Abstract 11885: Differential Contributions of Abdominal Visceral Fat and Epicardial Fat to Coronary Atherosclerosis in Non-Obese Japanese Patients
Introduction: Epicardial fat is a source of adipocytokines that have both paracrine and systemic effects and is implicated in coronary atherosclerosis. The relation between epicardial fat volume (EFV) and circulating adipocytokine levels has remained unknown, however.
Objectives: We assessed the relation between EFV and both plasma adipocytokine concentrations and coronary atherosclerotic plaque.
Methods: Consecutive Japanese patients suspected of having coronary artery disease (n = 216) were examined. Individuals with acute coronary syndrome or with inadequate CT imaging were excluded. A total of 164 patients (65 ± 10 years; 70% men; BMI, 23.8 ± 3.6 kg/m2) was enrolled. Plasma levels of adiponectin, interleukin-6 (IL-6), plasminogen activator inhibitor-1 (PAI-1), and vascular endothelial growth factor (VEGF) were measured. The characteristics of coronary plaque, abdominal visceral fat area, and EFV were determined by 64-slice CT.
Results: EFV was greater in subjects with noncalcified plaque than in those with no plaque or with calcified plaque (126 ± 39 vs. 98 ± 34 and 97 ± 45 mL, respectively; P = 0.010). EFV was significantly correlated with BMI, plasma triglyceride concentration, and the triglyceride/HDL-cholesterol ratio (r = 0.51, 0.19, and 0.20, respectively) but not with plasma adipocytokine levels, whereas plasma adiponectin and IL-6 levels were significantly correlated (r = -0.49 and 0.20, respectively) with visceral fat area, in patients with coronary plaque.
Conclusions: Patients with noncalcified plaque had increased EFV but their plasma adipocytokine levels had not increased. Adipocytokines in plasma may be derived mainly from abdominal visceral fat, whereas epicardial fat may promote coronary atherosclerosis directly through a paracrine mechanism rather than by systemic effects. In conclusion, abdominal visceral fat and epicardial fat may thus contribute to coronary atherosclerosis by distinct mechanisms in nonobese individuals.
Author Disclosures: K. Harada: None. T. Kataoka: None. M. Takeshita: None. K. Harada: None. A. Kunimura: None. S. Okumura: None. N. Shinoda: None. B. Kato: None. T. Uetani: None. M. Kato: None. N. Marui: None. H. Ishii: None. T. Matsubara: None. T. Amano: None. T. Murohara: None.
- © 2014 by American Heart Association, Inc.