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Hemostatic abnormalities in acute myocardial infarction as detected by specific blood markers
In order to elucidate the mechanism of thrombus formation in acute myocardial infarction (AMI), coagulation and fibrinolytic and inhibitory proteins were systemically examined in 12 patients with AMI and 29 normal subjects. Activities of factor XII, II and V and concentration of high molecular weight kininogen and Factor II were significantly lower in AMI patients than in normal control subjects. Factor XI activity was also increased in AMI patients as compared with normal controls. Von Willebrand Factor and fibrinogen levels were increased in patients with AMI. Plasma D-dimer concentration was also significantly higher in AMI patients than in controls. Activation of the intrinsic pathway, thrombin generation, fibrin formation and fibrin degradation may be present in patients with AMI just after the onset of coronary thrombus formation.
In order to elucidate the mechanism of thrombus formation in acute myocardial infarction (AMI), coagulation and fibrinolytic and inhibitory proteins were systemically examined in 12 patients with AMI and 29 normal subjects. Activities of factor XII, II and V and concentration of high molecular weight kininogen and Factor II were significantly lower in AMI patients than in normal control subjects. Factor XI activity was also increased in AMI patients as compared with normal controls. Von Willebrand Factor and fibrinogen levels were increased in patients with AMI. Plasma D-dimer concentration was also significantly higher in AMI patients than in controls. Activation of the intrinsic pathway, thrombin generation, fibrin formation and fibrin degradation may be present in patients with AMI just after the onset of coronary thrombus formation.