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.