title: Adipokines and endothelial dysfunction in acute myocardial infarction and the risk of recurrent cardiovascular events.
abstract: OBJECTIVE
  The aim of the study was to evaluate the prognostic role of adipokines (adiponectin, apelin, resistin, and visfatin) in patients with acute myocardial infarction (AMI) in relation to the extent of glucose metabolism impairment and intensity of systemic low-grade inflammation.
  
  
  METHODS
  This case-control study covered 131 patients with coronary artery disease: 104 consecutive patients with AMI (74% men, mean age of 62 ± 11 years) treated with primary percutaneous coronary intervention with stent implantation, and 27 patients with stable angina (70% men, mean age of 63 ± 11 years), who were initially assessed in terms of adipokine levels, C-reactive protein and various echocardiographic and vascular parameters. Major adverse cardiovascular events were recorded in the AMI group during 3-year follow-up.
  
  
  RESULTS
  Resistin and visfatin serum levels were significantly higher (P < 0.001), and adiponectin and apelin were lower (P < 0.001) in AMI patients as compared to patients with stable angina. In AMI patients, adipokine levels were not related to glucose metabolism disturbances, yet adiponectin (P = 0.03) and resistin (P = 0.001) concentrations were related to the number of affected coronary vessels. Serum adiponectin level correlated negatively (r = -0.608, P < 0.05), whereas resistin and visfatin correlated positively (r = 0.526, P < 0.05 and r = 0.352, P < 0.05, respectively) with C-reactive protein levels. All of the analyzed adipokines significantly accounted for the flow-mediated dilation variability (Radjusted 32%) in the AMI group. The Cox survival analysis indicated that resistin and visfatin were independent risk factors of recurrent AMI/unstable angina, with the diagnostic threshold above 12.2 ng/ml for resistin and above 11.8 ng/ml for visfatin concentrations.
  
  
  CONCLUSIONS
  An abnormal profile in serum adipokines observed in AMI is related to systemic inflammation and the degree of atherosclerosis independently of glucose metabolism disturbances and heralds major adverse cardiovascular event occurrence in long-term observation.
authors.affiliation: a2nd Department of Cardiology b1st Department of Cardiology, Medical University of Silesia in Katowice, Public Hospital No. 7 in Katowice, Upper Silesian Medical Center cDepartment of Pathophysiology, Medical University of Silesia in Katowice, Katowice, Poland.
authors.forename: Patryk
authors.initials: P
authors.lastname: Grzywocz
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Mizia-Stec
authors.forename: Maciej
authors.initials: M
authors.lastname: Wybraniec
authors.forename: Jerzy
authors.initials: J
authors.lastname: Chudek
mesh_terms: D054392:Adipokines / Q000097:blood*; D000368:Aged; D060050:Angina, Stable / Q000097:blood; D050197:Atherosclerosis / Q000150:complications; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000150:complications; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000175:diagnosis / Q000503:physiopathology; D011379:Prognosis; D011446:Prospective Studies; D012008:Recurrence; D018570:Risk Assessment
chemical_list: D054392:Adipokines; D015415:Biomarkers; D005947:Glucose