title: The relationship between inflammation and neoangiogenesis of epicardial adipose tissue and coronary atherosclerosis based on computed tomography analysis.
abstract: OBJECTIVE
  Previous studies indicate that epicardial adipose tissue (EAT) biologically contributes to the progression of coronary atherosclerosis. We evaluated the relationship between EAT pathology, represented by inflammation and neoangiogenesis, and coronary atherosclerosis on computed tomography (CT) images.
  
  
  METHODS
  We performed CT examination in 45 patients scheduled for cardiac surgery (coronary artery bypass graft [CABG], n = 21; non-CABG, n = 24) to assess visceral adipose tissue (VAT) area, EAT volume, coronary calcium score (CCS), and presence of non-calcified coronary plaque (NCP) on CT angiography. Each patient was assessed with the numbers of CD68(+) individual macrophages and CD31(+) neovessels in six random high-power fields (400×) of EAT samples subsequently obtained during cardiac surgery.
  
  
  RESULTS
  In three groups based on CCS (mild, 0-100; moderate, 101-400; severe, >400), the moderate group had the most extensive macrophage infiltration (p = 0.0025) and neoangiogenesis (p = 0.0036) in EAT. The patients with NCP had more extensive macrophage infiltration (p = 0.010) and neoangiogenesis (p = 0.0043) in EAT than those without. On multivariate analysis adjusted for age, sex, CABG versus. non-CABG, VAT area, and EAT volume, moderate CCS and the presence of NCP showed significant correlations 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.
  
  
  CONCLUSIONS
  Inflammation and neoangiogenesis in EAT independently correlate with moderate coronary calcification and presence of NCP, suggesting that these two factors may have a role in promoting coronary atherosclerosis.
authors.affiliation: Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan. Electronic address: toshirok@hiroshima-u.ac.jp.
authors.forename: Toshiro
authors.initials: T
authors.lastname: Kitagawa
authors.affiliation: Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan.
authors.forename: Hideya
authors.initials: H
authors.lastname: Yamamoto
authors.affiliation: Department of Molecular Pathology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Sentani
authors.affiliation: Department of Cardiovascular Surgery, Hiroshima University Hospital, Hiroshima, Japan.
authors.forename: Shinya
authors.initials: S
authors.lastname: Takahashi
authors.affiliation: Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Tsushima
authors.affiliation: Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan.
authors.forename: Atsuhiro
authors.initials: A
authors.lastname: Senoo
authors.affiliation: Department of Molecular Pathology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.
authors.forename: Wataru
authors.initials: W
authors.lastname: Yasui
authors.affiliation: Department of Cardiovascular Surgery, Hiroshima University Hospital, Hiroshima, Japan.
authors.forename: Taijiro
authors.initials: T
authors.lastname: Sueda
authors.affiliation: Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan.
authors.forename: Yasuki
authors.initials: Y
authors.lastname: Kihara
mesh_terms: D000273:Adipose Tissue / Q000473:pathology; D000368:Aged; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D015331:Cohort Studies; D017023:Coronary Angiography; D001026:Coronary Artery Bypass; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000473:pathology*; D003331:Coronary Vessels / Q000473:pathology; D018450:Disease Progression; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000000981:diagnostic imaging / Q000473:pathology; D050152:Intra-Abdominal Fat / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009389:Neovascularization, Pathologic / Q000000981:diagnostic imaging / Q000473:pathology*; D015588:Observer Variation; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D014057:Tomography, X-Ray Computed; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D019408:Platelet Endothelial Cell Adhesion Molecule-1; C067980:CD68 antigen, human; D000097382:CD68 Molecule
keywords: Coronary atherosclerosis; Epicardial adipose tissue; Inflammation; Neoangiogenesis