Ryan T Demmer1, Matthew A Allison2, Jianwen Cai2, Robert C Kaplan2, Ankit A Desai2, Barry E Hurwitz2, Jill C Newman2, Sanjiv J Shah2, Katrina Swett2, Gregory A Talavera2, Ashley Thai2, Marston E Youngblood2, Carlos J Rodriguez2. 1. From the Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY (R.T.D., A.T.); Department of Family Medicine and Public Health (M.A.A.) and Graduate School of Public Health (G.A.T.), University of California, San Diego; Department of Biostatistics, University of North Carolina at Chapel Hill (J.C., M.E.Y.); Department of Epidemiology and Population Health, Albert Einstein College of Medicine, New York, NY (R.C.K.); Department of Medicine, University of Illinois, Champaign (A.A.D.); Department of Psychology, Behavioral Medicine Research Center, University of Miami, Coral Gables, FL (B.E.H.); Wake Forest School of Medicine, Wake Forest University, Winston-Salem, NC (J.C.N., K.S., C.J.R.); and Division of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL (S.J.S.). rtd2106@cumc.columbia.edu. 2. From the Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY (R.T.D., A.T.); Department of Family Medicine and Public Health (M.A.A.) and Graduate School of Public Health (G.A.T.), University of California, San Diego; Department of Biostatistics, University of North Carolina at Chapel Hill (J.C., M.E.Y.); Department of Epidemiology and Population Health, Albert Einstein College of Medicine, New York, NY (R.C.K.); Department of Medicine, University of Illinois, Champaign (A.A.D.); Department of Psychology, Behavioral Medicine Research Center, University of Miami, Coral Gables, FL (B.E.H.); Wake Forest School of Medicine, Wake Forest University, Winston-Salem, NC (J.C.N., K.S., C.J.R.); and Division of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL (S.J.S.).
Abstract
BACKGROUND: We examined the relationship between glucose homeostasis and comprehensive measures of cardiac structure and function among a representative sample of US Hispanics. METHODS AND RESULTS: ECHO-SOL (Echocardiographic Study of Latinos), an echocardiographic ancillary study of the HCHS/SOL (Hispanic Community Health Study/Study of Latinos), enrolled 1818 Hispanic/Latino men (43%) and women (57%) aged ≥45 years (mean=56). Glucose intolerance was defined as follows: (1) prediabetes: hemoglobin (HbA1c) ≥5.7 and <6.5% and (2) diabetes mellitus: fasting plasma glucose ≥126 mg/dL, 2-hour postload glucose ≥200 mg/dL, HbA1c ≥6.5%, or hypoglycemic agent use. Uncontrolled diabetes mellitus was defined as HbA1c ≥7.0%. Insulin resistance was defined using the homeostatic model assessment for insulin resistance. Echocardiography examinations assessed left ventricular structure and systolic/diastolic function. Multivariable linear and logistic regression models were used. Prediabetes prevalence was 42%, and diabetes mellitus prevalence was 28% (47% uncontrolled). Glucose intolerance was associated with increased left ventricular posterior wall and interventricular septal and relative wall thicknesses (all P<0.05), reduced ejection fraction (P<0.01), reduced stroke and end-diastolic volumes (both P<0.001), decreased peak E' velocity (lateral and septal P<0.001), and increased E/E' ratio (lateral and septal P<0.01). The odds ratios (95% confidence intervals) for diastolic dysfunction among individuals with prediabetes and diabetes mellitus (versus diabetes mellitus free) were 1.36 (0.96-1.9) and 1.90 (1.3-2.8), respectively(P=0.006). Results were consistent for uncontrolled diabetes mellitus versus diabetes mellitus. Homeostatic model assessment for insulin resistance was associated with increased E/E' (P<0.001), and greater relative wall thickness and septal thickness (both P<0.05); lower stroke volume (P<0.0001); and lower peak lateral and septal E' velocities (both P<0.01). CONCLUSIONS: Glucose intolerance and insulin resistance are associated with unfavorable cardiac structure and function, particularly worsened measures of diastolic function, even before the development of diabetes mellitus.
BACKGROUND: We examined the relationship between glucose homeostasis and comprehensive measures of cardiac structure and function among a representative sample of US Hispanics. METHODS AND RESULTS: ECHO-SOL (Echocardiographic Study of Latinos), an echocardiographic ancillary study of the HCHS/SOL (Hispanic Community Health Study/Study of Latinos), enrolled 1818 Hispanic/Latino men (43%) and women (57%) aged ≥45 years (mean=56). Glucose intolerance was defined as follows: (1) prediabetes: hemoglobin (HbA1c) ≥5.7 and <6.5% and (2) diabetes mellitus: fasting plasma glucose ≥126 mg/dL, 2-hour postload glucose ≥200 mg/dL, HbA1c ≥6.5%, or hypoglycemic agent use. Uncontrolled diabetes mellitus was defined as HbA1c ≥7.0%. Insulin resistance was defined using the homeostatic model assessment for insulin resistance. Echocardiography examinations assessed left ventricular structure and systolic/diastolic function. Multivariable linear and logistic regression models were used. Prediabetes prevalence was 42%, and diabetes mellitus prevalence was 28% (47% uncontrolled). Glucose intolerance was associated with increased left ventricular posterior wall and interventricular septal and relative wall thicknesses (all P<0.05), reduced ejection fraction (P<0.01), reduced stroke and end-diastolic volumes (both P<0.001), decreased peak E' velocity (lateral and septal P<0.001), and increased E/E' ratio (lateral and septal P<0.01). The odds ratios (95% confidence intervals) for diastolic dysfunction among individuals with prediabetes and diabetes mellitus (versus diabetes mellitus free) were 1.36 (0.96-1.9) and 1.90 (1.3-2.8), respectively(P=0.006). Results were consistent for uncontrolled diabetes mellitus versus diabetes mellitus. Homeostatic model assessment for insulin resistance was associated with increased E/E' (P<0.001), and greater relative wall thickness and septal thickness (both P<0.05); lower stroke volume (P<0.0001); and lower peak lateral and septal E' velocities (both P<0.01). CONCLUSIONS:Glucose intolerance and insulin resistance are associated with unfavorable cardiac structure and function, particularly worsened measures of diastolic function, even before the development of diabetes mellitus.
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