CAPTOPRIL REDUCED PLASMINOGEN-ACTIVATOR INHIBITOR ACTIVITY IN PATIENTS WITH ACUTE MYOCARDIAL-INFARCTION

Recent clinical trials have demonstrated that the administration of an giotensin-converting enzyme (ACE) inhibitors to patients with myocardi al infarction reduces the incidence of recurrent myocardial infarction . It has also been reported that an elevated level of plasminogen acti vator inhibitor (PAI) appears to constitute a marker of the risk of re current coronary thrombosis. To determine whether the ACE inhibitor ca ptopril reduces plasma PAI inhibitor activity, we measured changes in plasma PAI activity (IU/ml), tissue plasminogen activator (t-PA) antig en (ng/ml), and serum ACE activity (IU/L) in 14 survivors of myocardia l 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 grou p, 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 ac tivity 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 dur ing the study period in the placebo group. Thus, our data indicate tha t the administration of captopril to patients with acute myocardial in farction may result in a reduced frequency of recurrent coronary throm bosis by increasing fibrinolytic capacity.