Author + information
- Received October 21, 2016
- Revision received February 1, 2017
- Accepted February 1, 2017
- Published online April 24, 2017.
- Roberta Florido, MDa,
- Chiadi E. Ndumele, MD, MHSa,b,
- Lucia Kwak, MSb,
- Yuanjie Pang, ScMb,
- Kunihiro Matsushita, MD, PhDb,
- Jennifer A. Schrack, PhDb,
- Mariana Lazo, MD, PhDb,c,
- Vijay Nambi, MD, PhDd,e,
- Roger S. Blumenthal, MDa,
- Aaron R. Folsom, MD, MPHf,
- Josef Coresh, MD, PhDb,
- Christie M. Ballantyne, MDe and
- Elizabeth Selvin, PhD, MPHb,∗ ()
- aJohns Hopkins Ciccarone Center for the Prevention of Heart Disease, Johns Hopkins University School of Medicine, Baltimore, Maryland
- bDepartment of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland
- cDepartment of General Internal Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland
- dMichael E. DeBakey Veterans Affairs Hospital, Houston, Texas
- eDivision of Atherosclerosis and Vascular Medicine, Baylor College of Medicine, and Center for Cardiovascular Disease Prevention, Methodist DeBakey Heart and Vascular Center, Houston, Texas
- fDivision of Epidemiology & Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota
- ↵∗Address for correspondence:
Dr. Elizabeth Selvin, Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, 2024 East Monument Street, Suite 2-600, Baltimore, Maryland 21287.
Objectives This study sought to evaluate the association of physical activity with chronic myocardial damage, assessed by elevated high-sensitivity cardiac troponin T (hs-cTnT), in individuals with and without obesity.
Background Physical activity is associated with reduced risk of heart failure (HF), particularly among obese people. The role of chronic myocardial damage in this association is uncertain.
Methods We studied 9,427 participants in the Atherosclerosis Risk in Communities Study without cardiovascular disease, with body mass index >18.5 kg/m2. Physical activity was categorized per American Heart Association guidelines as recommended, intermediate, or poor. We evaluated cross-sectional associations of physical activity and obesity with elevated hs-cTnT (≥14 ng/l). In prospective analyses, we quantified the association of elevated hs-cTnT with HF risk within cross-categories of baseline physical activity and obesity.
Results People with poor physical activity were more likely to have elevated hs-cTnT than those with recommended levels (odds ratio [OR]: 1.39; 95% confidence interval [CI]: 1.15 to 1.68). In cross-categories of physical activity and obesity, using the non-obese/recommended activity group as the reference, individuals with obesity and poor activity were most likely to have elevated hs-cTnT (OR: 2.46; 95% CI: 1.91 to 3.19), whereas the obese/recommended activity group had a weaker association (OR: 1.68; 95% CI: 1.28 to 2.21; p < 0.001 for interaction between physical activity and obesity). In prospective analyses, elevated hs-cTnT was strongly associated (p < 0.001) with incident HF in all obesity/physical activity cross-categories (p > 0.20 for interaction).
Conclusions Physical activity is inversely associated with chronic subclinical myocardial damage. Physical activity might lessen the association between obesity and subclinical myocardial damage, which could represent a mechanism by which physical activity reduces HF risk.
The views expressed in this article are those of the authors and do not necessarily represent the views of the Department of Veterans Affairs. ARIC is conducted as a collaborative study supported by National Heart, Lung, and Blood Institute contracts (HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN268201100008C, HHSN268201100009C, HHSN268201100010C, HHSN268201100011C, and HHSN268201100012C). This work was supported by a Robert Wood Johnson Amos Medical Faculty Development Award and a National Institutes of Health (NIH)/National Heart, Lung, and Blood Institute grant (K23HL12247) awarded to Dr. Ndumele and by an NIH/National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) grant (R01DK089174) awarded to Dr. Selvin. Dr. Selvin was also supported by NIH/NIDDK grant K24DK106414. Dr. Schrack is a consultant for EMD Serono Research & Development Institute, Inc. Dr. Nambi has served as an event adjudicator for a study sponsored by Siemens to evaluate a new high-sensitivity troponin assay. Drs. Selvin and Ballantyne have served on an advisory board for Roche Diagnostics. Drs. Ballantyne and Nambi, along with Roche and Baylor College of Medicine, have filed a provisional patent (patent #61721475) entitled “Biomarkers to Improve Prediction of Heart Failure Risk.” All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received October 21, 2016.
- Revision received February 1, 2017.
- Accepted February 1, 2017.
- 2017 American College of Cardiology Foundation