Intravenous streptokinase during acute myocardial infarction. A prospective open study

To evaluate the efficacy of intravenous streptokinase in acute myocardial infarction (AMI) 108 patients received a high-dose (1.5 million units), short-term infusion (60 minutes) within 6 hours after onset of symptoms, followed by anticoagulation. Before discharge a submaximal exercise test and a coronary arteriography were performed in 100 surviving patients. Sixty-seven patients had a patent infarct-related vessel. Clinical reocclusion occurred in 21 patients. Left ventricular function was slightly, but not significantly, better in patients with patent infarct-related vessels: ejection fraction 59.5 +/- 13% versus 57.4 +/- 13%. Additional procedures were performed in 20 patients: percutaneous transluminal coronary angioplasty (PTCA) in 8 and coronary artery bypass surgery (CABG) in 12. The results indicate that streptokinase applicated during a 6 hour-time window is a potent thrombolytic agent in acute myocardial infarction with limited effect on global left ventricular function. Pre-discharge evaluation is necessary to screen patients for residual ischemia.     

Intravenous streptokinase in acute myocardial infarction

Intravenous (IV) fibrinolytic therapy, a recent area of research, has a great deal of applicability in emergency medicine. We report our experience with 30 patients treated with this method. Thirty consecutive patients in the early stages of acute evolving myocardial infarction (AMI) were assigned to receive high-dose IV streptokinase, 1.5 million units over a 30-minute period. Patients presented to the treating hospital at a mean time of 1.21 +/- 1.08 hours, and treatment commenced at a mean time of 2.77 +/- 1.31 hours after the onset of symptoms. Using standard clinical criteria, 86.7% (n = 26) of the patients reperfused initially. Two, however, reoccluded within the first 48 hours, and their clinical symptoms of myocardial infarction reappeared. By clinical observation 80% (n = 24) of the patients reperfused, and myocardial salvage was observed. Twenty-four patients with clinical reperfusion and one additional patient had patency of the affected artery, yielding a reperfusion rate of 83.3% (n = 25) as judged by angiography within one week of AMI. Both patients who had reoccluded clinically also were found to be occluded on angiography. Clinical and angiographic methods yield very similar results for the judgment of reperfusion (80% vs 83%, respectively, with no significant difference, P not significant). The results of our study tend to confirm the efficacy of IV streptokinase as a valuable management tool for early myocardial infarction.     

Intravenous streptokinase in evolving acute myocardial infarction

Eighty-one consecutive patients presenting within 3 hours of the onset of acute myocardial infarction (AMI) and without contraindications to thrombolytic or anticoagulant therapy received a 15- to 30-minute intravenous infusion of 750,000 or 1.5 million units of streptokinase (STK) followed by anticoagulation. Treatment was instituted 130 +/- 41 minutes after the onset of symptoms and reperfusion was achieved 36 +/- 26 minutes later. Reperfusion of the "infarct artery" was recognized by indirect clinical criteria in 78 patients (96%). In all 66 patients who underwent coronary angiography 3 to 7 days later, there was complete concordance between indirect and angiographic evidence of reperfusion. In 6 patients there was early reocclusion within 24 hours of treatment; in 4 of these patients, the artery was reopened with an additional dose of STK. Two elderly patients suffered an intracranial hemorrhage and there were 8 other major hemorrhagic complications, of which 7 were related to procedural trauma. Five patients (6.2%) died in the hospital. The results of intravenous STK thrombolytic therapy are compared with those of our previous study using intracoronary STK.     

