title: Elevated levels of PAI-1 activity and t-PA antigen are associated with newly diagnosed abnormal glucose regulation in patients with ST-elevation myocardial infarction.
abstract: BACKGROUND
  Both Type 2 diabetes and cardiovascular disease have been associated with enhanced coagulation and suppressed fibrinolysis.
  
  
  OBJECTIVE
  To investigate a possible relationship between selected hemostatic variables and abnormal glucose regulation (AGR) in patients with acute ST-elevation myocardial infarction (STEMI) without known diabetes and to study changes in selected hemostatic variables from baseline to follow-up in STEMI patients with or without AGR.
  
  
  METHODS
  Plasminogen activator inhibitor-1 (PAI-1) activity, tissue plasminogen activator (t-PA) antigen, prothrombin fragment 1+2 (F(1+2)) and von Willebrand factor (vWF) were measured in fasting blood samples from 199 STEMI patients 16.5 h (median time) after admission and 3 months later. All patients were classified into normal glucose regulation (NGR) or AGR based on an oral glucose tolerance test at follow-up, according to the WHO criteria.
  
  
  RESULTS
  High PAI-1 activity (≥ 75th percentile) measured in-hospital was associated with AGR (n = 49) with an adjusted odds ratio of 2.2 (95% confidence interval, 1.1, 4.4). In addition, high levels of t-PA antigen (≥ 75th percentile) were associated with AGR (adjusted odds ratio, 3.5; 95% confidence inteval, 1.5, 8.2), but only in men. Changes in the levels of F(1+2) were significantly more pronounced in patients with AGR compared with NGR (adjusted P = 0.04).
  
  
  CONCLUSIONS
  Elevated levels of PAI-1 activity and t-PA antigen measured in-hospital in STEMI patients were associated with AGR classified at 3-month follow-up. Additionally, changes in the levels of F(1+2) were more pronounced in patients with AGR compared with NGR. The data suggest an enhanced prothrombotic state after an acute STEMI in patients with AGR without known diabetes.
authors.affiliation: Center for Clinical Heart Research, Oslo University Hospital, Ullevål, Oslo, Norway. knev@uus.no
authors.forename: E C
authors.initials: EC
authors.lastname: Knudsen
authors.forename: I
authors.initials: I
authors.lastname: Seljeflot
authors.forename: M
authors.initials: M
authors.lastname: Abdelnoor
authors.forename: J
authors.initials: J
authors.lastname: Eritsland
authors.forename: A
authors.initials: A
authors.lastname: Mangschau
authors.forename: C
authors.initials: C
authors.lastname: Müller
authors.forename: H
authors.initials: H
authors.lastname: Arnesen
authors.forename: G Ø
authors.initials: GØ
authors.lastname: Andersen
mesh_terms: D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism*; D016009:Chi-Square Distribution; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000175:diagnosis; D005260:Female; D018149:Glucose Intolerance / Q000097:blood* / Q000175:diagnosis; D005951:Glucose Tolerance Test; D006487:Hemostasis; D006801:Humans; D007297:Inpatients; D016015:Logistic Models; D008297:Male; D009203:Myocardial Infarction / Q000097:blood* / Q000175:diagnosis; D009664:Norway; D016017:Odds Ratio; D010446:Peptide Fragments / Q000097:blood; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D011446:Prospective Studies; D011516:Prothrombin; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000097:blood*; D015854:Up-Regulation; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D010446:Peptide Fragments; D017395:Plasminogen Activator Inhibitor 1; C051321:SERPINE1 protein, human; C045879:prothrombin fragment 1.2; D014841:von Willebrand Factor; D011516:Prothrombin; D010959:Tissue Plasminogen Activator