BACKGROUND: The coagulation and fibrinolytic activities increase in the setting of acute myocardial infarction (AMI) and has been shown to increase further after the administration of thrombolytic agents. The reocclusion rate was slightly higher in patients with recombinant tissue type plasminogen activator (rt-PA) than urokinase (UK). However, there are few studies on serial changes in coagulation and fibrinolytic activities during the thrombolytic therapy. METHODS: Twenty five AMI patients who visited Yongdong Severance Hospital from August 1996 to August 1997 were recruited. They were randomized two groups either double bolus UK or accelerated rt-PA. Plasma levels of fibrinogen, thrombin-antithrombin III complex (TAT), plasmin-alpha2 plasmin inhibitor complex (PIC), activities of protein C and protein S were checked before and 3, 12, 24hrs and 7days after the thrombolytic therapy. RESULTS: Plasma level of fibrinogen was decreased 3 and 12hrs after the initiation of thrombolytic therapy in both groups (p<0.05) however, the fibrinogen level in UK treated group (59.9+/-33.5 mg/dl) was decreased than rt-PA treated group (198.2+/-64.3 mg/dl) at 3hrs after thrombolytic therapy (p<0.05). Activities of protein C and protein S were increased at 3hrs after thrombolytic therapy in both groups and no difference was noticed between UK and rt-PA group. Concentrations of TAT and PIC were increased in both groups even before the thrombolytic therapy was initiated. The increment of TAT level was larger in rt-PA group (21.7+/-16.1, 8.9+/-5.4 ng/mL) compared with UK group (15.0+/-17.9, 4.6+/-1.9 ng/mL) at 3 and 12 hrs after thrombolytic therapy (p<0.05). PIC level was significantly increased at 3 and 12 hrs after the treatment in both groups and no difference was noted between UK and rt-PA group. CONCLUSION: Both coagulation and fibrinolytic activities, activated already before thrombolytic therapy, were further aug-mented after thrombolytic therapy in AMI patients. The increment of fibrinolytic activity showed no significant difference between UK and rt-PA treated group. However the coagulation activity in rt-PA treated group was increased more than UK treated group.
Antifibrinolytic Agents ; Fibrinogen ; Fibrinolytic Agents ; Humans ; Myocardial Infarction* ; Plasma ; Protein C ; Protein S ; Thrombolytic Therapy ; Tissue Plasminogen Activator* ; Urokinase-Type Plasminogen Activator*

BACKGROUND: The coagulation and fibrinolytic activities increase in the setting of acute myocardial infarction (AMI) and has been shown to increase further after the administration of thrombolytic agents. The reocclusion rate was slightly higher in patients with recombinant tissue type plasminogen activator (rt-PA) than urokinase (UK). However, there are few studies on serial changes in coagulation and fibrinolytic activities during the thrombolytic therapy. METHODS: Twenty five AMI patients who visited Yongdong Severance Hospital from August 1996 to August 1997 were recruited. They were randomized two groups either double bolus UK or accelerated rt-PA. Plasma levels of fibrinogen, thrombin-antithrombin III complex (TAT), plasmin-alpha2 plasmin inhibitor complex (PIC), activities of protein C and protein S were checked before and 3, 12, 24hrs and 7days after the thrombolytic therapy. RESULTS: Plasma level of fibrinogen was decreased 3 and 12hrs after the initiation of thrombolytic therapy in both groups (p<0.05) however, the fibrinogen level in UK treated group (59.9+/-33.5 mg/dl) was decreased than rt-PA treated group (198.2+/-64.3 mg/dl) at 3hrs after thrombolytic therapy (p<0.05). Activities of protein C and protein S were increased at 3hrs after thrombolytic therapy in both groups and no difference was noticed between UK and rt-PA group. Concentrations of TAT and PIC were increased in both groups even before the thrombolytic therapy was initiated. The increment of TAT level was larger in rt-PA group (21.7+/-16.1, 8.9+/-5.4 ng/mL) compared with UK group (15.0+/-17.9, 4.6+/-1.9 ng/mL) at 3 and 12 hrs after thrombolytic therapy (p<0.05). PIC level was significantly increased at 3 and 12 hrs after the treatment in both groups and no difference was noted between UK and rt-PA group. CONCLUSION: Both coagulation and fibrinolytic activities, activated already before thrombolytic therapy, were further aug-mented after thrombolytic therapy in AMI patients. The increment of fibrinolytic activity showed no significant difference between UK and rt-PA treated group. However the coagulation activity in rt-PA treated group was increased more than UK treated group.
Antifibrinolytic Agents ; Fibrinogen ; Fibrinolytic Agents ; Humans ; Myocardial Infarction* ; Plasma ; Protein C ; Protein S ; Thrombolytic Therapy ; Tissue Plasminogen Activator* ; Urokinase-Type Plasminogen Activator*