重组链激酶治疗急性心肌梗塞的疗效与安全性

目的观察国产重组链激酶在急性心肌梗塞治疗中的溶栓效果和不良反应。方法自１９９７年３月～１９９８年３月间对４７７例急性心肌梗塞患者予１５０万单位重组链激酶溶栓治疗,观察溶栓再通率、急性期死亡率、并发症以及不良反应发生率。结果溶栓再通率为８０２％,３５天死亡率５０％。不良反应中：过敏反应５５％（２６例）,低血压７８％（３７例）,出血１５１％（７２例）,１例发生颅内出血但未致残,肝功能损害１４％（７例）,半月后均恢复。结论国产重组链激酶为治疗急性心肌梗塞有效、安全的溶栓药物。     

Intravenous versus intracoronary streptokinase in acute myocardial infarction

One hundred sixty-four consecutive patients with acute myocardial infarction were enrolled in a prospective trial of coronary thrombolysis with streptokinase (STK). The first 98 patients received intracoronary (i.c.) STK after coronary angiography and the next 66 received a high-dose rapid infusion of STK (900,000 IU) intravenously (i.v.) before angiography. First-pass radionuclide ejection fraction (EF) was performed early (within 24 hours of admission) and late (10 to 14 days after admission) to evaluate left ventricular function. In the i.v. group, 42 of 66 (64%) of infarct-related arteries were patent at the initial angiogram and 6 (9%) opened with subsequent i.c. STK. In the i.c. group, 13 of 98 (13%) of infarct-related arteries were patent at the initial angiogram and 50 of 85 (59%) opened with the i.c. STK. The i.v. and i.c. groups did not differ in time from onset of chest pain to presentation, type of infarct or underlying severity of coronary artery disease. In the i.v. group, STK was begun 67 minutes earlier than in the i.c. group. In 62 patients in whom reperfusion was successful, mean EF increased from 39 +/- 11% early to 48 +/- 13% late. In 30 in whom it was not, the mean EF increased from 36 +/- 10% to 40 +/- 12%. The increase in EF was significantly greater in patients in the reperfused group (p less than 0.03). In 18 patients who underwent reperfusion by i.v. STK, the mean EF increased 11 +/- 12%, whereas in 44 patients who had reperfusion by i.c. STK, the mean EF increased 9 +/- 10% (difference not significant).(ABSTRACT TRUNCATED AT 250 WORDS)     

Intravenous versus intracoronary streptokinase in acute myocardial infarction

Nine studies specifically dealing with the comparison of intravenous streptokinase (IVSK) and intracoronary streptokinase (ICSK) in the treatment of acute myocardial infarction (MI) were analyzed to determine if IVSK is as efficacious as ICSK in achieving thrombolysis. Pooled data from the studies yielded success rates of 73% for IVSK and 72% for ICSK. Considering that the studies which did not perform preintervention angiogram may have overestimated the thrombolytic success rate in IVSK patients, there is a possibility that ICSK may be slightly more effective in achieving acute reperfusion. Bleeding complications were similar, and a systemic lytic state was observed in both treatment groups. No definitive conclusions can be drawn regarding the differences between groups in improvements of left ventricular function and mortality rates. ICSK has the advantage of direct documentation of reperfusion and spares the patient the risk of anticoagulation should the attempt fail. On the other hand, IVSK is cheaper, easier to administer, and can logistically be given earlier (even in the emergency room or ambulance) than ICSK; it is therefore more widely available, and may be the preferred mode of treatment in community hospitals where cardiac catheterization facilities are not readily available, if streptokinase is to be given at all.     

Intravenous short-term infusion of streptokinase in acute myocardial infarction

Clinically encouraging results can be obtained with an intravenous high dosage, short-term infusion of streptokinase in patients with evolving myocardial infarction. The feasibility and efficacy of the systemic approach of streptokinase therapy is discussed in this report and includes topics such as recanalization success rate, restoration of coronary blood flow, residual coronary artery lesions, salvage of jeopardized myocardium, time limits of effective reperfusion, transluminal angioplasty, coronary bypass surgery, and mortality. The value of high dosage intravenous short-term streptokinase infusion needs to be assessed with properly designed clinical trials.     

