title: Effects of captopril therapy on endogenous fibrinolysis in men with recent, uncomplicated myocardial infarction.
abstract: OBJECTIVE
  This study investigated the effects of captopril therapy on endogenous fibrinolysis in men with recent, uncomplicated myocardial infarction.
  
  
  BACKGROUND
  Angiotensin-converting enzyme inhibitors reduce the incidence of acute coronary syndromes in patients with mild left ventricular dysfunction after myocardial infarction. Abnormal endogenous fibrinolysis, reflected in increased levels of endogenous tissue-type plasminogen activator (t-PA) antigen and plasminogen activator inhibitor type 1 activity, is associated with an increased risk of myocardial infarction in patients with ischemic heart disease.
  
  
  METHODS
  In a randomized, double-blind crossover study beginning 8 weeks after uncomplicated myocardial infarction, patients received 4 weeks of placebo and 4 weeks of captopril (75 mg daily) therapy. At the end of each treatment period, we measured t-PA antigen and plasminogen activator inhibitor type 1 antigen and activity.
  
  
  RESULTS
  Median values in the 15 patients after placebo and in 12 normal men matched for age and body mass index were, respectively, t-PA antigen 16.0 versus 9.5 ng/ml (p = 0.001), plasminogen activator inhibitor type 1 antigen 17.3 versus 8.6 ng/ml (p = 0.29) and plasminogen activator inhibitor type 1 activity 13.2 versus 6.3 AU/ml (p = 0.04). After 4 weeks of treatment with captopril in the 15 patients, the estimated (95% confidence interval) median reduction in t-PA antigen was 7.3 ng/ml (-4.6 to -10.3 ng/ml, p = 0.001), in plasminogen activator inhibitor type 1 antigen 3.1 ng/ml (+1.5 to -8.4 ng/ml, p = 0.17) and in plasminogen activator inhibitor type 1 activity -2.2 AU/ml (-1.0 to -4.3 AU/ml, p = 0.02).
  
  
  CONCLUSIONS
  Treatment with captopril after uncomplicated myocardial infarction is associated with a significant decrease in elevated levels of t-PA antigen and plasminogen activator inhibitor type 1 activity. This may help to explain the reduction in risk of coronary thrombosis associated with the use of angiotensin-converting enzyme inhibitors.
authors.affiliation: Cardiovascular Research Unit, University of Edinburgh, United Kingdom.
authors.forename: R A
authors.initials: RA
authors.lastname: Wright
authors.forename: A D
authors.initials: AD
authors.lastname: Flapan
authors.forename: K G
authors.initials: KG
authors.lastname: Alberti
authors.forename: C A
authors.initials: CA
authors.lastname: Ludlam
authors.forename: K A
authors.initials: KA
authors.lastname: Fox
mesh_terms: D002216:Captopril / Q000008:administration & dosage / Q000494:pharmacology*; D003864:Depression, Chemical; D004311:Double-Blind Method; D005342:Fibrinolysis / Q000187:drug effects*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000175:diagnosis / Q000188:drug therapy* / Q000453:epidemiology; D010919:Placebos; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D013223:Statistics as Topic / Q000379:methods; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000097:blood / Q000187:drug effects
chemical_list: D010919:Placebos; D017395:Plasminogen Activator Inhibitor 1; D002216:Captopril; D010959:Tissue Plasminogen Activator