Epicardial adipose tissue volume predicts long term major adverse cardiovascular events in patients with Type 2 diabetes

Epicardial adipose tissue (EAT) is a metabolically active visceral fat depot that plays an important role in coronary atherosclerosis. In this study, our aim was to investigate the relationship between long-term major adverse cardiovascular events (MACEs) and EAT volume detected by coronary computed tomography angiography (CCTA) in patients with Type 2 diabetes mellitus (T2-DM) without previous coronary events. A total of 127 patients with diabetes who underwent CCTA between 2012 and 2014 were enrolled retrospectively. The study population was divided into 2 groups according to whether they experienced or did not experience MACE, which was defined as cardiac death, non-fatal myocardial infarction or unstable angina requiring hospitalization, coronary revascularizations (percutaneous coronary intervention or coronary artery bypass grafting surgery), heart failure, peripheral arterial disease, or ischemic stroke. In both groups, EAT volumes were measured by CCTA. During 60±7 months follow-up period, 22 participants experienced MACEs. Data were evaluated with univariate and multivariate analyses and receiver operating characteristic (ROC) analysis. Age, male sex, coronary artery disease, hemoglobin A1c, glucose, creatinine, C- reactive protein, and cholesterol levels were found to be associated with MACE. EAT volume (odds ratio [OR]: 1.027; 95% confidence interval [CI]: 1.010‒1.044, p=0.002) and low-density lipoprotein (OR: 1.015; 95% CI: 1.000‒1.030, p=0.050) were found to be independent predictors for MACE. ROC analysis indicated that EAT volumes >123.2 mL had a 72.7% sensitivity and a 77.1% specificity for predicting long-term MACE in patients with T2-DM (area under the curve: 0.820; 95% CI: 0.733-0.908). EAT volume is an independent predictor of long-term MACE in patients with T2-DM without previous coronary events. EAT volume may be used additionally in risk stratification for MACE besides the well-known vascular risk factors in patients with T2-DM.