Intravenous short-term infusion of streptokinase in acute myocardial infarction

Short-term i.v. infusion of streptokinase was performed in 93 patients within 6 hours after the onset of acute myocardial infarction. Twenty-six patients underwent angiography in the acute phase (group A) and 52 underwent angiography in the fourth week only (group B); 15 patients had no angiography. Seven patients died during the hospital stay and six suffered nonfatal reinfarctions. There were no bleeding complications. In 11 of 21 group A patients, occluded coronary arteries were opened within 1 hour after the streptokinase infusion was started. In 84% of groups A and B, the infarct-related coronary artery was patent in the fourth week. In 75% of the patent arteries, the residual luminal diameter stenosis was less than 70%. According to serial serum CK-MB curves, recanalization was achieved mostly within 1-2 hours. Myocardial salvage was indicated by improvement in local contraction disorders in the recanalized group A patients and by the significant relationship between infarct size and time from symptom onset to treatment in group B. These data suggest that a high-dose, short-term, i.v. infusion of streptokinase is a safe and efficient method of restoring coronary blood flow. Expeditious initiation of i.v. streptokinase infusion is a critical determinant for early recanalization and salvage of myocardium. Patients with thrombotically subtotal occlusion probably receive the most benefit. Evaluation of the true impact on survival and myocardial function will require controlled clinical trials.     

Intravenous versus intracoronary streptokinase for acute transmural myocardial infarction

In order to compare the thrombolytic efficacy of selective versus systemic administration of streptokinase, we gave this drug by either the intracoronary or intravenous routes to 25 patients during the first 6 hours of acute myocardial infarction. All patients had total occlusion of the infarct-related vessel, unresponsive to intracoronary nitroglycerin. Twelve patients received intravenous streptokinase and 13 received intracoronary administration of the drug. Angiograms were taken prior to and during streptokinase administration. Reopening was achieved in 11 of 13 intracoronary patients and 8 of 12 intravenous patients (P = Ns). Time to reopening was longer (54 minutes) in the intravenous patients than in the intracoronary patients (26 minutes) (P < 0.05). In this study, intravenous streptokinase reopened infarct-related vessels nearly as often as intracoronary streptokinase, but it took longer. Given the limited access and time to prepare for intracoronary infusion and the ease of intravenous administration, further study of intravenous streptokinase is justified.     

Intravenous streptokinase in acute myocardial infarction. Reduction of early in-hospital mortality

A randomized study of the effects of intravenous streptokinase was performed in 214 patients with an acute myocardial infarction of less than 4 hours of whom 110 were included in the therapeutic group (SK) and 104 in the control group (C). Incidence of angiographic recanalization was higher in SK group (71 vs 28%, p less than 0.001) as that of non-significant residual coronary artery stenosis (less than 70%, 16% vs 3%, p less than 0.005), particularly in young patients (less than 45 years; 42% vs 8%, p less than 0.05). However, SK group presented a higher incidence of severe residual stenosis (90-99%) (SK, 42% vs C, 22%, p less than 0.01). Ejection fraction was higher among recanalized patients in both groups. Peak CPK-MB occurred earlier in SK group (13 vs 19 hours, p less than 0.001) and also among the recanalized patients of each group (SK, 12 vs 16 hours, p less than 0.001; C, 15 vs 21 hours, 0.002). The course of ST segment was similar in the 2 groups. The occurrence of ventricular arrhythmias within the first hour was greater in SK group (40% vs 20%, p less than 0.002), whereas the incidence of pericarditis (14% vs 35%, p less than 0.001) and of early mortality (less than 5 days, 2% vs 10%, p less than 0.02) was lower in SK group. The incidence of cardiac rupture, confirmed at necropsy in each of the 5 cases studied, was also lower in SK group (1 vs 8).(ABSTRACT TRUNCATED AT 250 WORDS)     

Intravenous streptokinase versus heparin in recent acute myocardial infarction. Randomized multicenter study in the Franche-Comté

