ristocetin and Angina--Unstable

To assess the contribution of thrombus formation in the pathogenesis of unstable angina, we employed the recently developed assays of small fragments which reflect the degree of activation of various components of the haemostatic system. Such haemostatic measurements were undertaken in patients with unstable angina (n = 47) from the time of their admission to the coronary care unit (CCU) at 8-h intervals in the first 24 h and then daily for a total of 5 days. The results obtained were compared with healthy control values. Patients exhibited lower ATIII, prolongation of the APTT and TT, but not PT or the reptilase time, which is a consequence of heparinization. There was significant elevation of fibrinogen, factor VIII:C, von Willebrand factor:antigen and von Willebrand factor:ristocetin cofactor throughout the study period. There was also evidence of thrombin generation as indicated by the elevated levels of fibrinopeptide A (FPA) and thrombin-antithrombin complexes. The platelet release proteins, beta-thromboglobulin (BTG) and platelet factor 4 (PF4), were markedly elevated in the first 2 days and dropped gradually thereafter. The fibrinolytic inhibitor, plasminogen activator inhibitor (PAI), levels were elevated throughout. Proteins C and S, plasminogen and alpha 2-antiplasmin remained unchanged. It was concluded that in patients with unstable angina, there is significant activation of the clotting system and inhibition of fibrinolysis which confirms the existence of a tendency towards thrombus formation in patients with unstable angina.

Topics: Adult; Aged; Angina, Unstable; Antigens; Antithrombin III; beta-Thromboglobulin; Blood Coagulation; Factor VIII; Female; Fibrinogen; Fibrinopeptide A; Hemostasis; Humans; Male; Middle Aged; Peptide Hydrolases; Plasminogen Inactivators; Platelet Factor 4; Protein C; Protein S; Ristocetin; von Willebrand Factor