Author + information
- Received January 5, 2017
- Accepted January 10, 2017
- Published online February 27, 2017.
- Ambarish Pandey, MDa,
- Michael LaMonte, PhD, MPHb,
- Liviu Klein, MD, MSc,
- Colby Ayers, MSa,d,
- Bruce M. Psaty, MD, PhDe,
- Charles B. Eaton, MD, MSf,
- Norrina B. Allen, PhDg,
- James A. de Lemos, MDa,
- Mercedes Carnethon, PhDg,
- Philip Greenland, MDg and
- Jarett D. Berry, MD, MSa,d,∗ ()
- aDivision of Cardiology, UTSW Medical Center, Dallas, Texas
- bDepartment of Epidemiology and Environmental Health, School of Public Health and Health Professions, University of Buffalo, Buffalo, New York
- cDivision of Cardiology, University of California San Francisco, San Francisco, California
- dDepartment of Clinical Sciences, UTSW Medical Center, Dallas, Texas
- eCardiovascular Health Research Unit, Departments of Medicine, Epidemiology, and Health Services, University of Washington, Seattle, Washington
- fDepartment of Epidemiology, School of Public Health, Brown University, Providence, Rhode Island and Department of Family Medicine, Alpert Medical School of Brown University, Providence, Rhode Island
- gDepartment of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois
- ↵∗Address for correspondence:
Dr. Jarett D. Berry, Department of Cardiology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9047.
Background Lower leisure-time physical activity (LTPA) and higher body mass index (BMI) are independently associated with risk of heart failure (HF). However, it is unclear if this relationship is consistent for both heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF).
Objectives This study sought to quantify dose–response associations between LTPA, BMI, and the risk of different HF subtypes.
Methods Individual-level data from 3 cohort studies (WHI [Women’s Health Initiative], MESA [Multi-Ethnic Study of Atherosclerosis], and CHS [Cardiovascular Health Study]) were pooled and participants were stratified into guideline-recommended categories of LTPA and BMI. Associations between LTPA, BMI, and risk of overall HF, HFpEF (ejection fraction ≥45%), and HFrEF (ejection fraction <45%) were assessed by using multivariable adjusted Cox models and restricted cubic splines.
Results The study included 51,451 participants with 3,180 HF events (1,252 HFpEF, 914 HFrEF, and 1,014 unclassified HF). In the adjusted analysis, there was a dose-dependent association between higher LTPA levels, lower BMI, and overall HF risk. Among HF subtypes, LTPA in any dose range was not associated with HFrEF risk. In contrast, lower levels of LTPA (<500 MET-min/week) were not associated with HFpEF risk, and dose-dependent associations with lower HFpEF risk were observed at higher levels. Compared with no LTPA, higher than twice the guideline-recommended minimum LTPA levels (>1,000 MET-min/week) were associated with an 19% lower risk of HFpEF (hazard ratio: 0.81; 95% confidence interval: 0.68 to 0.97). The dose–response relationship for BMI with HFpEF risk was also more consistent than with HFrEF risk, such that increasing BMI above the normal range (≥25 kg/m2) was associated with a greater increase in risk of HFpEF than HFrEF.
Conclusions Our study findings show strong, dose–dependent associations between LTPA levels, BMI, and risk of overall HF. Among HF subtypes, higher LTPA levels and lower BMI were more consistently associated with lower risk of HFpEF compared with HFrEF.
This project was conducted in collaboration with the American Heart Association SFRN (Strategically Focused Research Network) centers for prevention at UTSW, Dallas, and Northwestern University, Chicago. The MESA (Multi-Ethnic Study of Atherosclerosis) study was supported by contracts HHSN268201500003I, N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, and N01-HC-95169 from the National Heart, Lung, and Blood Institute (NHLBI) and by grants UL1-TR-000040 and UL1-TR-001079 from the National Center for Research Resources. The Women’s Health Initiative program was supported by the NHLBI, the National Institutes of Health, and the U.S. Department of Health and Human Services fund through contracts HHSN268201100046C, HHSN268201100001C, HHSN268201100002C, HHSN268201100003C, HHSN268201100004C, and HHSN271201100004C.
The Cardiovascular Health Study was supported by contracts HHSN268201200036C, HHSN268200800007C, N01HC55222, N01HC85079, N01HC85080, N01HC85081, N01HC85082, N01HC85083, HL130114, and N01HC85086 and grant U01HL080295 from the NHLBI, with additional contribution from the National Institute of Neurological Disorders and Stroke. Additional support was provided by the National Institute on Aging (R01AG023629). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Dr. Berry receives funding from the Dedman Family Scholar in Clinical Care endowment at the University of Texas Southwestern Medical Center and from the American Heart Association prevention network (14SFRN20740000). Dr. Psaty has served on the Data and Safety Monitoring Board of a clinical trial funded by Zoll LifeCor and on the Steering Committee of the Yale Open Data Access project funded by Johnson & Johnson. Dr. Allen has received grant support from Novartis. Dr. de Lemos has served as a consultant for Abbott Diagnostics, Siemen's Health Care, and Amgen; and has received grant support from Abbott Diagnostics. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received January 5, 2017.
- Accepted January 10, 2017.
- American College of Cardiology Foundation