Ambarish Pandey1, Sushil Garg1, Monica Khunger1, Douglas Darden1, Colby Ayers1, Dharam J Kumbhani1, Helen G Mayo1, James A de Lemos1, Jarett D Berry2. 1. From Division of Cardiology (A.P., C.A., D.J.K., J.A.d.L., J.D.B.), Department of Internal Medicine (D.D.), and Department of Clinical Sciences (C.A., J.D.B.), University of Texas Southwestern Medical Center, Dallas; Department of Internal Medicine, University of Minnesota School of Medicine, Minneapolis (S.G.); Department of Internal Medicine, Cleveland Clinic, OH (M.K.); and University of Texas Southwestern Medical Center Library, Dallas (H.G.M.). 2. From Division of Cardiology (A.P., C.A., D.J.K., J.A.d.L., J.D.B.), Department of Internal Medicine (D.D.), and Department of Clinical Sciences (C.A., J.D.B.), University of Texas Southwestern Medical Center, Dallas; Department of Internal Medicine, University of Minnesota School of Medicine, Minneapolis (S.G.); Department of Internal Medicine, Cleveland Clinic, OH (M.K.); and University of Texas Southwestern Medical Center Library, Dallas (H.G.M.). jarett.berry@utsouthwestern.edu.
Abstract
BACKGROUND: Prior studies have reported an inverse association between physical activity (PA) and risk of heart failure (HF). However, a comprehensive assessment of the quantitative dose-response association between PA and HF risk has not been reported previously. METHODS AND RESULTS: Prospective cohort studies with participants >18 years of age that reported association of baseline PA levels and incident HF were included. Categorical dose-response relationships between PA and HF risk were assessed with random-effects models. Generalized least-squares regression models were used to assess the quantitative relationship between PA (metabolic equivalent [MET]-min/wk) and HF risk across studies reporting quantitative PA estimates. Twelve prospective cohort studies with 20 203 HF events among 370 460 participants (53.5% women; median follow-up, 13 years) were included. The highest levels of PA were associated with significantly reduced risk of HF (pooled hazard ratio for highest versus lowest PA, 0.70; 95% confidence interval, 0.67-0.73). Compared with participants reporting no leisure-time PA, those who engaged in guideline-recommended minimum levels of PA (500 MET-min/wk; 2008 US federal guidelines) had modest reductions in HF risk (pooled hazard ratio, 0.90; 95% confidence interval, 0.87-0.92). In contrast, a substantial risk reduction was observed among individuals who engaged in PA at twice (hazard ratio for 1000 MET-min/wk, 0.81; 95% confidence interval, 0.77-0.86) and 4 times (hazard ratio for 2000 MET-min/wk, 0.65; 95% confidence interval, 0.58-0.73) the minimum guideline-recommended levels. CONCLUSIONS: There is an inverse dose-response relationship between PA and HF risk. Doses of PA in excess of the guideline-recommended minimum PA levels may be required for more substantial reductions in HF risk.
BACKGROUND: Prior studies have reported an inverse association between physical activity (PA) and risk of heart failure (HF). However, a comprehensive assessment of the quantitative dose-response association between PA and HF risk has not been reported previously. METHODS AND RESULTS: Prospective cohort studies with participants >18 years of age that reported association of baseline PA levels and incident HF were included. Categorical dose-response relationships between PA and HF risk were assessed with random-effects models. Generalized least-squares regression models were used to assess the quantitative relationship between PA (metabolic equivalent [MET]-min/wk) and HF risk across studies reporting quantitative PA estimates. Twelve prospective cohort studies with 20 203 HF events among 370 460 participants (53.5% women; median follow-up, 13 years) were included. The highest levels of PA were associated with significantly reduced risk of HF (pooled hazard ratio for highest versus lowest PA, 0.70; 95% confidence interval, 0.67-0.73). Compared with participants reporting no leisure-time PA, those who engaged in guideline-recommended minimum levels of PA (500 MET-min/wk; 2008 US federal guidelines) had modest reductions in HF risk (pooled hazard ratio, 0.90; 95% confidence interval, 0.87-0.92). In contrast, a substantial risk reduction was observed among individuals who engaged in PA at twice (hazard ratio for 1000 MET-min/wk, 0.81; 95% confidence interval, 0.77-0.86) and 4 times (hazard ratio for 2000 MET-min/wk, 0.65; 95% confidence interval, 0.58-0.73) the minimum guideline-recommended levels. CONCLUSIONS: There is an inverse dose-response relationship between PA and HF risk. Doses of PA in excess of the guideline-recommended minimum PA levels may be required for more substantial reductions in HF risk.
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Authors: Roberta Florido; Chiadi E Ndumele; Lucia Kwak; Yuanjie Pang; Kunihiro Matsushita; Jennifer A Schrack; Mariana Lazo; Vijay Nambi; Roger S Blumenthal; Aaron R Folsom; Josef Coresh; Christie M Ballantyne; Elizabeth Selvin Journal: JACC Heart Fail Date: 2017-05 Impact factor: 12.035
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