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PubMed1988

Thrombolysis in Myocardial Infarction (TIMI) Trial--phase I: hemorrhagic manifestations and changes in plasma fibrinogen and the fibrinolytic system in patients treated with recombinant tissue plasminogen activator and streptokinase.

Two hundred ninety patients with acute myocardial infarction were treated according to random assignment with an intravenous infusion of either 80 mg of recombinant tissue plasminogen activator (rt-PA) over 3 h or 1.5 million units of streptokinase over 1 h. Patients received an intravenous bolus of heparin (5,000 U [USP]) before pretreatment coronary angiography and a continuous infusion (1,000 U/h) starting 3 h later. The frequency of major and minor hemorrhagic events (33% rt-PA, 31% streptokinase) and associated transfusions (22% rt-PA, 20% streptokinase) were comparable in both groups. More than 70% of bleeding episodes in each group occurred at catheterization or vascular puncture sites. Precipitable fibrinogen levels, measured in plasma samples collected in the presence of a protease inhibitor (aprotinin), declined in rt-PA and streptokinase groups by averages of 26 and 57% at 3 h and by 33 and 58% at 5 h, respectively (rt-PA versus streptokinase, p less than 0.001). At 5 h the plasma plasminogen declined by 57% (rt-PA) and 82% (streptokinase) (p less than 0.001); plasma fibrin(ogen) degradation products were higher in streptokinase-treated patients (244 +/- 12 micrograms/ml, mean +/- SE) than in rt-PA-treated patients (97 +/- 9 micrograms/ml, p less than 0.001). At 27 h, plasma fibrinogen and plasminogen levels were lower and fibrin(ogen) degradation products higher than pretreatment levels in both groups. The frequency of hemorrhagic events was higher in patients with greater changes in plasma factors at 5 h; within treatment groups the levels of fibrin(ogen) degradation products correlated with bleeding complications (p less than 0.005). Thus, in the doses administered, rt-PA induces systemic fibrinogenolysis that is substantially less intense than that induced by streptokinase. The high frequency of bleeding encountered is related to the protocol used, including vigorous anticoagulation, arterial punctures and thrombolytic therapy. These findings emphasize the need for avoidance of invasive procedures and for meticulous care in the selection and management of patients subjected to thrombolytic therapy.

Clinical Trials as Topic↗

PubMed1989

Plasminogen Activator Italian Multicenter Study (PAIMS): comparison of intravenous recombinant single-chain human tissue-type plasminogen activator (rt-PA) with intravenous streptokinase in acute myocardial infarction.

A single chain preparation of recombinant tissue-type plasminogen activator (rt-PA) was compared with intravenous streptokinase to determine coronary thrombolytic efficacy in patients with acute myocardial infarction less than 3 h old. Eighty-six patients were randomly selected to receive the intravenous cumulative dose of 100 mg rt-PA and 85 patients to receive 1.5 million units streptokinase. At 240 min after initiation of the thrombolytic therapy noninvasive signs of sustained reperfusion occurred in 79% of patients in both groups (p = NS). Patency of the infarct-related vessel at follow-up angiography was observed in 81% of patients in the rt-PA group and 74% of patients in the streptokinase group (p = NS). At hospital discharge, compared with admission, echocardiographically determined left ventricular ejection fraction increased from 52 +/- 11% to 56 +/- 10% (p less than 0.01) in the rt-PA group; changes in the streptokinase group (50 +/- 9% to 51 +/- 11%) were not significant. A nadir value of less than 1 g/liter fibrinogen plasma level occurred in 6 patients (7%) receiving rt-PA versus 74 patients (87%) receiving streptokinase (p less than 0.0001). Plasma levels of fibrin(ogen) degradation products were more than doubled in the streptokinase group (p less than 0.01). One patient in the streptokinase group developed a fatal intracranial hemorrhage; five others showed a decline in hemoglobin greater than or equal to 5 g/dl. Other clinical events in the streptokinase-treated group included allergic reactions (four patients) and intrahospital reinfarction (two patients). None of these events occurred in the rt-PA group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

Reduction in incidence of inducible ventricular tachycardia after myocardial infarction by treatment with streptokinase during infarct evolution.

