@article{5aa9b54be9b84adeb8ef10a8d7ed852d,
title = "Physical Activity, Subclinical Myocardial Injury, and Risk of Heart Failure Subtypes in Black Adults",
abstract = "Objectives: This study sought to evaluate the independent associations and interactions between high-sensitivity cardiac troponin I (hs-cTnI) and physical activity (PA) with risk of heart failure (HF) subtypes, HF with preserved ejection fraction (HFpEF) and HF with reduced ejection fraction (HFrEF). Background: Black adults are at high risk for developing HF. Physical inactivity and subclinical myocardial injury, as assessed by hs-cTnI concentration, are independent risk factors for HF. Methods: Black adults from the Jackson Heart Study without prevalent HF who had hs-cTnI concentration and self-reported PA assessed at baseline were included. Adjusted Cox models were used to evaluate the independent and joint associations and interaction between hs-cTnI concentrations and PA with risk of HFpEF and HFrEF. Results: Among 3,959 participants, 25.1% had subclinical myocardial injury (hs-cTnI ≥4 and ≥6 ng/l in women and men, respectively), and 48.2% were inactive (moderate-to-vigorous PA = 0 min/week). Over 12.0 years of follow-up, 163 and 150 participants had an incident HFpEF and HFrEF event, respectively. In adjusted analysis, higher hs-cTnI concentration (per 1-U log increase) was associated with higher risk of HFpEF (hazard ratio [HR]: 1.47; 95% confidence interval [CI]: 1.25 to 1.72]) and HFrEF (HR: 1.57; 95% CI: 1.35 to 1.83]). In contrast, higher PA (per 1-U log increase) was associated with a lower risk of HFpEF (HR: 0.93; 95% CI: 0.88 to 0.99]) but not HFrEF. There was a significant interaction between hs-cTnI and PA for risk of HFpEF (p interaction = 0.04) such that inactive participants with subclinical myocardial injury were at higher risk of HFpEF but active participants were not. Conclusions: Among Black adults with subclinical myocardial injury, higher levels of PA were associated with attenuated risk of HFpEF.",
keywords = "Black adults, heart failure, physical activity, subclinical myocardial injury",
author = "Patel, {Kershaw V.} and Shawn Simek and Colby Ayers and Neeland, {Ian J.} and Christopher deFilippi and Seliger, {Stephen L.} and Katy Lonergan and Nicole Minniefield and Mentz, {Robert J.} and Adolfo Correa and Yimer, {Wondwosen K.} and Hall, {Michael E.} and Rodriguez, {Carlos J.} and {de Lemos}, {James A.} and Berry, {Jarett D.} and Ambarish Pandey",
note = "Funding Information: Supported by a Strategically Focused Research Network Grant for Prevention from the American Heart Association to University of Texas Southwestern Medical Center, Dallas, and Northwestern University School of Medicine, Chicago. Dr. Neeland is a consultant for Boehringer Ingelheim/Lilly Alliance and Merck. Dr. deFilippi has received grant support from Roche Diagnostics, Ortho Diagnostics, and Siemens Healthineers; is a consultant for Roche Diagnostics, Abbott Diagnostics, Ortho Clinical Diagnostics, Quidel, FujiRebio, and Siemen{\textquoteright}s Health Care Diagnostics; has received royalty payments from UpToDate; co-owns a patent awarded to the University of Maryland (U.S. Patent Application: 15/309,754; Methods for Assessing Differential Risk for Developing Heart Failure); and has received an award, UL1TR003015, from the U.S. National Institutes of Health/Center for Advancing Translational Science. Dr. Seliger has received funding from Roche Diagnostics. Dr. Rodriguez has received research support from Amgen, the American Heart Association, and the National Health Lung and Blood Institute (2R01HL104199). Dr. de Lemos has received grant support from Roche Diagnostics and Abbott Diagnostics; is a consultant for Roche Diagnostics, Abbott Diagnostics, Ortho Clinical Diagnostics, Quidel Cardiovascular, and Siemen{\textquoteright}s Health Care Diagnostics; and is a co-owner of a patent awarded to the University of Maryland (U.S. Patent Application: 15/309,754; Methods for Assessing Differential Risk for Developing Heart Failure). Dr. Mentz has received research support and honoraria from Abbott, American Regent, Amgen, AstraZeneca, Bayer, Boehringer Ingelheim/Eli Lilly, Boston Scientific, Cytokinetics, Fast BioMedical, Gilead, Innolife, Medtronic, Merck, Novartis, Relypsa, Respicardia, Roche, Sanofi, Vifor, and Windtree Therapeutics. Dr. Berry has received a grant, 14SFRN20740000, from the American Heart Association prevention network and salary support from Abbott Diagnostics. Dr. Pandey has served on the advisory board of Roche Diagnostics; has received nonfinancial support from Pfizer and Merck; and has received research support from Texas Health Resources Clinical Scholarship, the Gilead Sciences Research Scholar Program, and the National Institute of Aging GEMSSTAR grant (1R03AG067960-01) and Applied Therapeutics. Funding Information: The authors thank the study participants, staff, and investigators of the Jackson Heart Study. The authors also thank Rachael Whitehead, Houston Methodist Research Institute, for helping create the Central Illustration. The funding for biomarker assays was provided by Abbott Diagnostics. Publisher Copyright: {\textcopyright} 2021 American College of Cardiology Foundation",
year = "2021",
month = jul,
doi = "10.1016/j.jchf.2021.04.003",
language = "English (US)",
volume = "9",
pages = "484--493",
journal = "JACC: Heart Failure",
issn = "2213-1779",
publisher = "Elsevier BV",
number = "7",
}