Jennifer E Ho1, Elizabeth L McCabe2, Thomas J Wang2, Martin G Larson2, Daniel Levy2, Connie Tsao2, Jayashri Aragam2, Gary F Mitchell2, Emelia J Benjamin2, Ramachandran S Vasan2, Susan Cheng2. 1. From the Cardiovascular Research Center and Cardiology Division, Department of Medicine, Massachusetts General Hospital, Boston (J.E.H.); National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study, Framingham, MA (J.E.H., E.L.M., M.G.L., D.L., C.T., E.J.B., R.S.V., S.C.); Cardiology Division, Department of Medicine, Vanderbilt University, Nashville, TN (T.J.W.); Department of Biostatistics (M.G.L.) and Department of Epidemiology (E.J.B., R.S.V.), Boston University School of Public Health, MA; Cardiovascular Division, Beth Israel Deaconess Medical Center, Boston, MA (C.T.); Division of Cardiology, Department of Medicine, Brigham and Women's Hospital, Boston, MA (J.A., S.C.); Division of Cardiology, Department of Medicine, Veterans Affairs Boston Healthcare System, MA (J.A.); Cardiovascular Engineering, Inc, Norwood, MA (G.F.M.); and Cardiovascular Medicine Section (E.J.B.), Section of Preventive Medicine and Epidemiology (E.J.B., R.S.V.), and Section of Cardiology (E.J.B., R.S.V.), Department of Medicine, Boston University School of Medicine, MA. jho1@mgh.harvard.edu. 2. From the Cardiovascular Research Center and Cardiology Division, Department of Medicine, Massachusetts General Hospital, Boston (J.E.H.); National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study, Framingham, MA (J.E.H., E.L.M., M.G.L., D.L., C.T., E.J.B., R.S.V., S.C.); Cardiology Division, Department of Medicine, Vanderbilt University, Nashville, TN (T.J.W.); Department of Biostatistics (M.G.L.) and Department of Epidemiology (E.J.B., R.S.V.), Boston University School of Public Health, MA; Cardiovascular Division, Beth Israel Deaconess Medical Center, Boston, MA (C.T.); Division of Cardiology, Department of Medicine, Brigham and Women's Hospital, Boston, MA (J.A., S.C.); Division of Cardiology, Department of Medicine, Veterans Affairs Boston Healthcare System, MA (J.A.); Cardiovascular Engineering, Inc, Norwood, MA (G.F.M.); and Cardiovascular Medicine Section (E.J.B.), Section of Preventive Medicine and Epidemiology (E.J.B., R.S.V.), and Section of Cardiology (E.J.B., R.S.V.), Department of Medicine, Boston University School of Medicine, MA.
Abstract
BACKGROUND: Obesity and cardiometabolic dysfunction are associated with increased risk of heart failure and other cardiovascular diseases. We sought to examine the association of cardiometabolic traits with left ventricular (LV) cardiac mechanics. We hypothesized that specific obesity-related phenotypes are associated with distinct aspects of LV strain. METHODS AND RESULTS: We evaluated the associations of obesity-related phenotypes, including central adiposity, diabetes mellitus, insulin resistance, and circulating adipokine concentrations with echocardiographic measures of LV mechanical function among participants of the Framingham Heart Study Offspring and Third Generation cohorts. Among 6231 participants, the mean age was 51±16 years, and 54% were women. Greater body mass index was associated with worse LV longitudinal strain, radial strain (apical view), and longitudinal synchrony (multivariable-adjusted P<0.0001). After accounting for body mass index, we found that central adiposity, as measured by waist circumference, was associated with worse global longitudinal strain and synchrony (P≤0.006). Measures of insulin resistance, dyslipidemia, and diabetes mellitus also were associated with distinct aspects of LV mechanical function. Circulating leptin concentrations were associated with global longitudinal and radial strain (apical view, P<0.0001), whereas no such association was found with leptin receptor, adiponectin, or C-reactive protein. CONCLUSIONS: Our findings highlight the association of central obesity and related cardiometabolic phenotypes above and beyond body mass index with subclinical measures of LV mechanical function. Interestingly, obesity-related traits were associated with distinct aspects of LV mechanics, underscoring potential differential effects along specific LV planes of deformation. These findings may shed light onto obesity-related cardiac remodeling and heart failure.
BACKGROUND:Obesity and cardiometabolic dysfunction are associated with increased risk of heart failure and other cardiovascular diseases. We sought to examine the association of cardiometabolic traits with left ventricular (LV) cardiac mechanics. We hypothesized that specific obesity-related phenotypes are associated with distinct aspects of LV strain. METHODS AND RESULTS: We evaluated the associations of obesity-related phenotypes, including central adiposity, diabetes mellitus, insulin resistance, and circulating adipokine concentrations with echocardiographic measures of LV mechanical function among participants of the Framingham Heart Study Offspring and Third Generation cohorts. Among 6231 participants, the mean age was 51±16 years, and 54% were women. Greater body mass index was associated with worse LV longitudinal strain, radial strain (apical view), and longitudinal synchrony (multivariable-adjusted P<0.0001). After accounting for body mass index, we found that central adiposity, as measured by waist circumference, was associated with worse global longitudinal strain and synchrony (P≤0.006). Measures of insulin resistance, dyslipidemia, and diabetes mellitus also were associated with distinct aspects of LV mechanical function. Circulating leptin concentrations were associated with global longitudinal and radial strain (apical view, P<0.0001), whereas no such association was found with leptin receptor, adiponectin, or C-reactive protein. CONCLUSIONS: Our findings highlight the association of central obesity and related cardiometabolic phenotypes above and beyond body mass index with subclinical measures of LV mechanical function. Interestingly, obesity-related traits were associated with distinct aspects of LV mechanics, underscoring potential differential effects along specific LV planes of deformation. These findings may shed light onto obesity-related cardiac remodeling and heart failure.
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