title: Epicardial adipose tissue and insulin resistance in patients with coronary artery disease with or without left ventricular dysfunction.
abstract: BACKGROUND
  Epicardial adipose tissue (EAT) is a visceral fat that fulfills two important functions: lipid-storage and secretion of adipokines with pro-inflammatory and pro-atherogenic properties. It has been suggested that EAT may affect the pathogenesis of atherosclerosis and the clinical course of coronary artery disease (CAD). In patients with obesity, diabetes and metabolic syndrome, the epicardial adipose tissue is enlarged. Little is known about the role of EAT in left ventricular dysfunction. Aim of this study was to evaluate the ability of insulin resistance to predict EAT thickness in patients with significant CAD and systolic dysfunction.
  
  
  METHODS
  We enrolled 114 subjects diagnosed with CAD by angiography. The majority underwent revascularization after an acute coronary syndrome. Patients were considered affected by significant left ventricular dysfunction when EF was < or = 40%. Three indexes of insulin resistance, the HOMA IR index, the insulin sensitivity QUICKI index, and the novel adiponectin/resistin index (ADIPO-IRAR) were calculated and correlated to EAT thickness. Epicardial fat was measured by echocardiography according to standardized methods.
  
  
  RESULTS
  Subjects with diabetes and with a history of hypercholesterolemia had thicker EAT compared to controls. Potassium levels and all three indexes of insulin resistance were the best independent predictors of EAT in the study population as a whole and in the subset of patients with left ventricular dysfunction. In the latter group the novel ADIPO-IRAR index displayed the strongest predictivity.
  
  
  CONCLUSIONS
  Insulin resistance is an independent predictor of EAT thickness in patients affected by CAD, also in the presence of significant left ventricular dysfunction.
authors.forename: Samuele
authors.initials: S
authors.lastname: Baldasseroni
authors.forename: Alessandra
authors.initials: A
authors.lastname: Pratesi
authors.forename: Francesco
authors.initials: F
authors.lastname: Orso
authors.forename: Claudia
authors.initials: C
authors.lastname: Di Serio
authors.forename: Alice
authors.initials: A
authors.lastname: Foschini
authors.forename: Andrea Giosafat
authors.initials: AG
authors.lastname: Marella
authors.forename: Nadia
authors.initials: N
authors.lastname: Bartoli
authors.forename: Mauro
authors.initials: M
authors.lastname: Di Bari
authors.forename: Stefano
authors.initials: S
authors.lastname: Fumagalli
authors.forename: Niccolò
authors.initials: N
authors.lastname: Marchionni
authors.forename: Francesca
authors.initials: F
authors.lastname: Tarantini
mesh_terms: D000273:Adipose Tissue / Q000000981:diagnostic imaging / Q000473:pathology*; D000368:Aged; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000150:complications* / Q000175:diagnosis / Q000378:metabolism; D005260:Female; D006801:Humans; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D010496:Pericardium / Q000000981:diagnostic imaging / Q000473:pathology*; D011237:Predictive Value of Tests; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000150:complications* / Q000175:diagnosis / Q000378:metabolism