Plasma and platelet plasminogen activator inhibitor-1 in patients with acute myocardial infarction

Several studies have demonstrated an increased level of plasma plasminogen activator inhibitor-1 (PAI-I) in patients with coronary artery disease (CAD ). However, the concentration of PAI-1 in platelets, which accounts for mor e than 90% of the blood PAI-I, is unknown in these patients. The present st udy evaluated the concentrations of PAI-I and several fibrinolytic factors in the plasma and platelets of patients with CAD and the serial changes in patients with acute myocardial infarction (AMI). All 72 subjects had corona ry angiography and were divided into 3 groups: CAD(-) group without coronar y artery stenosis or myocardial ischemia (n=20), CAD(+) group with either s table angina pectoris (n=18) or old myocardial infarction (n=12) with coron ary artery stenosis, and the AMI group admitted within 24 h of symptom onse t who underwent successful percutaneous transluminal coronary angioplasty ( n=22.). The concentrations of plasma PAI-I, tissue plasminogen activator (t -PA), and tPA PAI-1 complex were similar in the CAD(-) and CAD(+) groups, b ut were greater on day 1 in the AMI group compared with the 3 CAD groups. T here were no significant differences between the 3 groups in the plasma con centrations of thrombin antithrombin III complex (TAT), alpha 2-plasmin inh ibitor-plasmin complex (PIC), beta-thromboglobulin (beta-TG), and platelet factor 4 (PF-4). The platelet PAI-1 concentrations did not differ between t he CAD(-) and CAD(+) groups, but was greater on day 1 in the AMI group comp ared to the CAD groups. The platelet beta-TG and PF-4 were similar between the 3 groups. In the AMI group, both the plasma and platelet PAI-1 concentr ations were greater on day 1, but the plasma PAI-I rapidly decreased by day 5 and remained low on day 28 compared with day 1, The platelet PAI-I conce ntration gradually decreased by day 5 and was further decreased by day 28. The serial changes of the plasma t-PA and t-PA PAI-I complex during the cou rse of AMI were similar to those of the plasma PAI-I. A positive correlatio n was found between the plasma and platelet PAI-1 in all 72 patients, but n ot in the AML group alone. These results suggest that the PAI-1 that has ac cumulated in platelets at the onset of AMI might be released in large amoun ts into the plasma, resulting in an increase in thrombus formation.