The aim of this study was to determine whether intravenous streptokinase administered with or without oral aspirin to patients with evolving myocardial infarction reduces the inducibility of ventricular tachycardia at electrophysiologic study and thus the risk of sudden death in infarct survivors. Of 159 patients randomized at Westmead Hospital to the multicenter Second International Study of Infarct Survival (ISIS-2) after streptokinase and aspirin in acute myocardial infarction, 87 underwent electrophysiologic testing 6 to 28 days after infarction to determine their risk of subsequent ventricular arrhythmias (streptokinase 20 patients; aspirin 25 patients; streptokinase and aspirin 21 patients; both placebos 21 patients). Patients who underwent electrophysiologic testing had similar clinical characteristics to those of patients who did not. The stimulation protocol comprised up to and including four extrastimuli applied to the right ventricular apex at twice diastolic threshold. An abnormal result was defined as ventricular tachycardia with a cycle length greater than or equal to 230 ms lasting greater than or equal to 10 s. Ventricular tachycardia was inducible at electrophysiologic study in 8 patients who received placebo streptokinase, but in no patient who received active streptokinase (8 of 46 versus 0 of 41; p = 0.005, Fischer's exact test). Ventricular tachycardia was inducible in 4 patients who received aspirin therapy and 4 who did not (4 of 41 versus 4 of 46; p = NS). During a mean follow-up period of 39 +/- 9 months, there were no spontaneous episodes of ventricular tachycardia, ventricular fibrillation or witnessed sudden death in the streptokinase-treated group compared with three such events in the placebo-treated group (p = 0.13). When compared with placebo therapy, intravenous streptokinase substantially reduced the incidence of inducible ventricular tachycardia in infarct survivors. No similar benefit was attributable to aspirin therapy.

Aspirin↗

PubMed1992

Long-term survival in 618 patients from the Western Washington Streptokinase in Myocardial Infarction trials.

OBJECTIVES: The aim of this study was to determine whether streptokinase treatment improves long-term survival in patients with acute myocardial infarction. BACKGROUND: Thrombolytic treatment for acute myocardial infarction reduces early mortality and improves the 1-year survival rate, but the long-term (3 to 8 years) survival benefits of treatment and the relation between survival and baseline clinical characteristics, infarct size and ventricular function have not been established. METHODS: We assessed survival status at a minimum of 3 and a mean of 4.9 +/- 2.3 years in 618 patients randomized between 1981 and 1986 to receive conventional treatment (n = 293) or thrombolysis with streptokinase (n = 325) in the Western Washington Intracoronary (n = 250) and Intravenous (n = 368) Streptokinase in Myocardial Infarction trials. The relation between long-term survival and thrombolytic treatment, admission baseline clinical characteristics and late radionuclide tomographic thallium-201 infarct size and ejection fraction was assessed in a subset of patients. RESULTS: Survival at 6 weeks was 94% in patients who received streptokinase versus 88% in the control group (p = 0.01). However, survival at 3 years was 84% in the streptokinase group and 82% in the control group and for the total period of follow-up, there was no significant survival benefit (p = 0.16). Analysis by infarct location showed a higher survival rate at 3 years for patients treated with anterior infarction (76% vs. 67% for the control group), but no overall survival benefit (p = 0.14). Survival at 3 years for patients with an inferior infarction was 89% in the streptokinase group and 91% in the control group (p = 0.62). By stepwise Cox regression analysis, admission clinical variables associated with decreased long-term survival were anterior infarction, advanced age, history of prior infarction and the presence of pulmonary edema or hypotension. Although streptokinase therapy was associated with improved survival, it was not an independent determinant of survival (p = 0.069). Ejection fraction and thallium-201 infarct size measured approximately 8 weeks after enrollment had a strong association with long-term survival. Univariate analysis in a subgroup of 289 patients with complete data selected infarct size, ejection fraction, age and history of prior infarction as predictors of survival. In the multivariate model, only ejection fraction (p < 0.0001), age (p = 0.008) and prior myocardial infarction (p = 0.02) remained strong predictors. CONCLUSIONS: In these early trials of thrombolytic therapy for acute myocardial infarction, streptokinase improved early survival, but there was little long-term survival benefit. This failure to show an improvement in the 3- to 8-year survival rate may also reflect the need to study a larger group of patients or to initiate treatment earlier after symptom onset.

