To assess the contribution of thrombus formation in the pathogenesis o
f 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 underta
ken in patients with unstable angina (n = 47) from the time of their a
dmission 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, whi
ch is a consequence of heparinization. There was significant elevation
of fibrinogen, factor VIII:C, von Willebrand factor:antigen and von W
illebrand factor:ristocetin cofactor throughout the study period. Ther
e was also evidence of thrombin generation as indicated by the elevate
d levels of fibrinopeptide A (FPA) and thrombin-antithrombin complexes
. The platelet release proteins, beta-thromboglobulin (BTG) and platel
et factor 4 (PF4), were markedly elevated in the first 2 days and drop
ped gradually thereafter. The fibrinolytic inhibitor, plasminogen acti
vator inhibitor (PAI), levels were elevated throughout. Proteins C and
S, plasminogen and alpha2-antiplasmin remained unchanged. It was conc
luded that in patients with unstable angina, there is significant acti
vation of the clotting system and inhibition of fibrinolysis which con
firms the existence of a tendency towards thrombus formation in patien
ts with unstable angina.