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Tissue plasminogen activator activity and inhibition in acute myocardial infarction and angiographically normal
Insights
Reduced tissue plasminogen activator (tPA) activity and increased tPA inhibition may contribute to coronary thrombosis, even without significant coronary artery disease. These findings highlight potential factors in acute myocardial infarction origins.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Thrombosis Research
Background:
- Acute myocardial infarction (AMI) can occur despite normal coronary arteries.
- Understanding the underlying mechanisms of thrombosis in such cases is crucial for effective treatment and prevention.
Purpose of the Study:
- To investigate the roles of blood coagulation, platelet reactivity, and fibrinolysis in patients with AMI and normal coronary arteries.
- To compare these parameters with AMI patients who have obstructive coronary artery disease and healthy controls.
Main Methods:
- Analysis of blood coagulation, platelet reactivity, and fibrinolysis in three groups: AMI with normal coronaries, AMI with single-vessel disease, and healthy volunteers.
- Measurement of plasma activity and inhibitory activity of tissue plasminogen activator (tPA).
Main Results:
- Blood coagulation and platelet reactivity were similar across groups, with higher fibrinogen in the patient control group.
- Significantly lower plasma tissue plasminogen activator (tPA) activity was observed in the AMI with normal coronaries group compared to both control groups.
- Elevated plasma tPA inhibitory activity was found in both AMI groups compared to healthy controls.
Conclusions:
- Reduced plasma tPA activity and enhanced tPA inhibition are potential key factors in the development of coronary thrombosis, particularly in the absence of obstructive coronary artery disease.
- These findings suggest a distinct thrombotic pathway in some AMI patients with normal coronary arteries.
Abstract:
Parameters of blood coagulation, blood platelet reactivity and fibrinolysis were analyzed in 18 patients with acute myocardial infarction (AMI) and angiographically normal coronary arteries. This study group was compared with a patient control group of 18 AMI patients with 1-vessel obstructive coronary artery disease. Patients were matched for sex, age and AMI date. A healthy control group consisted of 18 sex- and age-matched volunteers. Blood coagulation measurements and platelet reactivity were similar in the 3 groups, except for fibrinogen, which was significantly higher in the patient control group. Plasma activity of tissue plasminogen activator (tPA) was detectable in only 2 patients in the study group, 9 in the patient control group (p less than 0.02) and 12 in the healthy control group (p less than 0.0001). Median plasma tPA inhibitory activity was higher in the study group (10.3 IU/ml) and the patient control group (8.1 IU/ml) than in the healthy control group (2.7 IU/ml, p less than 0.0001 and p less than 0.03). Thus, reduced activity and enhanced inhibition of plasma tPA may be important factors in the origin of coronary thrombosis, especially in the absence of coronary artery disease.