[The effects of intravenous urokinase administration in patients with acute myocardial infarction].

The effects of intravenous urokinase administration were assessed in patients with acute myocardial infarction (AMI). Of 146 patients with AMI, 101 were admitted within 12 hours of onset of chest pain, and classified in four groups according to the method of administering urokinase. PTCR group (15 cases); PTCR was performed within six hours of onset, using less than 960,000 I.U.; Group A (20 cases); 1.5 million I.U. administered in one hour or 960,000 I.U. in 30 min; Group B (48 cases); 240,000 I.U. in two hours; and 4) Group C (18 cases); 240,000 I.U. in 12 hours. In groups A, B and C, urokinase was administered intravenously. The remaining 45 patients did not receive urokinase, and served as a control group. In the chronic stage, infarction-related coronary arteries were patent at rates of 93% in the PTCR group, 82% in group A, 76% in group B, 62% in group C, and 46% in the control group. In the PTCR group and in group A, alpha 2-plasmin inhibitor showed a steep decline to the lowest level on the day after urokinase administration, as did the summation of elevation of ST segments in conventional twelve-lead electrocardiograms. Peak CK times, which represent the duration (hours) from onset to the peak serum CK value increased in the following order: 13.3 +/- 4.8 in the PTCR group, 17.3 +/- 4.9 in group A, 17.3 +/- 6.9 in group B, 20.7 +/- 6.7 in group C and 22.5 +/- 6.4 in the control group. These data suggest early recanalization of occluded coronary arteries in the group A, and intravenous administration of high doses of urokinase in the early phase of AMI seemed to contribute to salvage the ischemic myocardium. However, assessment of ventricular wall motion by two-dimensional echocardiography failed to confirm appreciable improvement in the PTCR group and group A in comparison with the other groups.