OBJECTIVES: Epicardial adipose tissue (EAT) is a component of visceral adiposity with endocrine and paracrine effects. It is also associated with metabolic syndrome (MetS). In this study, we investigated the relationship between EAT thickness and hypertension that is a component of MetS. STUDY DESIGN: Enrolled in this study were 140 hypertensive patients and 60 age- and sex-similar normotensive controls. EAT thickness was measured using 2-D echocardiography from the parasternal long- and short-axis views. EAT thicknesses were compared between patients with hypertension and controls. The effects of hypertension on EAT thickness were evaluated like other components of MetS. RESULTS: EAT thickness was increased in hypertensive patients compared to normotensive controls (6.3 ± 1.7 mm vs. 5.3 ± 1.6 mm; p<0.001). EAT thickness correlated with systolic and diastolic blood pressures (r=0.233, p=0.001; r=0.144, p=0.047, respectively). EAT thickness was further increased in patients with uncontrolled hypertension than in those with controlled hypertension (6.6 ± 1.7 mm vs. 5.9 ± 1.8 mm, p=0.046). When linear regression analysis was performed to assess the effect of hypertension on EAT thickness like the other components of MetS, hypertension (p=0.009, 95% CI 0.236-1.619), waist circumference (p=0.003, 95%CI 0.339-1.640), HDL-cholesterol (p=0.046, 95% CI, -0.054 - 0.001) and blood glucose levels (p=0.007, 95% CI, 0.003-0.002) were found to be independent correlates of EAT thickness. CONCLUSION: EAT thickness is associated with hypertension. Hypertension could be contributing factor for the development of EAT thickness like the other components of MetS.
OBJECTIVES: Epicardial adipose tissue (EAT) is a component of visceral adiposity with endocrine and paracrine effects. It is also associated with metabolic syndrome (MetS). In this study, we investigated the relationship between EAT thickness and hypertension that is a component of MetS. STUDY DESIGN: Enrolled in this study were 140 hypertensivepatients and 60 age- and sex-similar normotensive controls. EAT thickness was measured using 2-D echocardiography from the parasternal long- and short-axis views. EAT thicknesses were compared between patients with hypertension and controls. The effects of hypertension on EAT thickness were evaluated like other components of MetS. RESULTS: EAT thickness was increased in hypertensivepatients compared to normotensive controls (6.3 ± 1.7 mm vs. 5.3 ± 1.6 mm; p<0.001). EAT thickness correlated with systolic and diastolic blood pressures (r=0.233, p=0.001; r=0.144, p=0.047, respectively). EAT thickness was further increased in patients with uncontrolled hypertension than in those with controlled hypertension (6.6 ± 1.7 mm vs. 5.9 ± 1.8 mm, p=0.046). When linear regression analysis was performed to assess the effect of hypertension on EAT thickness like the other components of MetS, hypertension (p=0.009, 95% CI 0.236-1.619), waist circumference (p=0.003, 95%CI 0.339-1.640), HDL-cholesterol (p=0.046, 95% CI, -0.054 - 0.001) and blood glucose levels (p=0.007, 95% CI, 0.003-0.002) were found to be independent correlates of EAT thickness. CONCLUSION: EAT thickness is associated with hypertension. Hypertension could be contributing factor for the development of EAT thickness like the other components of MetS.
Authors: A Temiz; S Ozcan; F Gökmen; E Gazi; A Barutcu; A Bekler; B Altun; A Akbal; F Güneş; H Şen Journal: Z Rheumatol Date: 2014-12 Impact factor: 1.372
Authors: Mustafa Cetin; Musa Cakici; Mustafa Polat; Arif Suner; Cemil Zencir; Idris Ardic Journal: Int J Endocrinol Date: 2013-05-09 Impact factor: 3.257