A multicentre randomised therapeutic trial was undertaken in 8 hospitals in the Franche-Comté department of France (Belfort, Besan?on, Dole, Lons-le-Saunier, Luxeuil, Montbéliard, Vesoul, Pontarlier) in which 101 patients with acute primary myocardial infarction were treated within 5 hours of onset of symptoms with either intravenous streptokinase (1,500,000 U in 30 mn) or conventional heparin therapy. The results were assessed on the clinical outcome, arterial patency in the necrosed territory and global and regional ejection fractions (EF) at the 3rd week. After randomisation, 51 patients were given heparin and 50 received streptokinase. Seven patients died in the heparin group and 4 in the streptokinase group (NS). At the third week, the artery in the necrosed zone was patent in 69% of the heparin group and in 68% of the streptokinase group (NS). The EF was significantly higher in the patients with patent arteries in the necrosed zone than in those with occluded arteries (0.49 +/- 0.12 vs 0.41 +/- 0.15, p less than 0.01). There was no significant difference in EF between the heparin and streptokinase groups. The EF was significantly higher in patients with anterior infarction who received streptokinase than in those who received heparin (0.40 +/- 0.10 vs 0.33 +/- 0.09 p less than 0.05). Segmental wall motion was significantly better at the apex and free wall. There was no significant difference between the two groups in posterior infarction. These results show that reestablishment or maintenance of arterial patency in the necrosed zone improves left ventricular function and that patients with anterior wall infarction are the ones most likely to benefit from streptokinase therapy.     

Intravenous streptokinase treatment and serum C-reactive protein in patients with acute myocardial infarction.

Serum concentrations of C-reactive protein were studied in 23 patients with acute myocardial infarction. In 14 patients who did not receive thrombolytic treatment there was a linear relation between infarct size (determined by serial creatine kinase-MB determinations and thallium-201 isotope emission tomography) and the C-reactive protein response. The correlation coefficient between the concentration-time integrals of creatine kinase-MB and C-reactive protein was 0.96. The correlation coefficient between the creatine kinase-MB concentration-time integral and the peak serum value of C-reactive protein was 0.93. In the nine patients who received intravenous streptokinase treatment there was also a positive correlation between the concentration-time integrals of creatine kinase-MB and C-reactive protein. The relation, however, depended on the success of the treatment. In patients with successful reperfusion the C-reactive protein response was only approximately 20% of that in patients in whom reperfusion failed or who received no thrombolytic treatment and who were matched by infarct size. When thrombolysis was successful the correlation coefficient between the concentration-time integrals of creatine kinase-MB and C-reactive protein was 0.86. Daily measurement of serum C-reactive protein is useful in evaluating infarct size in patients with acute myocardial infarction who do not receive thrombolytic treatment. In patients treated with streptokinase C-reactive protein concentrations may be used to assess the success of thrombolysis.     

Intravenous versus intracoronary streptokinase therapy for acute myocardial infarction in community hospitals

A consecutive series of 184 patients with acute myocardial infarction (AMI) received thrombolytic therapy. The first 63 were treated in the catheterization laboratory with intracoronary streptokinase (IC-STK), and 44 (70%) had successful thrombolysis. One hundred twenty-one patients received intravenous (IV) STK immediately after diagnosis of AMI, and 99 (82%) were found to have an open infarct artery. Only 58% of patients (14 of 24) who required transfer from out-of-town hospitals for IC-STK treatment had successful thrombolysis; in contrast, IV-STK given in the local hospital resulted in an 85% (72 of 85) rate of thrombolysis (p = 0.005). IV-STK thus appears at least as effective as IC-STK for AMI and is more effective for patients treated in hospitals without catheterization facilities.     

Intravenous streptokinase for acute myocardial infarction reduces the occurrence of ventricular late potentials.

