Plasma Plasminogen Activator Inhibitor-1, Tissue Plasminogen Activator and Serum Lipoprotein(a) after Reperf usion Therapy in Acute Myocardial Infarction: Comparison between Sequential and Direct Percutaneous Transluminal Coronary Angioplasty

Abstract

To determine which reperfusion therapy for acute myocardial infarction (AMI) is advantageous to avoid subsequent thrombotic coronary occlusion, 8 patients with AMI were studied. Four of them (group S) underwent sequential PTCA following unsuccessful intracoronary thrombolysis and the others (group D) direct PTCA. Serial changes in plasma plasminogen activator inhibitor-1 (PAI-1), plasma tissue plasminogen activator (t-PA) antigen and serum lipoprotein(a) levels were compared between the two groups. In group S, plasma PAI-1 levels showed no significant serial change after PTCA. However, in group D, plasma PAI-1 levels increased significantly 4-24 h after PTCA. We suggest that more attention should be focused on the prevention of thrombotic coronary closure as well as mechanical abrupt occlusion after direct PTCA.

The status of plasminogen activator inhibitor-1 as a therapeutic target

“…Plasma PAI-1 is raised 4 -24 h after percutaneous transluminal coronary angioplasty (PTCA) [79], and, after PTCA, PAI-1 levels are significantly higher in patients with restenosis than in patients without restenosis [80]. The impaired fibrinolysis resulting from raised PAI-1 might affect the repair process, and thus contribute to restenosis.…”