Aged↗

PubMed1994

Immediate coronary angioplasty versus intravenous streptokinase in acute myocardial infarction: left ventricular ejection fraction, hospital mortality and reinfarction.

OBJECTIVES: The purpose of the present study was to compare intravenous streptokinase therapy with immediate coronary angioplasty without antecedent thrombolytic therapy with regard to left ventricular function and hospital mortality and reinfarction. BACKGROUND: Despite the widespread use of intravenous thrombolytic therapy and immediate percutaneous transluminal coronary angioplasty, these two strategies to treat patients with an acute myocardial infarction have only recently been compared in randomized trials. Coronary angioplasty has been shown to result in a higher patency rate of the infarct-related coronary artery, with a less severe residual stenotic lesion, compared with streptokinase therapy, but whether this more favorable coronary anatomy results in clinical benefit remains to be established. METHODS: We studied 301 patients with acute myocardial infarction randomly assigned to undergo immediate coronary angioplasty without antecedent thrombolytic therapy or to receive intravenous streptokinase therapy. Before discharge left ventricular ejection fraction was measured by radionuclide scanning. RESULTS: The in-hospital mortality rate in the streptokinase group was 7% (11 of 149 patients) compared with 2% (3 of 152 patients) in the angioplasty group (p = 0.024). In the streptokinase group recurrent myocardial infarction occurred in 15 patients (10%) versus in 2 (1%) in the angioplasty group (p < 0.001). Either death or nonfatal reinfarction occurred in 23 patients (15%) in the streptokinase group and in 5 patients (3%) in the angioplasty group (p = 0.001). Left ventricular ejection fraction was 44 +/- 11% (mean +/- SD) in the streptokinase group versus 50 +/- 11% in the angioplasty group (p < 0.001). CONCLUSIONS: These findings indicate that immediate coronary angioplasty without antecedent thrombolytic therapy results in better left ventricular function and lower risk of death and recurrent myocardial infarction than treatment with intravenous streptokinase.

Aged↗

PubMed1985

Percutaneous transluminal coronary angioplasty, alone or in combination with streptokinase therapy, during acute myocardial infarction.

The treatment strategy in 66 consecutive patients who underwent invasive therapy for acute myocardial infarction was analyzed, and specific attention was focused on the role of percutaneous transluminal coronary angioplasty. The following four treatment regimens were used: angioplasty alone (11 patients), angioplasty followed immediately by administration of streptokinase (15), streptokinase therapy alone (11), and streptokinase therapy followed by angioplasty (29). Reperfusion was achieved in 91%, 80%, 82%, and 72% of these subgroups, respectively. Angioplasty was particularly helpful in patients with severe residual stenoses after intracoronary administration of streptokinase and in patients in whom streptokinase therapy failed to reopen the occluded artery. Angioplasty further reduced the residual stenosis in 11 of 15 patients (73%) with successful thrombolysis, and it restored blood flow in 10 of 14 patients (71%) in whom thrombolysis had failed to do so. The incidence of reinfarction after therapy was similar in all four treatment groups. Patients in whom angioplasty was used either alone or in combination with streptokinase therapy had a significantly decreased incidence of subsequent revascularization (less than 30% compared with 82%). Angioplasty is of considerable value in patients undergoing invasive therapy for acute infarction. In some patients, it may be used as the only treatment; in others, it may be used to treat severe residual stenosis after initial streptokinase therapy. Finally, angioplasty achieves reperfusion in most patients in whom streptokinase therapy has failed.

Adult↗

PubMed1987

Comparison of cost effectiveness of streptokinase and urokinase in the treatment of deep vein thrombosis.

