Abstract 9384: Differential Association of Epicardial Fat with Coronary Plaque in Patients with Acute Coronary Syndrome or Stable Angina Pectoris: Analysis by Integrated Backscatter Intravascular Ultrasound
Introduction: Epicardial fat is implicated in the pathogenesis of coronary atherosclerosis, but its precise contribution to this condition remains unclear.
Objective: To evaluate the relations between epicardial adipose tissue and coronary plaque in patients with acute coronary syndrome (ACS) and those with stable angina pectoris (SAP).
Methods: Atotal of 62 individuals (mean age, 67 ± 11 years; 64% men) who underwent percutaneous coronary intervention, including 20 patients with ACS and 42 patients with SAP, were enrolled in the study. Conventional and integrated backscatter intravascular ultrasound (IB-IVUS) was performed to assess coronary plaque in the patients. Plaque components were classified as calcified, dense-fibrous, fibrous, or lipid with the IB-IVUS system. The average plaque volume (total plaque volume/lesion length) and the percentage volumes of individual plaque components were calculated. Epicardial fat volume (EFV) was also measured by 64-slice computed tomography within 1 week of percutaneous coronary intervention.
Results: There was no significant difference between ACS and SAP patient characteristics. EFV was significantly higher in patients with ACS than in those with SAP (117 ± 36 vs. 103 ± 40 ml, p < 0.05). Multivariate regression analysis revealed that EFV was positively correlated with the percentage volume of dense-fibrous plaque (r = 1.49, p < 0.05) and negatively correlated with average plaque volume (r = -0.58, p < 0.05) in patients with ACS. However, no correlation between EFV and coronary plaque profile was apparent in patients with SAP.
Conclusions: EFV was associated with the development of dense-fibrous plaque in ACS patients, whereas the average plaque volume decreased with increasing EFV in these patients. Our findings support the hypothesis that increased epicardial fat may contribute to the pathogenesis of ACS.
- © 2011 by American Heart Association, Inc.