Alvin Chandra1, Ian J Neeland2, Jarett D Berry3, Colby R Ayers4, Anand Rohatgi2, Sandeep R Das2, Amit Khera2, Darren K McGuire3, James A de Lemos2, Aslan T Turer5. 1. Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas. 2. Division of Cardiology, University of Texas Southwestern Medical Center, Dallas, Texas. 3. Division of Cardiology, University of Texas Southwestern Medical Center, Dallas, Texas; Department of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, Texas. 4. Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas; Department of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, Texas. 5. Division of Cardiology, University of Texas Southwestern Medical Center, Dallas, Texas. Electronic address: aslan.turer@utsouthwestern.edu.
Abstract
BACKGROUND: Obesity has been linked to the development of hypertension, but whether total adiposity or site-specific fat accumulation underpins this relationship is unclear. OBJECTIVES: This study sought to determine the relationship between adipose tissue distribution and incident hypertension. METHODS: Normotensive participants enrolled in the Dallas Heart Study were followed for a median of 7 years for the development of hypertension (systolic blood pressure [SBP] ≥140 mm Hg, diastolic blood pressure ≥90 mm Hg, or initiation of blood pressure medications). Visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) was quantified by magnetic resonance imaging and proton-spectroscopic imaging, and lower body fat (LBF) was imaged by dual-energy x-ray absorptiometry. Multivariable relative risk regression was performed to test the association between individual fat depots and incident hypertension, adjusting for age, sex, race/ethnicity, diabetes, smoking, SBP, and body mass index (BMI). RESULTS: Among 903 participants (median age, 40 years; 57% women; 60% nonwhite; median BMI 27.5 kg/m(2)), 230 (25%) developed incident hypertension. In multivariable analyses, higher BMI was significantly associated with incident hypertension (relative risk: 1.24; 95% confidence interval: 1.12 to 1.36, per 1-SD increase). However, when VAT, SAT, and LBF were added to the model, only VAT remained independently associated with incident hypertension (relative risk: 1.22; 95% confidence interval: 1.06 to 1.39, per 1-SD increase). CONCLUSIONS: Increased visceral adiposity, but not total or subcutaneous adiposity, was robustly associated with incident hypertension. Additional studies will be needed to elucidate the mechanisms behind this association.
BACKGROUND: Obesity has been linked to the development of hypertension, but whether total adiposity or site-specific fat accumulation underpins this relationship is unclear. OBJECTIVES: This study sought to determine the relationship between adipose tissue distribution and incident hypertension. METHODS: Normotensive participants enrolled in the Dallas Heart Study were followed for a median of 7 years for the development of hypertension (systolic blood pressure [SBP] ≥140 mm Hg, diastolic blood pressure ≥90 mm Hg, or initiation of blood pressure medications). Visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) was quantified by magnetic resonance imaging and proton-spectroscopic imaging, and lower body fat (LBF) was imaged by dual-energy x-ray absorptiometry. Multivariable relative risk regression was performed to test the association between individual fat depots and incident hypertension, adjusting for age, sex, race/ethnicity, diabetes, smoking, SBP, and body mass index (BMI). RESULTS: Among 903 participants (median age, 40 years; 57% women; 60% nonwhite; median BMI 27.5 kg/m(2)), 230 (25%) developed incident hypertension. In multivariable analyses, higher BMI was significantly associated with incident hypertension (relative risk: 1.24; 95% confidence interval: 1.12 to 1.36, per 1-SD increase). However, when VAT, SAT, and LBF were added to the model, only VAT remained independently associated with incident hypertension (relative risk: 1.22; 95% confidence interval: 1.06 to 1.39, per 1-SD increase). CONCLUSIONS: Increased visceral adiposity, but not total or subcutaneous adiposity, was robustly associated with incident hypertension. Additional studies will be needed to elucidate the mechanisms behind this association.
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Authors: Poghni A Peri-Okonny; Colby Ayers; Naim Maalouf; Sandeep R Das; James A de Lemos; Jarett D Berry; Aslan T Turer; Ian J Neeland; Philipp E Scherer; Wanpen Vongpatanasin Journal: Diabetes Metab Res Rev Date: 2016-08-18 Impact factor: 4.876