This study examines the comparative efficacy, safety, and cost associated with treatment of deep vein thrombosis with streptokinase or urokinase. Sixty patients were analyzed retrospectively, 30 treated with streptokinase and 30 treated with urokinase. Statistically significant greater fibrinogenolysis was noted when streptokinase was used to treat patients with deep venous thrombosis (p = 0.01). The mean decrease in fibrinogen from preinfusion value was 83% in the streptokinase treated group and 61% in the urokinase treated group. Five of 30 (17%) of the streptokinase treated patients experienced major complications. No major complications were seen in the urokinase treated group (p = 0.019). Cost analysis demonstrates that therapy with urokinase was $11.40 per patient more than streptokinase. If complications are not included in the cost analysis, then urokinase becomes only $650 per patient more expensive than streptokinase therapy. These data support that deep vein thrombosis treatment with urokinase is effective, safer and more cost efficient when compared to streptokinase.

Adolescent↗

PubMed1983

A randomized trial of intracoronary streptokinase in the treatment of acute myocardial infarction.

Fifty patients with acute myocardial infarction were randomly assigned to receive either intracoronary streptokinase or standard (control) therapy within about three hours after the onset of pain. Coronary perfusion was reestablished in 19 of 24 patients receiving streptokinase. Streptokinase alleviated pain (as indicated by differences in subsequent morphine use). The Killip class was significantly improved after therapy with streptokinase, as were changes in radionuclide ejection fraction between Days 1 and 10 in surviving patients (+3.9 vs. -3.0 per cent, P less than 0.01). The echocardiographic wall-motion index also showed greater improvement after streptokinase treatment (P less than 0.01). Streptokinase therapy was associated with rapid evolution of electrocardiographic changes, which were essentially complete within three hours after therapy, but loss of R waves, ST elevation, and development of Q waves in the convalescent period were greater in the control group (P less than 0.01). The time required to reach peak plasma enzyme concentrations was significantly shorter after streptokinase. The incidence of early and late ventricular arrhythmias was not affected by treatment. We conclude that intracoronary streptokinase appears to have a beneficial effect on the early course of acute myocardial infarction.

Adult↗

PubMed1993

A comparison of immediate coronary angioplasty with intravenous streptokinase in acute myocardial infarction.

BACKGROUND: Despite the widespread use of intravenous thrombolytic therapy and of immediate percutaneous transluminal coronary angioplasty for the treatment of acute myocardial infarction, randomized comparisons of the two approaches to reperfusion are lacking. We report the results of a prospective, randomized trial comparing immediate coronary angioplasty (without previous thrombolytic therapy) with intravenous streptokinase treatment. METHODS: A total of 142 patients with acute myocardial infarction were randomly assigned to receive one of the two treatments. The left ventricular ejection fraction was measured by radionuclide scanning before hospital discharge. Quantitative coronary angiography was performed to assess the degree of residual stenosis in the infarct-related arteries. RESULTS: A total of 72 patients were assigned to receive streptokinase and 70 patients to undergo immediate angioplasty. Angioplasty was technically successful in 64 of the 65 patients who underwent the procedure. Infarction recurred in nine patients assigned to receive streptokinase, but in none of those assigned to receive angioplasty (P = 0.003). Fourteen patients in the streptokinase group had unstable angina after their infarction, but only four in the angioplasty group (P = 0.02). The mean (+/- SD) left ventricular ejection fraction as measured before discharge was 45 +/- 12 percent in the streptokinase group and 51 +/- 11 percent in the angioplasty group (P = 0.004). The infarct-related artery was patent in 68 percent of the patients in the streptokinase group and 91 percent of those in the angioplasty group (P = 0.001). Quantitative coronary angiography revealed stenosis of 36 +/- 20 percent of the luminal diameter in the angioplasty group, as compared with 76 +/- 19 percent in the streptokinase group (P < 0.001). CONCLUSIONS: Immediate angioplasty after acute myocardial infarction was associated with a higher rate of patency of the infarct-related artery, a less severe residual stenotic lesion, better left ventricular function, and less recurrent myocardial ischemia and infarction than was intravenous streptokinase.

Angioplasty, Balloon, Coronary↗

PubMed2005

U.K. Controlled trial of intrapleural streptokinase for pleural infection.

