To examine the procoagulant effects of thrombolytic agent on h emostasis and study the role of hemostatic markers as predictors of clinical outcomes. Methods. In the present study, eighteen patients with acute m...To examine the procoagulant effects of thrombolytic agent on h emostasis and study the role of hemostatic markers as predictors of clinical outcomes. Methods. In the present study, eighteen patients with acute myocardial in farction(AMI) received 1.5 or 2.0 million U nonspecific urokinase(UK), or 70～80 mg fibrin specific recombinant tissue plasminogen activator(rt PA)and did not use heparin until 8 hours after intravenous injection of the above agents. Eig ht patients with AMI and without thrombolytic therapy were enrolled as controls. Coagulant and thrombolytic activity markers included thrombin antithrombin Ⅲ complex (TAT), D dimer, fibrinogen (Fg), FMPV/Amax. All markers were determined before,immediately,1,2,4 and 8 hours after the administration of thrombolytic a gents respectively. Results. Molecular marker of thrombin generation——TAT showed an activated coa gulant state immediately after thrombolytic therapy. Level of TAT showed no sign ificant changes between every two observed phases in controls. However, level of TAT increased significantly from 4.95±1.75μg/L ( 4.63±1.37μg/L) to 14.71±3 .31μg/L ( 14.25±2.53μg/L) before and immediately after administration of thro mbolytic agents UK(or rt PA). There was significant difference between level of serum TAT of patients with and without thrombolytic therapy (P< 0.05). Patients achieving clinical reperfusion had lower TAT level than those failing in thromb olytic therapy, and higher FMPV/Amax level than controls. D dimer, a surrogate of thrombolytic activity increased markedly and Fg significantly declined afte r thrombolytic therapy(P< 0.05).Conclusions. Thrombin generation occurred in plasma in response to excess fibri nolysis induced by thrombolytic therapy. Both urokinase and rt PA had procoagul ant action. This transient activation of the coagulant system might contribute t o early reocclusion. These data provided the theoretical support for simultaneou s administration of anticoagulant therapy with thrombolytic agents. These result s also suggested that TAT might be useful in predicting clinical outcomes of p atients treated with thrombolytic therapy for AMI.展开更多
Objective To investigate the influence and mechanism of incidence of atrioventricular block (AVB) treated with thrombolytic therapy in acute inferior myocardial infarction (AIMI).Methods A total of 46 patients with A...Objective To investigate the influence and mechanism of incidence of atrioventricular block (AVB) treated with thrombolytic therapy in acute inferior myocardial infarction (AIMI).Methods A total of 46 patients with AIMI were divided into the thrombolytic group (n = 23) and the nonthrornboytic group (n = 23). Intravenous or intracoronary urokinase was given to the former group. We observed the advancing courses of AVB, and further assessed the relationship between occurrence of AVB and stenosis of infarct-related artery (IRA) with coronary angiography.Results Two cases died of Ⅲ o AVB in the non-thrombolytic group, but none was found in the thrombolytic group. The occurrence rate of AVB was similar in both groups; but that of Ⅲ ° AVB was much lower in the thrombolytic group (4 cases) than that in the non-thrombolytic group (11 cases, P ＜ 0.05), and the duration of AVB decreased from 201 ± 113 hours to 102±60 hours after thrombolytic therapy ( P＜0.01 ),which was mainly due to the decrease of AVB in the vanishing interval, but not in the developing interval.The coronary angiography demonstrated that there were an increasing reperfusion flow and a decreasing coronary stenosis of the infarct-related artery after thrombolytic therapy.Conclusion Thrombolytic therapy can reduce the incidence of severe AVB, shorten its duration and decrease the mortality by increasing the coronary reperfusion flow in the patients with AIMI.展开更多
文摘To examine the procoagulant effects of thrombolytic agent on h emostasis and study the role of hemostatic markers as predictors of clinical outcomes. Methods. In the present study, eighteen patients with acute myocardial in farction(AMI) received 1.5 or 2.0 million U nonspecific urokinase(UK), or 70～80 mg fibrin specific recombinant tissue plasminogen activator(rt PA)and did not use heparin until 8 hours after intravenous injection of the above agents. Eig ht patients with AMI and without thrombolytic therapy were enrolled as controls. Coagulant and thrombolytic activity markers included thrombin antithrombin Ⅲ complex (TAT), D dimer, fibrinogen (Fg), FMPV/Amax. All markers were determined before,immediately,1,2,4 and 8 hours after the administration of thrombolytic a gents respectively. Results. Molecular marker of thrombin generation——TAT showed an activated coa gulant state immediately after thrombolytic therapy. Level of TAT showed no sign ificant changes between every two observed phases in controls. However, level of TAT increased significantly from 4.95±1.75μg/L ( 4.63±1.37μg/L) to 14.71±3 .31μg/L ( 14.25±2.53μg/L) before and immediately after administration of thro mbolytic agents UK(or rt PA). There was significant difference between level of serum TAT of patients with and without thrombolytic therapy (P< 0.05). Patients achieving clinical reperfusion had lower TAT level than those failing in thromb olytic therapy, and higher FMPV/Amax level than controls. D dimer, a surrogate of thrombolytic activity increased markedly and Fg significantly declined afte r thrombolytic therapy(P< 0.05).Conclusions. Thrombin generation occurred in plasma in response to excess fibri nolysis induced by thrombolytic therapy. Both urokinase and rt PA had procoagul ant action. This transient activation of the coagulant system might contribute t o early reocclusion. These data provided the theoretical support for simultaneou s administration of anticoagulant therapy with thrombolytic agents. These result s also suggested that TAT might be useful in predicting clinical outcomes of p atients treated with thrombolytic therapy for AMI.
文摘Objective To investigate the influence and mechanism of incidence of atrioventricular block (AVB) treated with thrombolytic therapy in acute inferior myocardial infarction (AIMI).Methods A total of 46 patients with AIMI were divided into the thrombolytic group (n = 23) and the nonthrornboytic group (n = 23). Intravenous or intracoronary urokinase was given to the former group. We observed the advancing courses of AVB, and further assessed the relationship between occurrence of AVB and stenosis of infarct-related artery (IRA) with coronary angiography.Results Two cases died of Ⅲ o AVB in the non-thrombolytic group, but none was found in the thrombolytic group. The occurrence rate of AVB was similar in both groups; but that of Ⅲ ° AVB was much lower in the thrombolytic group (4 cases) than that in the non-thrombolytic group (11 cases, P ＜ 0.05), and the duration of AVB decreased from 201 ± 113 hours to 102±60 hours after thrombolytic therapy ( P＜0.01 ),which was mainly due to the decrease of AVB in the vanishing interval, but not in the developing interval.The coronary angiography demonstrated that there were an increasing reperfusion flow and a decreasing coronary stenosis of the infarct-related artery after thrombolytic therapy.Conclusion Thrombolytic therapy can reduce the incidence of severe AVB, shorten its duration and decrease the mortality by increasing the coronary reperfusion flow in the patients with AIMI.
