title: Relationship between serum angiotensin-converting enzyme activity and plasma plasminogen activator inhibitor activity in patients with recent myocardial infarction.
abstract: BACKGROUND
  An elevated level of angiotensin-converting enzyme (ACE) has been demonstrated to increase the risk of myocardial infarction. Plasminogen activator inhibitor (PAI) is the most important physiological inhibitor of tissue plasminogen activator in plasma. An elevated level of PAI has been reported to be associated with decreased fibrinolytic capacity and to constitute a marker of the risk for recurrent coronary thrombosis.
  
  
  METHODS
  We measured the serum ACE activity and plasma PAI activity in 34 patients with recent myocardial infarction, and evaluated the correlation between these two values by linear regression analysis. We also administered captopril (37.5 mg/day) to 17 of these patients and placebo to the other 17 patients at random, and compared the changes in PAI activity and ACE activity in these two groups over a 1-month period.
  
  
  RESULTS
  There was a significant correlation between the serum ACE activity and the plasma PAI activity at baseline in the patients (r = 0.498, P < 0.01). The captopril-treated patients showed significantly reduced PAI activity (P < 0.01), and a concomitant decrease in ACE activity.
  
  
  CONCLUSIONS
  These results suggest that elevated ACE activity is associated with impaired fibrinolysis and that treatment with an ACE inhibitor improves the fibrinolytic function in patients with recent myocardial infarction. The results also suggest that the renin-angiotensin system plays a role in the increased risk of ischemic cardiovascular events when it is activated, and in the reduction of risk of recurrent myocardial infarction by ACE inhibition.
authors.affiliation: Department of Cardiovascular Medicine, Kumamoto University School of Medicine, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Moriyama
authors.forename: H
authors.initials: H
authors.lastname: Ogawa
authors.forename: S
authors.initials: S
authors.lastname: Oshima
authors.forename: H
authors.initials: H
authors.lastname: Arai
authors.forename: K
authors.initials: K
authors.lastname: Takazoe
authors.forename: H
authors.initials: H
authors.lastname: Shimomura
authors.forename: N
authors.initials: N
authors.lastname: Hirai
authors.forename: H
authors.initials: H
authors.lastname: Suefuji
authors.forename: H
authors.initials: H
authors.lastname: Soejima
authors.forename: K
authors.initials: K
authors.lastname: Nishiyama
authors.forename: K
authors.initials: K
authors.lastname: Misumi
authors.forename: H
authors.initials: H
authors.lastname: Yasue
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D002216:Captopril / Q000627:therapeutic use; D017023:Coronary Angiography; D003402:Creatine Kinase / Q000097:blood; D004562:Electrocardiography; D005260:Female; D005342:Fibrinolysis / Q000187:drug effects / Q000502:physiology; D005500:Follow-Up Studies; D006801:Humans; D007527:Isoenzymes; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000175:diagnosis / Q000188:drug therapy; D007703:Peptidyl-Dipeptidase A / Q000097:blood* / Q000187:drug effects; D015849:Plasminogen Inactivators / Q000097:blood*; D011379:Prognosis; D015635:Radionuclide Ventriculography; D012008:Recurrence
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D015415:Biomarkers; D007527:Isoenzymes; D008055:Lipids; D015849:Plasminogen Inactivators; D002216:Captopril; D003402:Creatine Kinase; D007703:Peptidyl-Dipeptidase A