BACKGROUND: Intrapleural fibrinolytic agents are used in the drainage of infected pleural-fluid collections. This use is based on small trials that did not have the statistical power to evaluate accurately important clinical outcomes, including safety. We conducted a trial to clarify the therapeutic role of intrapleural streptokinase. METHODS: In this double-blind trial, 454 patients with pleural infection (defined by the presence of purulent pleural fluid or pleural fluid with a pH below 7.2 with signs of infection or by proven bacterial invasion of the pleural space) were randomly assigned to receive either intrapleural streptokinase (250,000 IU twice daily for three days) or placebo. Patients received antibiotics and underwent chest-tube drainage, surgery, and other treatment as part of routine care. The number of patients in the two groups who had died or needed surgical drainage at three months was compared (the primary end point); secondary end points were the rates of death and of surgery (analyzed separately), the radiographic outcome, and the length of the hospital stay. RESULTS: The groups were well matched at baseline. Among the 427 patients who received streptokinase or placebo, there was no significant difference between the groups in the proportion of patients who died or needed surgery (with streptokinase: 64 of 206 patients [31 percent]; with placebo: 60 of 221 [27 percent]; relative risk, 1.14 [95 percent confidence interval, 0.85 to 1.54; P=0.43), a result that excluded a clinically significant benefit of streptokinase. There was no benefit to streptokinase in terms of mortality, rate of surgery, radiographic outcomes, or length of the hospital stay. Serious adverse events (chest pain, fever, or allergy) were more common with streptokinase (7 percent, vs. 3 percent with placebo; relative risk, 2.49 [95 percent confidence interval, 0.98 to 6.36]; P=0.08). CONCLUSIONS: The intrapleural administration of streptokinase does not improve mortality, the rate of surgery, or the length of the hospital stay among patients with pleural infection.

Anti-Bacterial Agents↗

PubMed2001

The mechanism of a bacterial plasminogen activator intermediate between streptokinase and staphylokinase.

The therapeutic properties of plasminogen activators are dictated by their mechanism of action. Unlike staphylokinase, a single domain protein, streptokinase, a 3-domain (alpha, beta, and gamma) molecule, nonproteolytically activates human (h)-plasminogen and protects plasmin from inactivation by alpha(2)-antiplasmin. Because a streptokinase-like mechanism was hypothesized to require the streptokinase gamma-domain, we examined the mechanism of action of a novel two-domain (alpha,beta) Streptococcus uberis plasminogen activator (SUPA). Under conditions that quench trace plasmin, SUPA nonproteolytically generated an active site in bovine (b)-plasminogen. SUPA also competitively inhibited the inactivation of plasmin by alpha(2)-antiplasmin. Still, the lag phase in active site generation and plasminogen activation by SUPA was at least 5-fold longer than that of streptokinase. Recombinant streptokinase gamma-domain bound to the b-plasminogen.SUPA complex and significantly reduced these lag phases. The SUPA-b.plasmin complex activated b-plasminogen with kinetic parameters comparable to those of streptokinase for h-plasminogen. The SUPA-b.plasmin complex also activated h-plasminogen but with a lower k(cat) (25-fold) and k(cat)/K(m) (7.9-fold) than SK. We conclude that a gamma-domain is not required for a streptokinase-like activation of b-plasminogen. However, the streptokinase gamma-domain enhances the rates of active site formation in b-plasminogen and this enhancing effect may be required for efficient activation of plasminogen from other species.

Amino Acid Sequence↗

PubMed1998

Meta-analysis of streptokinase and heparin in deep vein thrombosis.

