title: Captopril reduced plasminogen activator inhibitor activity in patients with acute myocardial infarction.
abstract: Recent clinical trials have demonstrated that the administration of angiotensin-converting enzyme (ACE) inhibitors to patients with myocardial infarction reduces the incidence of recurrent myocardial infarction. It has also been reported that an elevated level of plasminogen activator inhibitor (PAI) appears to constitute a marker of the risk of recurrent coronary thrombosis. To determine whether the ACE inhibitor captopril reduces plasma PAI inhibitor activity, we measured changes in plasma PAI activity (IU/ml), tissue plasminogen activator (t-PA) antigen (ng/ml), and serum ACE activity (IU/L) in 14 survivors of myocardial infarction receiving captopril therapy (37.5 mg daily) and compared them with the values in 15 placebo-treated patients chosen at random. Blood sampling was performed at 07.00 h. In the captopril-treated group, serum ACE activity decreased significantly, from 14.0 +/- 0.8 to 11.5 +/- 1.2 IU/L 24 h after captopril therapy (p < 0.01), and those of PAI activity and t-PA antigen also decreased significantly-from 11.9 +/- 2.8 to 5.5 +/- 2.2 IU/ml (p < 0.02) and from 9.9 +/- 1.0 to 7.5 +/- 0.9 ng/ml (p < 0.05), respectively 48 h after captopril therapy. However, the levels of ACE activity, PAI activity, and t-PA antigen remained unchanged during the study period in the placebo group. Thus, our data indicate that the administration of captopril to patients with acute myocardial infarction may result in a reduced frequency of recurrent coronary thrombosis by increasing fibrinolytic capacity.
authors.affiliation: Division of Cardiology, Fukuoka Tokusyukai Hospital, 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: K
authors.initials: K
authors.lastname: Takazoe
authors.forename: Y
authors.initials: Y
authors.lastname: Honda
authors.forename: O
authors.initials: O
authors.lastname: Hirashima
authors.forename: H
authors.initials: H
authors.lastname: Arai
authors.forename: T
authors.initials: T
authors.lastname: Sakamoto
authors.forename: H
authors.initials: H
authors.lastname: Sumida
authors.forename: H
authors.initials: H
authors.lastname: Suefuji
authors.forename: K
authors.initials: K
authors.lastname: Kaikita
authors.forename: H
authors.initials: H
authors.lastname: Yasue
mesh_terms: D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D010959:Tissue Plasminogen Activator / Q000097:blood
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D017395:Plasminogen Activator Inhibitor 1; D002216:Captopril; D010959:Tissue Plasminogen Activator