis.

Results 4959 citations were reviewed. After exclusions, 29 studies were analysed. A ‘J curve’ relationship was observed between body mass index (BMI) and risk of HF with maximum risk in the morbidly obese (1.73 (95% CI 1.30 to 2.31), p<0.001, n=11). Although ‘obesity paradox’ was observed for all-cause mortality, the overweight group was associated with lower cardiovascular (CV) mortality (OR=0.86 (95% CI 0.79 to 0.94), n=11) with no significant differences across other BMI groups. Intentional weight loss induced by bariatric surgery in obese patients (n=9) without established HF, atrial fibrillation or known coronary artery disease, was associated with a reduction in left ventricular mass index (p<0.0001), improvement in left ventricular diastolic function (p≤0.0001) and a reduction in left atrial size (p=0.02).

Conclusions Despite the increased risk of HF with obesity, an ‘obesity paradox’ is observed for all-cause mortality. However, the nadir for CV mortality is observed in the overweight group. Importantly, intentional weight loss was associated with improvement in indices of cardiac structure and myocardial function in obese patients.

Trial registration number APP 74412.

  • obesity
  • heart failure
  • obesity paradox
  • weight loss
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Footnotes

  • DL and PS contributed equally.

  • RM and MS contributed equally.

  • Contributors RM, MS, AE, DL and PS had full access to all the data in the study and take responsibility for the integrity of the data and accuracy of the data analysis. Study concept and design: RM and PS. Acquisition of data: RM and MS. Analysis and interpretation of data: RM, MS, AE, DL and PS. Drafting of manuscript: RM, MS and PS. Critical revision of the manuscript for important intellectual content: all authors. Statistical analysis: RM, MS and AE. Study supervision: RM and PS.

  • Funding This study was supported by funds from the Centre of Heart Rhythm Disorders at the University of Adelaide. RM is supported by an Early Career Fellowship from the National Health and Medical Research Council (NHMRC) and National Heart Foundation (NHF) of Australia and by the Leo J. Mahar Lectureship by the University of Adelaide. MS is supported by the Dawes Scholarship from the Royal Adelaide Hospital. AE and JH are supported by the Early Career Fellowship from NHF of Australia. DAM is supported by the Robert J. Craig Scholarship from the University of Adelaide and by the Indonesia Endowment Fund for Education, Ministry of Finance, The Republic of Indonesia. KBK is supported by Asia Pacific Heart Rhythm Society and the New Zealand Heart Foundation overseas fellowship. JH is supported by the Derek Frewin Lectureship from the University of Adelaide. DL is supported by a Beacon Research Fellowship from the University of Adelaide. CG is supported a Fellowship from the University of Adelaide. DK is supported by a Senior Research Fellowship from the NHMRC. DL is supported by the Robert J. Craig Lectureship from the University of Adelaide. PS is supported by Practitioner Fellowships from the NHMRC and by the NHF of Australia. The sponsor of the study is the University of Adelaide. Several of the authors are employees of the University of Adelaide. The sponsor has had no direct involvement in the management or outcomes of the study.

  • Competing interests The University of Adelaide reports receiving on behalf of RM lecture and/or consulting fees from Abbott and Medtronic. The University of Adelaide reports receiving on behalf of RM research funding from Abbott and Medtronic. DL reports having served on the advisory board of LivaNova and Medtronic. The University of Adelaide reports receiving on behalf of DL reports lecture and/or consulting fees from LivaNova, Medtronic, Pfizer and ResMed. The University of Adelaide reports receiving on behalf of DL research funding from Sanofi, ResMed and Medtronic. PS reports having served on the advisory board of Biosense-Webster, Medtronic, Abbott, Boston Scientific and CathRx. The University of Adelaide reports receiving on behalf of PS lecture and/or consulting fees from Biosense-Webster, Medtronic, Abbott and Boston Scientific. The University of Adelaide reports receiving on behalf of PS research funding from Medtronic, Abbott, Boston Scientific, Biotronik and Liva Nova.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data sharing statement There are no data in this work.

  • Patient consent for publication Not required.

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