Related Experiment Videos
Reduced fibrinolytic activity in coronary heart disease in basal conditions and after exercise
Insights
Coronary heart disease patients show impaired fibrinolysis, likely due to increased tissue-plasminogen activator inhibitor. This defective fibrinolytic activity was observed in tissue-plasminogen activator activity assays.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Thrombosis Research
Background:
- Fibrinolysis, the breakdown of blood clots, may be impaired in patients with coronary heart disease (CHD).
- Understanding fibrinolytic function is crucial for managing cardiovascular health and preventing thrombotic events.
Purpose of the Study:
- To investigate fibrinolytic and hemostatic parameters in patients with established coronary heart disease.
- To assess the impact of exercise on these parameters in CHD patients compared to controls.
Main Methods:
- Examined 20 CHD patients and 10 controls for tissue-plasminogen activator (t-PA) activity and antigen, t-PA inhibitor, and other fibrinolytic markers.
- Assays were performed before and after an exercise test to evaluate dynamic changes.
Main Results:
- CHD patients exhibited defective tissue-plasminogen activator activity (50% at baseline, 77% post-exercise, p<0.01).
- Tissue-plasminogen activator antigen levels were similar between groups.
- A persistent, though not statistically significant, increase in tissue-plasminogen activator inhibitor activity was noted in CHD patients.
Conclusions:
- Coronary heart disease is associated with defective fibrinolytic activity.
- Increased tissue-plasminogen activator inhibitor activity is a probable cause of impaired fibrinolysis in CHD patients.
Abstract:
Fibrinolysis may be impaired in coronary heart disease patients. 20 coronary heart disease patients and 10 control subjects were examined for tissue-plasminogen activator activity, tissue-plasminogen activator antigen, fast tissue-plasminogen activator inhibitor and other fibrinolytic and haemostatic parameters including antigenic and functional protein C. Both patient and control groups were similar in age and smoking habits. All of these patients had a myocardial infarction between 1-3 months before this study. Assays were evaluated before and after an exercise test. Prothrombin time, activated partial thromboplastin time, protein C, plasminogen, alpha 2-antiplasmin, fibrinogen/fibrin degradation products and contact-activated fibrinolysis were similar before and after exercise in both groups. Fibrinolytic activity assayed by the euglobulin lysis time and fibrin-plate lysis methods was decreased in the patient group as compared with the control group but the difference was not significant. In basal conditions, tissue-plasminogen activator activity was defective in 50% of the coronary heart disease patients (p less than 0.01) and after exercise this percentage rose to 77% (p less than 0.01). However, tissue-plasminogen activator antigen in the coronary heart disease group was similar to that of the control group, both before and after exercise. The activity of the tissue-plasminogen activator inhibitor was persistently increased in coronary heart disease though this increase was not statistically significant. It is concluded that in coronary heart disease patients there is a defective fibrinolytic activity probably due to an increase in tissue-plasminogen activator inhibitor.