HEIGHTENED THROMBIN FORMATION BUT NORMAL PLASMA-LEVELS OF ACTIVATED FACTOR-VII IN PATIENTS WITH ACUTE CORONARY SYNDROMES

Plaque rupture with the exposure of a tissue factor-rich procoagulant surface is considered the common pathogenetic mechanism of unstable angina and myocardial infarction. Activated factor VII, the key enzyme for initiating blood coagulation under resting conditions, is increased in pathological situations associated with tissue factor exposure. We measured the plasma levels of activated factor VII and studied their relation with signs of coagulation enzyme activity in patients with acute coronary syndromes. The plasma levels of activated factor VII, prothrombin fragment 1+2, and fibrinopeptide A were measured on admission in consecutive patients presenting with acute myocardial infarction (n=28), unstable angina (n=32), and stable angina (n=17) and in age- and sex-matched healthy individuals (n=33). Plasma determinations of the same markers were also repeated at 15 days and 3 and 6 months. On admission, the patients with unstable angina or myocardial infarction had significantly higher plasma levels of prothrombin fragment 1+2 (P<.0001) and fibrinopeptide A (P<.0001) than those with stable angina or healthy individuals, whereas no differences were detected in the plasma levels of activated; factor VII. During follow-up there was a significant decrease in the plasma levels of fibrinopeptide A both in patients with unstable angina (P<.001) and in those with myocardial infarction (P<.001), whereas no changes in plasma prothrombin fragment 1+2 or activated factor VII levels were observed. Hence, in the acute and chronic phases of myocardial infarction and unstable angina, heightened coagulation enzyme activity is not accompanied by an increase in activated factor VII.