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Tissue plasminogen activator release and plasminogen activator inhibitor levels in coronary artery disease
D G Meyers1, W D Haire, J K Rasmussen
1Department of Internal Medicine, College of Medicine, University of Nebraska, Omaha.
Insights
This study found no evidence that impaired fibrinolysis contributes to coronary thrombosis in patients with unstable angina or myocardial infarction. Fibrinolytic system variables were similar across patient groups and controls, suggesting systemic fibrinolysis is not a key factor.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Thrombosis Research
Background:
- Unstable angina and myocardial infarction are linked to coronary thrombosis.
- Impaired fibrinolysis is a potential contributing factor to thrombosis.
Purpose of the Study:
- To investigate the role of the extrinsic fibrinolytic system in thrombus-associated coronary syndromes.
- To compare fibrinolysis variables in patients with and without coronary thrombosis.
Main Methods:
- Assessed tissue plasminogen activator antigen, plasminogen activator inhibitor activity/antigen, and euglobulin clot lysis time.
- Evaluated 56 patients with chest pain syndromes and 16 healthy controls.
- Measured fibrinolysis variables before and after venous occlusion.
Main Results:
- Fibrinolysis variables were similar in patients with thrombus-associated coronary syndromes compared to those without coronary thrombosis.
- No significant differences were observed between patient groups and healthy controls.
- Systemic fibrinolytic function did not appear to differ significantly.
Conclusions:
- Defective systemic fibrinolysis is unlikely to be a primary factor in the pathogenesis of thrombus-associated coronary artery syndromes.
- The study suggests other mechanisms may be more critical in the development of coronary thrombosis.
Abstract:
Unstable angina and Q wave myocardial infarction are associated with intraluminal 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 antigen, and euglobulin clot lysis time before and after venous occlusion in 56 patients undergoing coronary angiography for chest pain syndromes and in 16 healthy controls. Fibrinolysis variables were similar (with greater than 95% confidence) in the patients with thrombus-associated coronary syndromes as compared with those with chest pain syndromes not due to coronary thrombosis. These fibrinolytic variables were also similar to those in patients without coronary artery disease and in healthy controls. Their data suggest that defective fibrinolysis is not involved, at least systemically, in the pathogenesis of thrombus-associated coronary artery syndromes.