Vol 13, No 6 (2006): Folia Cardiologica
Original articles
Published online: 2006-07-10

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Evaluation of thrombinogenesis in vivo in acute myocardial infarction in relation to concentrations of thrombin-antithrombin III complexes and antithrombin III activity

Władysław Sinkiewicz, Jan Błażejewski, Robert Bujak, Ewa Żekanowska, Jacek Kubica, Jacek Budzyński, Joanna Dudziak
Folia Cardiol 2006;13(6):465-472.

Abstract

Background: Thrombotic processes play an essential role in the progression of the atheromatosis and pathogenesis of acute coronary syndromes. The role of haemostatic factors in the development of circulatory system diseases, ischaemic heart disease in particular, has met with great research interest. The purpose of the present research is to define the role of haemostatic factors in the pathogenesis of atheromatosis and ischaemic heart disease and also to deal with their impact on diagnosis and prognosis. The aim of the present study was to evaluate thrombin generation in vivo and to define the role of the main inhibitor of coagulation in patients with acute myocardial infarction.
Methods: The study was performed using a group of 70 patients with acute myocardial infarction with ST segment elevation (STEMI). The control group comprised 25 healthy subjects matched for age and gender. Concentrations of thrombin-antithrombin III complexes (TAT complexes) and antithrombin III (AT III) activity were measured; the sample was taken before essential treatment was administered.
Results: In a group of patients with myocardial infarction, significantly higher average concentrations of TAT complexes (p < 0.0001) and AT III activity (p < 0.001) were found. An inverse correlation between AT III activity and kinase phosphocreatine concentration (p < 0.02) was shown as well as a positive correlation between AT III activity and the time elapsing from the onset of infarction symptoms to admission (p < 0.05). The increase in TAT complex concentration and AT III activity did not depend on sex, age and risk factors for ischaemic heart disease, nor did it predict late complications.
Conclusions: The results provide evidence of an intensification of thrombinogenesis processes in patients with acute myocardial infarction. The increase of AT III activity may reflect a compensatory mechanism of the haemostatic system with regard to intensified thrombinogenesis.

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