Hypercoagulation state in acute coronary syndromes. A brief review of the issue as seen by the clinician
Abstract
The communication points to the pathogenesis of thrombus formation as the cause of clinical manifestations of acute coronary syndromes. An increase in the activation of the procoagulation markers fibrinopeptide A, prothrombin fragment1+2, thrombin-antithrombin complex on admission of patients presenting with acute myocardial infarction (AMI) and a further rise in their activity during thrombolysis were shown.
AMI patients have been shown to have a reduced fibrinolysis activity. The authors note that concomitant administration of heparin and hirudin markedly affects fibrinopeptide A activity by inhibiting the effect of thrombin on fibrinogen.
The modulation of thrombin activity by heparin and hirudin administered during thrombolysis is less marked.