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[Blood coagulation and fibrinolysis in ischemic heart disease]
1Division of Cardiology, Kumamoto University School of Medicine.
Insights
Coronary artery spasm may trigger thrombus formation by increasing fibrinopeptide A (FPA). Increased plasminogen activator inhibitor (PAI) activity in unstable angina may impair clot removal, potentially leading to myocardial infarction.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Biochemistry
Context:
- Intracoronary thrombus formation is implicated in acute myocardial infarction and unstable angina.
- Investigating alterations in coagulation and fibrinolytic systems in ischemic heart diseases is crucial.
Purpose:
- To examine plasma levels of fibrinopeptide A (FPA) and plasminogen activator inhibitor (PAI) in patients with ischemic heart diseases.
- To elucidate the role of FPA and PAI in the pathogenesis of variant angina, coronary spastic angina, and unstable angina.
Summary:
- Plasma FPA levels were elevated in variant angina patients, with circadian variation peaking overnight, and increased post-ischemic attack in coronary spastic angina.
- FPA release into coronary circulation occurred after acetylcholine-induced angina, suggesting spasm induces thrombin generation and thrombus formation.
- Plasma PAI activity was higher in unstable and coronary spastic angina than stable exertional angina, decreasing with treatment in unstable cases.
Impact:
- Findings suggest coronary artery spasm can initiate thrombin generation and intracoronary thrombus formation.
- Elevated PAI activity may reduce fibrinolysis, hindering thrombus removal and contributing to acute myocardial infarction in susceptible patients.
- This research provides insights into the pro-thrombotic state in certain ischemic heart conditions, aiding in understanding disease mechanisms.
Abstract:
Intracoronary thrombus formation has been thought to play an important role in the genesis of acute myocardial infarction an unstable angina. To examine whether the coagulation and fibrinolytic systems are altered in such ischemic heart diseases, the plasma levels of fibrinopeptide A (FPA) and plasminogen activator (PAI) were measured. The plasma level of FPA was increased in patients with variant angina as compared with those with stable exertional angina and there was a significant circadian variation in the plasma level of FPA in parallel with that of the frequency of the attacks with the peak level occurring from midnight to early morning in patients with variant angina. The plasma FPA level increased in patients with coronary spastic angina after the ischemic attack induced by hyperventilation. Furthermore, FPA was released into the coronary circulation after the anginal attack induced by intracoronary injection of acetylcholine. These findings suggest that the coronary artery spasm may induce thrombin generation and trigger thrombus formation in the coronary artery. On the other hand, the plasma level of PAI activity was higher in patients with unstable angina and coronary spastic angina than in those with stable exertional angina. Moreover, the PAI activity in patients with unstable angina decreased to the level in patients with stable exertional angina after the stabilization of their symptoms by drugs. Our findings suggest that the increased plasma PAI activity may reduce fibrinolytic activity and attenuate removal of the thrombus and may ultimately lead to acute myocardial infarction in some patients with unstable angina and coronary spastic angina.(ABSTRACT TRUNCATED AT 250 WORDS)