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Tissue Plasminogen Activator Release and Plasminogen Activator Inhibitor Levels in Coronary Artery Disease

Sections of Cardiology and Hematology, Department of Internal Medicine, College of Medicine, University of Nebraska, Omaha, Nebraska

William D. Haire

Sections of Cardiology and Hematology, Department of Internal Medicine, College of Medicine, University of Nebraska, Omaha, Nebraska

Julie K. Rasmussen

Sections of Cardiology and Hematology, Department of Internal Medicine, College of Medicine, University of Nebraska, Omaha, Nebraska

Eric J. Boyd

Sections of Cardiology and Hematology, Department of Internal Medicine, College of Medicine, University of Nebraska, Omaha, Nebraska

Unstable angina and Q wave myocardial infarction are associated with in traluminal coronary thrombosis, a process to which impaired fibrinolysis may contribute. The authors examined the extrinsic fibrinolytic system, including tissue plasminogen activator antigen, plasminogen activator inhibitor activity and an tigen, and euglobulin clot lysis time before and after venous occlusion in 56 pa tients undergoing coronary angiography for chest pain syndromes and in 16 healthy controls. Fibrinolysis variables were similar (with > 95% confidence) in the patients with thrombus-associated coronary syndromes as compared with those with chest pain syndromes not due to coronary thrombosis. These fibrino lytic variables were also similar to those in patients without coronary artery dis ease and in healthy controls. Their data suggest that defective fibrinolysis is not involved, at least systemically, in the pathogenesis of thrombus-associated coro nary artery syndromes.

Angiology, Vol. 42, No. 7, 561-567 (1991)
DOI: 10.1177/000331979104200707


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