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Increased plasma factor VIII:c activity in patients with unstable angina pectoris
D Olinic1, I Brudaşcă, D Colhon
1First Medical Clinic, University of Medicine and Pharmacy Cluj-Napoca, Romania.
Insights
Patients with unstable angina pectoris have significantly higher plasma factor VIII:c activity and fibrinogen levels compared to healthy individuals. These findings suggest a potential role in the thrombotic propensity of unstable angina.
Area of Science:
- Cardiology
- Hematology
- Thrombosis
Background:
- Unstable angina pectoris is a critical condition associated with increased thrombotic risk.
- The role of specific coagulation factors in the pathophysiology of unstable angina requires further elucidation.
Purpose of the Study:
- To investigate plasma levels of factor VIII:c, fibrinogen, and antithrombin III in patients with unstable angina pectoris.
- To determine the potential contribution of these hemostatic factors to the thrombotic propensity in unstable angina.
Main Methods:
- Comparative analysis of plasma factor VIII:c activity, fibrinogen levels, and antithrombin III activity.
- Study included 17 patients with unstable angina pectoris and 10 healthy control subjects.
Main Results:
- Significantly elevated plasma factor VIII:c activity (p < 0.01) in unstable angina patients (201% +/- 121) versus controls (97% +/- 16).
- Significantly higher plasma fibrinogen levels (p < 0.003) in patients (455 mg/dl +/- 188) compared to controls (260 mg/dl +/- 35).
- No significant difference in antithrombin III activity between patients and controls; no correlation between factor VIII:c and fibrinogen within the patient group.
Conclusions:
- Increased factor VIII:c activity in unstable angina may stem from acute phase reactions or adrenergic stimulation.
- Elevated factor VIII:c and fibrinogen suggest a heightened systemic thrombotic propensity in unstable angina.
- These hemostatic alterations could be pathogenically relevant to plaque rupture outcomes.
Abstract:
Plasma factor VIII:c activity was found to be significantly (p < 0.01) higher in the 17 patients with unstable angina pectoris (201% +/- 121; x +/- SD) than in the 10 healthy control subjects (97% +/- 16). Plasma fibrinogen level was also significantly (p < 0.003) higher in patients (455 mg/dl +/- 188) than in controls (260 mg/dl +/- 35) but there was no significant correlation between these two variables within the group of patients with unstable angina. No difference could be noted between plasma antithrombin III activities in patients and in controls. It is considered that the increased factor VIII:c activity in patients with unstable angina pectoris could be subsequent to the acute phase reaction induced by cytokines and/or by an enhanced adrenergic stimulation, although the possible presence of genetically-conditioned hyperactive factor VIII:c molecules can not be excluded. Since the outcome of a ruptured plaque may also depend on the systemic thrombotic propensity at the time of rupture, the presently reported findings could be pathogenically relevant.