title: Epicardial adipose tissue volume and adipocytokine imbalance are strongly linked to human coronary atherosclerosis.
abstract: OBJECTIVE
  The impact of epicardial adipose tissue (EAT) over abdominal or overall adiposity on coronary artery disease (CAD) is currently unknown. We compared the association among EAT volume (EATV), cytokine/adipocytokine profiles in EAT and subcutaneous fat, and atherogenic CAD.
  
  
  RESULTS
  Paired samples were obtained from EAT and subcutaneous adipose tissue during elective cardiac surgery for CAD (n=50) or non-CAD (n=50). EATV was the sum of cross-sectional EAT areas, and visceral and subcutaneous fat areas were determined at the umbilicus level on computed tomography scans. CD68(+), CD11c(+), and CD206(+) cells were counted using immunohistochemical staining. Cytokine/adipocytokine expression was evaluated using quantitative real-time polymerase chain reaction. Multivariate analysis indicated that male sex, age, diabetes mellitus, high triglycerides, and low high-density lipoprotein cholesterol, and EATV index (EATV/body surface area, cm(3)/m(2)) were significant CAD predictors (corrected R(2)=0.401; P<0.001); visceral fat area, hypertension, smoking, low-density lipoprotein cholesterol (140 mg/dL [3.63 mmol/L]) or statin use were not predictors. The EATV index positively correlated with the CD68(+) and CD11c(+) cell numbers and nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3), interleukin-1β, and interleukin-1R expression; and negatively correlated with adiponectin expression in EAT. A multivariate analysis model, including CD68(+) cells and interleukin-1β, and adiponectin expression in EAT strongly predicted CAD (corrected R(2)=0.756; P<0.001).
  
  
  CONCLUSIONS
  EATV and macrophage and cytokine/adipocytokine signals in EAT strongly correlated with CAD. Our findings suggest that EATV and adipocytokine imbalance are strongly linked to human coronary atherosclerosis.
authors.affiliation: Department of Cardio-Diabetes Medicine, The University of Tokushima Graduate School of Health Biosciences, 3-18-15 Kuramoto, Tokushima 770-8503, Japan. mshimabukuro-ur@umin.ac.jp
authors.forename: Michio
authors.initials: M
authors.lastname: Shimabukuro
authors.forename: Yoichiro
authors.initials: Y
authors.lastname: Hirata
authors.forename: Minoru
authors.initials: M
authors.lastname: Tabata
authors.forename: Munkhbaatar
authors.initials: M
authors.lastname: Dagvasumberel
authors.forename: Hiromi
authors.initials: H
authors.lastname: Sato
authors.forename: Hirotsugu
authors.initials: H
authors.lastname: Kurobe
authors.forename: Daiju
authors.initials: D
authors.lastname: Fukuda
authors.forename: Takeshi
authors.initials: T
authors.lastname: Soeki
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Kitagawa
authors.forename: Shuichiro
authors.initials: S
authors.lastname: Takanashi
authors.forename: Masataka
authors.initials: M
authors.lastname: Sata
mesh_terms: D054392:Adipokines / Q000378:metabolism*; D000273:Adipose Tissue / Q000473:pathology*; D000368:Aged; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D039521:CD11c Antigen / Q000032:analysis; D008076:Cholesterol, HDL / Q000097:blood; D003324:Coronary Artery Disease / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D005260:Female; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D010496:Pericardium / Q000473:pathology*; D000097382:CD68 Molecule
chemical_list: D054392:Adipokines; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D039521:CD11c Antigen; D008076:Cholesterol, HDL; C067980:CD68 antigen, human; D000097382:CD68 Molecule