The efficacy and safety of streptokinase and heparin in deep vein thrombosis (DVT) were compared in a meta-analysis. Randomized trials in which streptokinase (followed by heparin) and heparin alone were compared in treating phlebographically documented acute DVT were identified from MEDLINE and other sources for a meta-analysis. Odds ratios (ORs) and 95% confidence intervals (CIs) based on the logit method were computed for each study. A fixed-effect model was used to combine the study results, enabling differences between streptokinase recipients and recipients of heparin alone to be expressed as summary ORs with 95% CIs. Significantly more streptokinase recipients achieved thrombolysis than recipients of heparin alone (summary OR, 6.24; 95% CI, 3.62 to 10.78). One study was identified as an outlier and excluded from the analysis. The meta-analysis then showed that streptokinase recipients were significantly less likely to have postthrombotic changes (summary OR, 0.40; 95% CI, 0.18 to 0.88) and postphlebitic changes (summary OR, 0.32; 95% CI, 0.12 to 0.86) in phlebographic evaluation. The frequency of major bleeding was significantly higher among streptokinase recipients than recipients of heparin alone (summary OR, 3.78; 95% CI, 1.26 to 11.32). A meta-analysis showed that, compared with heparin alone, streptokinase therapy for DVT was associated with significantly more frequent thrombolysis and major bleeding; after exclusion of one outlying study, analysis showed that streptokinase therapy was associated less frequently than heparin alone with postthrombotic changes (assessed by phlebographic evaluation) and postphlebitic syndrome.

Fibrinolytic Agents↗

PubMed1993

Hypersensitivity reactions to streptokinase in patients with high pre-treatment antistreptokinase antibody and neutralisation titres.

After streptokinase or antistreplase administration, raised antibody levels can persist for many years, but it is unclear if these antibodies can cause allergic reactions following streptokinase re-administration for myocardial re-infarction. Pretreatment antistreptokinase antibody (AB) and neutralisation titres (NT) were measured in 189 consecutive patients (57 received streptokinase or anistreplase). Seven patients had previous exposure to streptokinase or anistreplase; they had high mean (SEM) antibody titres of 1:801 (332) and neutralisation titres of 3.3 (1.7) million units. The 182 patients without previous thrombolysis had mean (SD) antibody titres of 1:25 (3) and neutralisation titres of 0.14 (0.08) million units; nine patients (4.95%), however, had raised antibody titres of > or = 1:160 and neutralisation titres of > or = 0.3 million units. Of the 15 patients with antibody titres of > or = 1:160, three received streptokinase or anistreplase. Hypersensitivity reactions occurred in all three patients--neutralisation titres 0.48, 1.5 and 1.1 million units respectively. Two became severely hypotensive with systolic pressures of 70 mmHg; one developed a serum sickness-like reaction. Importantly, none of the 54 patients with antibody titres of < 1:160 who received streptokinase or antistreplase reacted adversely to the thrombolytic agents (chi 2 with Yates's correction = 38.71, P < 0.01). High antibody titres are associated with hypersensitivity reactions to streptokinase. This has important implications in reinfarction thrombolysis. In patients whose antistreptokinase antibody titres are likely to be raised the avoidance of streptokinase-related thrombolytic agents should be considered.

Adult↗

PubMed1993

Evaluation of in vivo immune complex formation and complement activation in patients receiving intravenous streptokinase.

The usefulness of several different methods for detecting immune complex formation and complement activation in the circulation were applied to samples from patients receiving intravenous Streptokinase therapy for myocardial infarction. Streptokinase is a foreign antigen and can cause immune reactions. We collected samples from 13 patients, before Streptokinase administration (baseline), at the end of infusion (1 h), 12 h later and on day 7. We measured IgG containing immune complexes (IgG-IC), free C3d and antibodies to Streptokinase by ELISA, and CR1, C3d and C4d on erythrocytes by flow cytometric assay. Antibodies to Streptokinase are common, as all but two of the patients had measurable antibody levels. During Streptokinase treatment there was a drop in antibody levels, most prominent in those patients who had high baseline levels. At the same time increased levels of free C3d and erythrocyte-bound C3d were observed. After 12 h free C3d was usually back to baseline level, but C3d on erythrocytes was still raised. These data indicate the formation of Streptokinase immune complexes in patients with high Streptokinase antibody levels, and show that these complexes are cleared rapidly from the circulation, leaving more persistent signs of complement activation. We conclude that free C3d is a good indicator of ongoing complement activation, whereas C3d on erythrocytes indicates that complement activation has recently taken place.

Antibodies↗

PubMed1986

Streptokinase alters myocardial creatine kinase depletion after ischaemia and reperfusion in rabbits.

