STUDIES RELATED TO COAGULATION ACTIVATION AFTER THROMBOLYTIC THERAPY IN ACUTE MYOCARDIAL INFARCTION

摘要

Objective:Thrombolytic therapy is an established modality in the management ofacute myocardial infarction(AMI).But early reocclusion of 5-15% limits its effectsand modifies the prognosis of involved patients,To identify the coagulation-relatedfactors predisposing to rethrombosis and consequent reocclusion after thrombolytictherapy,this study was designed to dynamically observe the changes of plasmacoagulation activities before and after thrombolytic therapy.Materials and methods:Consecutive 37 patients presenting with AMI were included,28 of which matched with the inclusion criteria for thrombolysis,Either 1500 000U ofurokinase or 1 500 000U of streptokinase was infused intravenously within 30min.0.3g of aspirin was taken sublingually by all the patients before the start ofthrombolysis and maintained 150mg once daily.Subcutaneous calcium heparan,7500U twice daily was administered 12 hours after the initiation of thrombolytic therapyand sustained for 4-10 days.Upon the diagnosis of the AMI established,blcodsampling was performed periodically and plasma ATM(antithrombin Ⅲ modified)and D-D(D-Dimer) determined by ELISA.Changes of these two parameters within andbetween different subgroups were analyzed.Results:Plasma ATM and D-D increased significantly 2 hours after thrombolysisinitiation.Plasma ATM levels peaked 4 hours later,sustained for at least 3 days,Plasma D-D peaked in 2 hours and returned progressively to normal 12 hours afterthrombolysis In patients without thrombolysis,no significant changes were found inplasma ATM and D-D levels during the whole monitoring period.A positivecorrelation was present between plasma ATM and D-D levels in thrombolytic patients.By subgroup analysis,coagulation activation occurred upon infusion of thromnbolytics.no matter whether the infarct-related vessels were reperfused or not,or which kind ofthromboiytics we chosen,Conclusion:1)Thrombolytic therapy activates coagulation system,which is positivelyrelated to clot lysis.2)Burst of coagulation cascade is only related to thrombolyticsinfusion.3)The anticoagulant regimen we now used could net sufficiently suppress theactivation of coagulation.Earlier or simultancous administration of intensiveanticoagulation may benefit more from thrombolytic therapy for patients with AMI.