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Plasma resistance to activated protein C regulates the activation of coagulation induced by thrombolysis in patients with ischaemic heart disease.
  1. O. D. Pedersen,
  2. J. Gram,
  3. J. Jespersen
  1. Department of Internal Medicine, Ribe County Hospital, Esbjerg, Denmark.

    Abstract

    OBJECTIVE: To determine whether there was a relation between plasma resistance to activated protein C and the coagulation activation induced during thrombolysis with 100 mg alteplase in 25 patients with acute ischaemic heart disease. METHODS: Blood samples were collected before (t = 0 h), during (t = 2.25 h), and after (t = 4 h, t = 12 h, and t = 24 h) thrombolysis to examine the relation between baseline activated protein C resistance ratio and markers of coagulation activation-that is, thrombinantithrombin III-complexes and prothrombin fragment 1 + 2 generated during thrombolysis. RESULTS: There was a negative correlation between activated protein C resistance ratio and area under the curve of thrombin-antithrombin III-complexes (rs = - 0.60; P < 0.003) and there was a trend to a negative correlation between activated protein C resistance ratio and area under the curve of prothrombin fragment 1 + 2 (rs = - 0.37; P = 0.07). This accorded with the negative correlation between activated protein C resistance ratio and the peak value of thrombin-antithrombin III-complexes (rs = - 0.55; P < 0.005) and between activated protein C resistance ratio and the peak value of prothrombin fragment 1 + 2 (rs = - 0.42; P < 0.04). Components of the protein C/S system or known inhibitors of activated protein C may influence the activated protein C resistance ratio. There were no associations between the activated protein C resistance ratio and protein C, protein C inhibitor, or plasminogen activator inhibitor type-1, whereas there was a trend to a negative correlation between activated protein C resistance ratio and protein S. CONCLUSIONS: The results indicate that plasma resistance to activated protein C may be one of the main mechanisms regulating the activation of coagulation induced by thrombolysis. This study suggests that it may be possible to single out individuals with a high risk of reocclusion before the start of thrombolytic therapy.

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