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Epicardial adipose tissue thickness is an indicator for coronary artery stenosis in asymptomatic type 2 diabetic patients: its assessment by cardiac magnetic resonance

DOI: 10.1186/1475-2840-11-83

Keywords: Epicardial adipose tissue, Cardiovascular magnetic resonance, Silent ischemia, Coronary artery stenosis, Type 2 diabetes

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The study included 100 type 2 diabetic subjects (51 male and 49 female; mean age: 56 ± 7 years). Silent myocardial ischemia, as determined by CMR, was defined as evidence of inducible ischemia or myocardial infarction. Signal reduction or stenosis of ≥ 50% in the vessel diameter was used as the criteria for significant coronary artery stenosis on coronary magnetic resonance (MR) angiography.EAT thickness was positively correlated with body mass index (BMI), waist-to-hip ratio, systolic blood pressure, postprandial glucose, fasting/postprandial triglyceride (TG), serum glycated hemoglobin (HbA1c) level, and homeostasis model assessment of insulin resistance (HOMA-IR) score. Significant coronary artery stenosis was found in 24 patients, while 14 patients had silent myocardial ischemia in CMR (1 with silent myocardial infarction, 11 with inducible ischemia, and 2 with both). EAT thickness was greater in patients who had coronary artery stenosis (13.0 ± 2.6 mm vs. 11.5 ± 2.1 mm, p = 0.01), but did not differ between the subjects with or without silent myocardial ischemia on CMR images (12.8 ± 2.1 vs. 11.7 ± 2.3 mm, p = 0.11). Multivariate logistic regression analysis indicated that EAT thickness was an independent indicator for significant coronary artery stenosis after adjusting for traditional risk factors (OR 1.403, p = 0.026).Increased EAT thickness assessed by CMR is an independent risk factor for significant coronary artery stenosis in asymptomatic type 2 diabetes. However, EAT thickness was not associated with silent myocardial ischemia.Epicardial adipose tissue (EAT) is a metabolically active visceral fat deposit found around the heart, between the pericardium and myocardium [1]. Transthoracic echocardiography (TTE) and multi-slice computed tomography (MSCT) scanning have been conventional methods for quantifying EAT [2]. Growing evidence suggests that EAT has clinical relevance in that it produces several proatherogenic molecules and influences the development


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