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Gender disparities in the association between epicardial adipose tissue volume and coronary atherosclerosis: A 3-dimensional cardiac computed tomography imaging study in Japanese subjects

DOI: 10.1186/1475-2840-11-106

Keywords: Atherosclerosis, Gender difference, Epicardial adipose tissue, Obesity

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Abstract:

The study population consisted of 90 consecutive subjects (age: 63 ± 12 years; men: 47, women: 43) who underwent 256-slice multi-detector computed tomography (MDCT) coronary angiography. EATV was measured as the sum of cross-sectional epicardial fat area on CT images, from the lower surface of the left pulmonary artery origin to the apex. Subjects were segregated into the CAD group (coronary luminal narrowing > 50%) and non-CAD group.EATV/body surface area (BSA) was higher among men in the CAD group than in the non-CAD group (62 ± 13 vs. 33 ± 10 cm3/m2, p < 0.0001), but did not differ significantly among women in the 2 groups (49 ± 18 vs. 42 ± 9 cm3/m2, not significant). Multivariate logistic analysis showed that EATV/BSA was the single predictor for >50% coronary luminal narrowing in men (p < 0.0001). Predictors excluded were age, body mass index, hypertension, diabetes mellitus, and hyperlipidemia.Increased EATV is strongly associated with coronary atherosclerosis in men.Epicardial adipose tissue (EAT) is the visceral fat located between the outer layer of the myocardium and the visceral pericardium [1-4]. EAT volume (EATV) is correlated with various cardiovascular risk factors, independent of abdominal visceral adiposity, body mass index (BMI), hypertension, and diabetes mellitus [5-7]. Two population-based studies, the Multi-Ethnic Study of Atherosclerosis and the Framingham Heart Study, showed that EATV is an independent risk predictor for cardiovascular disease [5,8,9]. EAT is shown to be metabolically active and the source of pro-atherogenic mediators and adipocytokines [1-5]. Because EAT and the myocardium are located close anatomically, it is predicted that cytokines/adipocytokines produced by infiltrated macrophages or by adipocytes could locally modulate myocardial function or contribute to the pathogenesis of coronary atherosclerosis [1-5]. Recently, we [10,11] and others [12] showed that proinflammatory cytokines and adipocytokines are expressed and sec

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