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PubMed1994

Inactivation of the streptokinase gene prevents Streptococcus equisimilis H46A from acquiring cell-associated plasmin activity in the presence of plasminogen.

The streptokinase gene of Streptococcus equisimilis H46 was inactivated by plasmid insertion mutagenesis to study the relationship between elaboration of streptokinase and acquisition of cell-associated plasmin activity after incubation of wild-type and mutant cells in media containing plasminogen or plasmin. The results showed that H46A binds both the zymogen and active enzyme, generates surface-associated plasmin activity in the presence of plasminogen when producing streptokinase, and expresses its plasmin(ogen) receptor(s) independently of a functional streptokinase gene. At least part of the plasmin(ogen) binding capacity may be due to the glyceraldehyde-3-phosphate dehydrogenase type of receptor molecule, as judged by the detection of the corresponding gene.

Base Sequence↗

PubMed1996

RcsC-mediated induction of colanic acid by secretion of streptokinase in Escherichia coli K-12.

The introduction of a plasmid containing skc (streptokinase-coding gene) fused with ompA signal sequence into Escherichia coli K-12 strains, rendered the bacteria mucoid. Measurement of the synthesis of beta-galactosidase from a cps-lacZ fusion (lacZ fusion to a gene necessary for capsule synthesis) showed that the mucoid phenotype was due to induction of the capsular polysaccharide colanic acid synthesis. The introduction of a plasmid carrying skc fused with malE (gene encoding maltose-binding protein) also induced cps-lacZ expression, but intracellular expression of streptokinase in E. coli did not. The cps expression by secretion of streptokinase was diminished to the basal level in a cps-lacZ strain carrying a rcsC mutation. These results show that the secretion of streptokinase in E. coli induces colanic acid synthesis through the RcsC-dependent pathway.

Bacterial Proteins↗

PubMed1994

Intraventricular streptokinase increases cerebrospinal fluid D dimer in preterm infants with posthaemorrhagic ventricular dilatation.

Failure to lyse multiple small blood clots in the cerebrospinal fluid (CSF) reabsorption pathways may be one of the mechanisms leading to posthaemorrhagic ventricular dilatation (PHVD). It has been suggested that intraventricular administration of streptokinase may resolve PHVD but it is not known whether such treatment produces an increase in fibrin degradation products in the CSF. Ventricular CSF was collected from six infants with PHVD before and during intraventricular treatment with streptokinase 1000 units/h. In all six infants, CSF D dimer increased during streptokinase treatment. Median D dimer before treatment was 1642 micrograms/l and during treatment 5440 micrograms/l (p < 0.05). Undetectable D dimer levels in plasma during streptokinase treatment ruled out the possibility that D dimer had merely diffused into the CSF. This augmentation of local fibrinolysis may have therapeutic potential. There was no evidence of systemic fibrinolysis.

Cerebral Hemorrhage↗

PubMed2004

Randomized controlled trial of intrapleural streptokinase in empyema thoracis in children.

AIM: To compare intrapleural streptokinase and placebo in paediatric empyema. METHODS: Children with empyema greater than stage 5 received intrapleural streptokinase (n = 19) or normal saline (n = 21) along with intercostal drainage. Clinical and serial sonographic outcomes were compared. RESULTS: Although there was no difference in clinical and sonographic outcome, none of the children with stage 7 empyema (multi-loculated empyema) who received streptokinase developed pleural thickening 30 d later. CONCLUSION: There is no short-term clinical benefit of intrapleural streptokinase in paediatric empyema; this therapy may be reserved for those with stage 7 empyema to prevent pleural thickening in the long term.

Anti-Bacterial Agents↗

PubMed1974

Comparison by controlled clinical trial of streptokinase and heparin in treatment of life-threatening pulmonay embolism.

Treatment with heparin or streptokinase was allocated randomly to 30 patients with life-threatening pulmonary embolism verified by angiography. Treatment was given for 72 hours and pulmonary angiography was repeated. There was significantly greater (P < 0.001) evidence of thrombolysis in those patients treated with streptokinase compared with those treated with heparin. The reduction of systolic and mean pulmonary arterial pressures was also significantly greater (P < 0.05 and P < 0.02 respectively) in the streptokinase group.Seven patients failed to complete 72 hours of the trial treatment: five successfully underwent pulmonary embolectomy. Six of these "failures" had initial pulmonary angiographic scores of 24 or more and systemic systolic blood pressure recordings of 100 mm Hg or less. Patients with these features should probably be considered for pulmonary embolectomy as the initial treatment.A febrile reaction commonly occurred in the streptokinase group; otherwise side effects were no more common than in the heparin group.