The occurrence of ventricular late potentials in survivors of acute myocardial infarction treated with intravenous streptokinase was compared with that in a conservatively treated group and the relation between ventricular late potentials and patency of the infarct related artery was examined. Of 115 patients admitted with a first infarct, 55 were treated with intravenous streptokinase (streptokinase group) and 60 were treated conservatively (non-streptokinase group). A signal averaged electrocardiogram was recorded in all patients and coronary angiography was performed in 45 (81.8%) of the streptokinase group and in 21 (35%) of the non-streptokinase group. At a 40 Hz filter setting ventricular late potentials were significantly less common in patients treated with streptokinase (9 (16.4%) of 55) than in those who were not (26 (43.3%) of 60). A total of 66 patients underwent angiography. Of the 26 who had closed infarct-related arteries, 17 had ventricular late potentials at a 40 Hz filter setting (sensitivity 65.4%, specificity 95%) and 38 of the 40 patients with a patent infarct-related artery did not have ventricular late potentials (sensitivity 80.9%, specificity 89.5%). Patients with acute myocardial infarction treated with intravenous streptokinase were significantly less likely to have ventricular late potentials than conservatively treated patients and the absence of ventricular late potentials at 40 Hz filter setting was a good non-invasive predictor that the infarct-related artery was patent.     

Intravenous streptokinase for acute myocardial infarction. Effects on global and regional systolic function

The Western Washington Intravenous Streptokinase Trial randomized 368 patients with acute myocardial infarction to receive either intravenous streptokinase or standard therapy. The ventriculograms and coronary angiograms obtained in 170 patients 10.4 +/- 7.4 days after infarction were analyzed to evaluate the effects of thrombolytic therapy on global and regional systolic function. Streptokinase treatment resulted in a higher patency rate of the infarct-related artery (68.5%) than did standard therapy (44.8%) (p = 0.003). Ejection fraction was higher in streptokinase-treated patients (54% vs. 51%, p = 0.056), and the difference was most marked in patients with anterior myocardial infarction (53% vs. 44%, p = 0.03). Regional wall motion was measured by the centerline method and expressed in mean +/- SD motion in 52 normal subjects. There was a trend toward better function of the infarct zone in streptokinase-treated patients (SD, -2.48 vs. -2.70, p = 0.24). Additionally, streptokinase-treated patients had significantly better wall motion of noninfarct areas (SD, 0.36 vs. -0.08, p = 0.02). Treatment effects on function of noninfarct regions were most apparent in the subset of patients with multivessel disease. Thus, intravenous streptokinase preserves left ventricular function in patients with acute myocardial infarction. This benefit includes favorable effects on the function of regions remote from the site of infarction.     

Intravenous streptokinase treatment and serum C-reactive protein in patients with acute myocardial infarction

Serum concentrations of C-reactive protein were studied in 23 patients with acute myocardial infarction. In 14 patients who did not receive thrombolytic treatment there was a linear relation between infarct size (determined by serial creatine kinase-MB determinations and thallium-201 isotope emission tomography) and the C-reactive protein response. The correlation coefficient between the concentration-time integrals of creatine kinase-MB and C-reactive protein was 0.96. The correlation coefficient between the creatine kinase-MB concentration-time integral and the peak serum value of C-reactive protein was 0.93. In the nine patients who received intravenous streptokinase treatment there was also a positive correlation between the concentration-time integrals of creatine kinase-MB and C-reactive protein. The relation, however, depended on the success of the treatment. In patients with successful reperfusion the C-reactive protein response was only approximately 20% of that in patients in whom reperfusion failed or who received no thrombolytic treatment and who were matched by infarct size. When thrombolysis was successful the correlation coefficient between the concentration-time integrals of creatine kinase-MB and C-reactive protein was 0.86. Daily measurement of serum C-reactive protein is useful in evaluating infarct size in patients with acute myocardial infarction who do not receive thrombolytic treatment. In patients treated with streptokinase C-reactive protein concentrations may be used to assess the success of thrombolysis.