Cor Vasa 2003, 44(6):323-327
Hypercoagulation state in acute coronary syndromes. A brief review of the issue as seen by the clinician
- I. interní klinika, Fakultní nemocnice a Lékařská fakulta Univerzity Karlovy, Hradec Králové, Česká republika
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. A decrease in thrombin production was demonstrated when determining prothrombin fragment1+2 (statistically significant; p = 0.02), but not when determining the thrombin-antithrombin complex. Persistent thrombin activity-despite thrombolytic therapy-may be, along with activated thrombocytes, the source of new thrombosis. Patients with AMI and reduced coronary artery flow rates (TIMI flow rates 0, 1, 2) show significantly higher fibrinopeptide A and thrombin-antithrombin complex levels compared with TIMI 3 flow rate patients. Patients who died also had significantly higher values of both markers compared with survivors. Patients with unstable angina (UA) associated with a complicated course (recurrent pain, AMI) have been reported to show increased procoagulant activity and, conversely, decreased fibrinolytic activity. The effects of thrombocyte activation and thromboxane production are discussed.
Keywords: Coronary syndromes; Prothrombin fragment1+2; Fibrin peptide A; Thrombin-antithrombin complex; Tissue plasminogen activator; PAF; Thromboxane A2
Published: June 1, 2003 Show citation