Angiography↗

PubMed1986

High dose intravenous streptokinase in acute myocardial infarction--short and long term prognosis.

Streptokinase (1 million international units) was given intravenously over 30 or 60 minutes to 50 patients four hours or less after the onset of acute myocardial infarction. All were aged less than or equal to 70 years and had 4 mm or greater ST segment elevation in anterior or inferior leads. Rapid (mean 95 min) ST segment resolution, which was taken to indicate reperfusion of the myocardium, occurred in 36 (72%) patients. In these 36 the average time from onset of symptoms to peak creatine kinase, creatine kinase MB, and myoglobin was 9.45 hours, whereas it was 17 hours in the 14 patients in whom indirect criteria did not indicate reperfusion. Reperfusion arrhythmias were invariably present and ventricular tachycardia developed in five patients and ventricular fibrillation in two. The infarct related artery was seen to be open in 28 (70%) of the 40 patients who had delayed coronary arteriography. The frequency of patency in the infarct related artery was no different in patients given streptokinase less than 2 hours or between 2-4 hours from onset of symptoms nor did it differ when streptokinase was infused over 30 or 60 minutes. Mean left ventricular ejection fraction was 57% in those with a patient infarct related artery and 48% in those with an occluded vessel. Eight patients subsequently underwent elective percutaneous transluminal coronary angioplasty after successful thrombolysis and six had coronary artery bypass grafting. There were nine in-hospital reocclusions of the infarct related coronary arteries. Two bleeding episodes occurred; one required transfusion. Five of the 50 patients died in hospital. All of them had had an anterior myocardial infarction; four had bifascicular block and one had right bundle branch block. During follow up, four patients died, two suddenly and two from reinfarction. During follow up (mean 15 months) the frequency of reinfarction, dyspnoea, and angina was low and there was no difference in the proportions of patients returning to work between those with an open infarct related artery and those with a closed infarct related artery. Intravenous administration of high dose streptokinase to selected patients during the acute phase of myocardial infarction is a safe, effective, and practical method of thrombolysis. It must, however, be followed by coronary arteriography to select those patients in whom percutaneous transluminal coronary angioplasty or coronary artery bypass grafting will be helpful.

Adult↗

PubMed1990

Streptokinase treatment for femoral artery thrombosis after arterial cardiac catheterisation in infants and children.

Data on 205 children who underwent retrograde arterial catheterisation were studied to assess the frequency of femoral artery thrombosis and the safety and efficacy of systemic streptokinase treatment for this complication. In 29 (14%) a transarterial balloon dilatation was performed. In 15 (7.3%) patients impaired arterial perfusion due to vascular spasm with or without thrombus formation was seen in the cannulated leg after catheterisation. Despite heparinisation, signs of impaired arterial circulation persisted in nine patients (4.4% of the total). In these patients femoral artery thrombosis was strongly suspected. Six (53%) of these had undergone a balloon dilatation. Therefore in this study the risk of femoral artery thrombosis developing was 12 times greater after transarterial balloon dilatation than after arterial catheterisation without dilatation (20.6% v 1.7%). Systemic infusion of streptokinase was started in all patients with femoral artery thrombosis. Arterial perfusion became normal in all patients, though in one this was delayed. Haematological monitoring showed lengthening of the thrombin time and a decrease of the fibrinogen concentration during streptokinase treatment. There were no serious complications. Systemic infusion of streptokinase is a safe and useful treatment in children with persistent femoral artery thrombosis after arterial cardiac catheterisation.

Cardiac Catheterization↗

PubMed1990

Enhanced thrombolytic efficacy and reduction of infarct size by simultaneous infusion of streptokinase and heparin.

