Abstract 10411: Significance of Inflammation and Neoangiogenesis of Epicardial Adipose Tissue on Coronary Atherosclerosis Based on Computed Tomography Analysis
Background: Previous studies indicate that epicardial adipose tissue (EAT) biologically contributes to coronary atherosclerosis progression. The inflammation and neoangiogenesis have been reported to be biological markers of ‘diseased’ adipose tissues. We evaluated the relation of EAT pathologies, represented by inflammation and neoangiogenesis, to computed tomography (CT)-based coronary atherosclerosis.
Methods: We enrolled 45 patients undergoing cardiac CT examination before elective cardiac surgery (coronary artery bypass graft [CABG], n = 21; non-CABG, n = 24). Each patient was evaluated with visceral adipose tissue (VAT) area, EAT volume, coronary calcium score (CCS), and presence of non-calcified coronary plaque (NCP) on CT angiography. During each cardiac surgery, histological samples for immunohistochemistry were obtained from EATs adjacent to the left anterior descending and right coronary arteries. Each patient was assessed with the numbers of CD-68+ individual macrophages and CD-31+ neovessels in a total of 6 random high-power fields (x400) of EAT samples.
Results: The EAT volume had no correlation with macrophage infiltration (r = 0.09, p = 0.53) or neoangiogenesis (r = 0.08, p = 0.59) in EAT. In the comparisons of EAT pathologies based on CCS levels or NCP presence, the moderate CCS (101-400) or NCP present group had more macrophage infiltration and neoangiogenesis in EAT (Fig 1). On multivariate analyses adjusting for age, sex, CABG vs. non-CABG, VAT area, and EAT volume, both the moderate CCS and NCP presence showed significant correlation with increased macrophage infiltration (β = 0.65; p < 0.0001, and β = 0.49; p = 0.0089, respectively) and neoangiogenesis (β = 0.55; p = 0.0011, and β = 0.53; p = 0.012, respectively) in EAT (Fig 2).
Conclusions: The EAT biological activities independently correlate with moderate, rather than severe, coronary calcium and NCP formation, suggesting the stage in the process of coronary atherosclerosis growing.
Author Disclosures: T. Kitagawa: Research Grant; Significant; JSPS Grants-in-Aid for Scientific Research Grant Number 26870395, Japan Heart Foundation Research Grant. H. Yamamoto: None. H. Tsushima: None. A. Senoo: None. K. Sentani: None. W. Yasui: None. Y. Kihara: None.
- © 2015 by American Heart Association, Inc.