The efficacy of streptokinase as an intracoronary thrombolytic agent is well-recognized. The effect of streptokinase, distinct from its thrombolytic action, on ischaemic myocardium distal to an area of coronary artery occlusion when reperfusion occurs has not been well-defined. In order to do this, myocardial creatine kinase depletion and the histopathology of infarctions produced in rabbits after 1 h of circumflex coronary artery occlusion and mechanical release of the occlusion were assessed. Streptokinase or saline was infused intravenously for 1 h beginning 0.5 h after occlusion. Rabbits were divided into two time intervals: early (less than 10 h) and late (24 h) after release of coronary artery occlusion. When streptokinase was infused in early infarctions, haemorrhage did not correlate with infarction cross-sectional area or myocardial creatine kinase depletion. However, myocardial creatine kinase depletion was 40% less when streptokinase was infused than when saline was infused, suggesting that streptokinase might limit infarct size. In late infarctions, the degree of haemorrhage, infarction cross-sectional area, and myocardial creatine kinase depletion were similar after reperfusion with streptokinase or saline. By 24 h, the beneficial effect of a single dose of streptokinase given early in the course of occlusion-reperfusion myocardial injury was no longer evident in limiting infarct size.

Animals↗

PubMed1990

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.

Arrhythmias, Cardiac↗

PubMed1984

Intracoronary thrombolysis in patients with acute myocardial infarction: comparison of the efficacy of urokinase with streptokinase.

The efficacy of intracoronary urokinase and streptokinase were compared in 80 patients with acute myocardial infarction in a prospective, randomized, double-blind study. Urokinase was infused into the occluded coronary artery at 6000 U/min, and streptokinase was infused at 2000 U/min. Maximal duration of infusion was 2 hr. The frequency of successfully opening the artery was similar for patients receiving urokinase (27 of 45, 60%) and those receiving streptokinase (20 of 35, 57%). Fibrinogen levels after infusion were measured in 63 patients. Nineteen of 29 streptokinase recipients had fibrinogen levels less than 100 mg/dl compared with levels of two of 34 urokinase recipients (p less than .001). Five of 45 (11%) patients receiving urokinase and 10 of 35 receiving streptokinase (29%) had bleeding complications (p less than .05). Major bleeding after early coronary artery bypass surgery was more frequent in the streptokinase group (four of five compared with a similar group of patients receiving urokinase (none of five). This study demonstrates that while urokinase and streptokinase have equal intracoronary thrombolytic efficacy, patients receiving urokinase have less systemic fibrinolysis and less perioperative bleeding with early surgery than do patients receiving streptokinase.

Adult↗

PubMed1974

Resolution of experimental pulmonary emboli with heparin and streptokinase in different dosage regimens.

Thrombolytic agents may be useful in acute pulmonary embolism, but their optimal dosage remains uncertain. We have examined the relative efficacy of heparin and different doses of streptokinase, either alone or in combination, in acute experimental pulmonary embolism. A standardized massive embolus of autologous blood clot incorporating canine [(125)I]-fibrinogen was given to 40 dogs; the degree of resolution after 24 h was quantitated by measuring the radioactivity in the lungs and was compared with detailed postmortem observations. The amount of residual embolus was 49% in control animals, 28% after heparin (200 U/kg loading dose and 800 U/kg/24 h maintenance dose), and 6% after high dose streptokinase (250,000 U loading dose and 100,000 U/h maintenance dose); it was 31% after low dose streptokinase (25,000 U loading dose and 10,000 U/h maintenance dose), 7% after low dose streptokinase with heparin, 14% after very low dose streptokinase (5,000 U/h without a loading dose) with heparin, and 9% after short course streptokinase (250,000 U loading dose and no maintenance dose) with heparin. The combination of heparin and low doses or brief courses of streptokinase appeared to be synergistic and produced as much resolution as did standard high dose streptokinase alone. The enhanced resolution of pulmonary emboli in heparin-treated animals may have been due to the prevention by heparin of further deposition of fibrin on the embolus. It appears that dosage regimens of thrombolytic therapy other than those in current use may be worthy of clinical examination.

Animals↗