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Reduced synthesis of tissue plasminogen activator by vascular endothelium during acute myocardial infarction
R M Norris1, P A Ockelford, D B Cross
1Coronary-Care Unit, Green Lane Hospital, Auckland, New Zealand.
Insights
Impaired vascular endothelium release of tissue plasminogen activator (t-PA) is linked to acute myocardial infarction. This suggests a role for t-PA production in acute coronary thrombosis.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Thrombosis Research
Background:
- Acute myocardial infarction (AMI) involves coronary thrombosis.
- Tissue plasminogen activator (t-PA) is crucial for fibrinolysis.
- Endothelial function may be altered during AMI.
Purpose of the Study:
- To investigate t-PA antigen levels and release capacity in AMI patients.
- To assess von Willebrand factor release during acute infarction.
- To explore the relationship between t-PA production and acute coronary thrombosis.
Main Methods:
- Measured t-PA antigen and von Willebrand factor in AMI patients, chronic angina patients, and normal subjects.
- Assessed endothelial t-PA release after venous occlusion.
- Repeated measurements in AMI patients at three weeks post-infarction.
Main Results:
- Resting t-PA antigen levels did not differ significantly between groups.
- Endothelial t-PA release capacity was significantly impaired in AMI patients (p < 0.01).
- Acute phase von Willebrand factor release was significantly increased in AMI patients (p < 0.01).
Conclusions:
- Impaired t-PA production is associated with acute coronary thrombosis.
- The findings suggest a potential role for compromised t-PA release in AMI pathogenesis.
- Further research is needed to determine if impaired t-PA production is causative or a secondary response.
Abstract:
We measured levels of tissue plasminogen activator (t-PA) antigen in 100 patients within six hours of the onset of acute myocardial infarction, in 34 patients with chronic angina but no recent infarction, and in 36 normal subjects. We also assayed von Willebrand factor in the acute patients and in the normal subjects. Measurements were repeated in 40 acute patients at three weeks after myocardial infarction. Although resting levels of t-PA antigen were not significantly different from normal during myocardial infarction, the capacity of the vascular endothelium to release t-PA after five minutes of venous occlusion was impaired (p less than 0.01). The acute phase vessel wall release of von Willebrand factor was increased during acute infarction (p less than 0.01). We conclude that impairment of t-PA production is associated with acute coronary thrombosis, although it is not possible to differentiate between a causative role or a secondary response due to exhaustion of the t-PA producing mechanism.