Several studies have demonstrated an increased level of plasma
plasminogen activator inhibitor-1 (PAI-1) in patients with
coronary artery disease (CAD). However, the concentration of
PAI-1 in platelets, which accounts for more than 90% of the blood
PAI-1, is unknown in these patients. The present study evaluated the concentrations of
PAI-1 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 coronary angiography and were divided into 3 groups: CAD(-) group without
coronary artery stenosis or
myocardial ischemia (n=20), CAD(+) group with either
stable angina pectoris (n=18) or old
myocardial infarction (n=12) with
coronary artery stenosis, and the AMI group admitted within 24h of symptom onset who underwent successful percutaneous transluminal coronary angioplasty (n=22). The concentrations of plasma
PAI-1,
tissue plasminogen activator (t-PA), and t-PA x
PAI-1 complex were similar in the CAD(-) and CAD(+) groups, but were greater on day 1 in the AMI group compared with the 2 CAD groups. There were no significant differences between the 3 groups in the plasma concentrations of
thrombin antithrombin III complex (TAT),
alpha2-plasmin inhibitor-plasmin complex (PIC),
beta-thromboglobulin (beta-TG), and
platelet factor 4 (PF-4). The platelet
PAI-1 concentrations did not differ between the CAD(-) and CAD(+) groups, but was greater on day 1 in the AMI group compared 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 concentrations were greater on day 1, but the plasma
PAI-1 rapidly decreased by day 5 and remained low on day 28 compared with day 1. The platelet
PAI-1 concentration gradually decreased by day 5 and was further decreased by day 28. The serial changes of the plasma t-PA and t-PA
PAI-1 complex during the course of AMI were similar to those of the plasma
PAI-1. A positive correlation was found between the plasma and platelet
PAI-1 in all 72 patients, but not in the AMI group alone. These results suggest that the
PAI-1 that has accumulated in platelets at the onset of AMI might be released in large amounts into the plasma, resulting in an increase in
thrombus formation.