Increased Epicardial Adipose Tissue in Patients with Isolated Coronary Artery Ectasia

PubMed: 22504235Background Epicardial adipose tissue (EAT), localized beneath the visceral pericardium, is a metabolically active endocrine and paracrine organ with possible interactions within the heart. Coronary artery ectasia (CAE) is a clinical entity characterized with localized or diffuse dilatation, of the coronary arteries, with a diameter of greater than 1.5 times that of adjacent segments. Although the etiopathogenesis is not clearly understood, some studies have revealed that CAE may be a form of atherosclerosis that has greater inflammatory properties than atherosclerosis. The goal of this study was to investigate whether EAT and the level of C-reactive protein (CRP) are increased in patients with isolated CAE compared to normal subjects. Methods Thirty-three patients with isolated CAE (mean age: 57±9 years) and 32 age- and gender-matched control participants with NCA, but without CAE (mean age: 56±10 years), were included in the study. The relationship between EAT thickness, CRP levels and the presence of CAE was investigated. Results Epicardial adipose tissue thickness was significantly higher in CAE group compared to NCA group (7.2±3.2 vs. 4.7±2.1 mm, p<0.001). Body mass index (BMI, p=0.013), CRP (p=0.047), and the percentage of isolated CAE (p=0.012) were significantly higher in patients with an increased EAT thickness. While CRP correlated with increased EAT, it was not related to CAE. However, CRP levels were higher in patients with diffuse coronary ectatic involvement than the focal lesions (0.58±0.32 vs. 0.31±0.11 mg/dL, p=0.046). When we performed multiple logistic regression analysis, only increased EAT thickness was related to CAE independent of CRP and BMI (OR: 1.442, 95%CI: 1.066-1.951, p=0.018). Conclusion This is the first study, displaying a significantly higher EAT-thickness in patients with isolated CAE. We believe that further studies are needed to clarify the role of adipose tissue in patients with isolated CAE. © 2012 The Japanese Society of Internal Medicine