A review was done on 631 patients with acute myocardial infarction who underwent coronary angiography within 30 days after onset of myocardial infarction at Yonsei University Severance Hospital from January, 1985, to August, 1993. The incidence of acute myocardial infarction in patients under 40 years of age was 10.3% (65/631). Acute myocardial infarction below the fourth decades was the predominant disease of men. Risk factor analysis revealed a history of cigarette smoking and hypercholesterolemia were more frequently found in the young patients, but a history of hypertension and diabetes were more frequently found in the elderly patients. Angiographically, the incidence of one vessel disease and normal or minimal lesion coronary anatomy were more frequent in the young patients and incidence of multi-vessel disease were more frequent in the elderly patients. Of the 65 patients under 40 with acute myocardial infarction, the patients with multi-vessel disease tended to have a history of diabetes mellitus in comparison with those with normal coronary anatomy or one vessel disease.
Adult ; Age Factors ; Female ; Human ; Incidence ; Korea/epidemiology ; Male ; Middle Age ; Myocardial Infarction/*epidemiology ; Prevalence ; Risk Factors

BACKGROUND: The early coronary reperfusion with tissue type plasminogen activator(t-PA) influenced on the short term mortality and long term mobidity in acute myocardial infarction. The attention for thrombolysis with t-PA has been focused in identifying the optimal t-PA regimen and on the possibility of achieving effective and safe thrombolysis with a bolus of t-PA. Experimental data demonstrates that rapid t-PA infusion resulted in improved thrombolysis with minimal fibrinogenolysis and without excessive bleeding than prolonged infusion. METHODS: Consecutive patients presenting up to 6 hour from the onset of symptoms were recruited for the study. Aspirin(200mg daily) should be given immediately, 100mg t-PA was administered as two intravenous bolus injections of 50mg t-PA each given 30 minute apart, and followed by 5,000 unit heparin IV bolus with continuous infusion for 5 days. Angiography was performed at 60 and 90min after the first bolus and between 12-24 hour after study entry. After 7-10 days of myocardial infacrtion, coronary angiograms were performed in all patients who had been taken ddouble bolus t-PA. RESULTS: At 60min, angiography revealed infarct-related coronary artery patency of TIMI flow grade 3 in 15(88%) of 17 patients. At 90min, infarct-related coronary artery patency of TIMI flow grade 3 was achieved in 16(94%) of 17 patients. Bleeding episodes were mostly minor(6 of 33 patients, 18%), and hemorrhagic stroke was developed in 1 patients(1/33, 3.0%). Three patients(9.0%) died in hospitalization probably due to ventricular rupture. CONCLUSION: The administration of 100mg of double bolus t-PA in acute myocardial infarcion results in remarkably high early TIMI flow grade 3 on infarct-related coronary artery patency rates(88% and 94% at 60 and 90min, respectively). The bolus injection of t-PA may be simple and effective strategy in the treatment of acute myocardial infarction. However, large numbers of prospective study would be required.
Angiography ; Coronary Vessels ; Hemorrhage ; Heparin ; Hospitalization ; Humans ; Mortality ; Myocardial Infarction* ; Myocardial Reperfusion ; Plasminogen ; Rupture ; Stroke ; Tissue Plasminogen Activator*