title: Circulating vaspin levels and epicardial adipose tissue thickness are associated with impaired coronary flow reserve in patients with nonalcoholic fatty liver disease.
abstract: BACKGROUND
  Patients with nonalcoholic fatty liver disease (NAFLD) have a reduced coronary flow reserve (CFR) and an increased risk of cardiovascular disease. The fat cells that surround coronary arteries may play a central and underrecognized role in development of cardiovascular disease through the systemic secretion of adipokines. We therefore evaluated the relation of epicardial fat thickness, serum levels of epicardial fat-related adipokines (chemerin and vaspin), and CFR in patients with NAFLD.
  
  
  METHODS
  We investigated 54 patients with biopsy-proven NAFLD and 56 age- and sex-matched controls. CFR and epicardial fat thickness (EFT) were measured by transthoracic echocardiography. Serum levels of chemerin and vaspin were measured by ELISA.
  
  
  RESULTS
  EFT was significantly higher (0.64 ± 0.13 vs. 0.54 ± 0.10 cm, P<0.001) and CFR significantly lower (2.11 ± 0.45 vs. 2.52 ± 0.62, P < 0.001) in patients with NAFLD than in controls. Serum levels of vaspin and chemerin were both significantly increased in patients with NAFLD compared with controls. Stepwise regression analysis showed that EFT (β=-0.53, t=-3.7, P<0.001), serum vaspin levels (β=-0.30, t=-2.5, P=0.014), and liver fibrosis (β=-0.31, t=-2.11, P=0.041), in the order they entered into the model, were independent predictors of CFR in NAFLD patients.
  
  
  CONCLUSIONS
  Our data suggest the presence of a complex interplay between EFT, serum vaspin, and liver histology in promoting an impaired hyperemic stimulation of coronary blood flow in patients with NAFLD.
authors.affiliation: Department of Gastroenterology, Marmara University, School of Medicine, Pendik, 34899 Istanbul, Turkey. yusufyilmaz@uludag.edu.tr
authors.forename: Yusuf
authors.initials: Y
authors.lastname: Yilmaz
authors.forename: Ramazan
authors.initials: R
authors.lastname: Kurt
authors.forename: Ahmet
authors.initials: A
authors.lastname: Gurdal
authors.forename: Yesim Ozen
authors.initials: YO
authors.lastname: Alahdab
authors.forename: Oya
authors.initials: O
authors.lastname: Yonal
authors.forename: Ebubekir
authors.initials: E
authors.lastname: Senates
authors.forename: Nihat
authors.initials: N
authors.lastname: Polat
authors.forename: Fatih
authors.initials: F
authors.lastname: Eren
authors.forename: Nese
authors.initials: N
authors.lastname: Imeryuz
authors.forename: Huseyin
authors.initials: H
authors.lastname: Oflaz
mesh_terms: D054392:Adipokines / Q000378:metabolism; D000273:Adipose Tissue / Q000473:pathology*; D000328:Adult; D016022:Case-Control Studies; D003326:Coronary Circulation; D005234:Fatty Liver / Q000097:blood* / Q000473:pathology*; D005260:Female; D006801:Humans; D008099:Liver / Q000473:pathology; D008297:Male; D008875:Middle Aged; D065626:Non-alcoholic Fatty Liver Disease; D010496:Pericardium / Q000473:pathology*; D019707:Receptors, Chemokine / Q000378:metabolism; D012044:Regression Analysis; D012306:Risk; D015843:Serpins / Q000097:blood*
chemical_list: D054392:Adipokines; C102741:CMKLR1 protein, human; D019707:Receptors, Chemokine; C507339:SERPINA12 protein, human; D015843:Serpins