Because paradoxical increase in thrombin activity was reported after the administration of streptokinase in patients with acute myocardial infarction the velocity of reperfusion and degree of myocardial damage were studied when heparin was infused during rather than after streptokinase infusion. Thirty seven consecutive patients with acute myocardial infarction were randomised to receive intravenous heparin during (group 1, n = 18) or after (group 2, n = 19) streptokinase (1.5 megaunits over 60 minutes). Markers of reperfusion were monitored every 15 minutes for 3 hours. The serum concentration of creatine kinase was measured every 2 hours. The two groups were similar in terms of age and sex distribution, infarct site, time to treatment, and baseline myocardial ischaemia. Patients in group 1 had a significantly shorter mean (SD) reperfusion time (57 (35) minutes v 101 (47)). From 60 to 120 minutes after randomisation there were significant differences in ST segment elevation between the groups. Serum creatine kinase MB peaked earlier (8 (2) hours) in group 1 than in group 2 (10 (4) hours). The peak concentration was significantly lower in group 1 (87 (47) mU/ml) than in group 2 (134 (96) mU/ml) and infarcts were smaller (25.2 (9.8) gram equivalents/m2) in group 1 than in group 2 (35.1 (10.2) gram equivalents/m2). Simultaneous infusion of heparin and streptokinase speeds up the appearance of signs of reperfusion and reduces infarct size.

Aged↗

PubMed1991

Holter monitoring of ventricular arrhythmias in a randomised, controlled study of intravenous streptokinase in acute myocardial infarction.

The occurrence of ventricular arrhythmias attributed to streptokinase treatment in acute myocardial infarction is not well defined. Holter monitoring was performed for 24 hours in 81 patients with suspected acute myocardial infarction randomised in a ratio of 2:1 to intravenous streptokinase 1.5 x 10(6) IU (n = 55) or placebo infusion (n = 26) 6.7 hours (mean) after the onset of symptoms. No episodes of ventricular fibrillation were recorded. For the whole 24 hour period and during the first three hours after the start of treatment the incidence and frequency of ventricular arrhythmias were similar in the patients randomised to streptokinase and to placebo. But when the results in patients randomised "early" after the onset of symptoms of suspected acute myocardial infarction were analysed separately the frequency of abnormal complexes, pairs, runs, and repetitive arrhythmias seemed to be higher in patients allocated to streptokinase. This may reflect arrhythmias associated with reperfusion.

Arrhythmias, Cardiac↗

PubMed1996

Time course of platelet alpha granule release in acute myocardial infarction treated with streptokinase.

OBJECTIVE: To determine the time course of platelet alpha granule release in patients with acute myocardial infarction treated with streptokinase. DESIGN: A prospective study. SETTING: Coronary care unit. PATIENTS: Nine with myocardial infarction treated with both streptokinase and aspirin, and nine with acute chest pain but without myocardial infarction, who were treated with aspirin only. METHODS: All patients received 250 mg aspirin on admission and 150 mg once daily thereafter. All patients who fulfilled the indications for streptokinase received 1.5 megaunits, in a single infusion. After the initial medication, serial measurements of plasma beta thromboglobulin and plasma platelet factor 4 were performed at fixed intervals after the onset of chest pain. The primary endpoint sought was the peak value of beta thromboglobulin and platelet factor 4 in each individual. RESULTS: The median peak plasma beta thromboglobulin in the infarction group was substantially higher than in those without infarction, at 37 (range 12 to 210) v 15 (9 to 36) mg/litre, P < 0.01. The corresponding values for plasma platelet factor 4 were 4.6 (2.4 to 60.0) v 2.2 (< 2 to 8.5) mg/litre, P < 0.01. Increased values were seen only within the first 12 h after onset of chest pain, and after 12 h there was no difference between the patients with myocardial infarction and those without. Aspirin treatment did not abolish alpha granule release. CONCLUSIONS: In patients with acute myocardial infarction treated with streptokinase the content of the alpha granules is released within the first 12 h after the onset of chest pain. Aspirin apparently does not abolish this release.

Adult↗

PubMed1983

Streptokinase and transluminal angioplasty in the treatment of acutely thrombosed hemodialysis access fistulas.

Streptokinase was selectively infused into nine thrombosed hemodialysis access fistulas in eight patients. Lysis occurred in all but one case. Of the eight infusions producing lysis, seven resulted in some clinical benefit. Three grafts functioned adequately for 2 to 6 months after streptokinase infusion alone. A fourth patient had good function for over 11 months after streptokinase treatment and transluminal angioplasty. In a fifth patient, graft function was partially restored, but a persistent arterial defect led to elective graft replacement. Moderate fibrinolysis in the sixth case was of no clinical benefit; rethrombosis developed promptly after SK was discontinued because of bleeding from a recent puncture site. In cases 7 and 8, fibrinolysis restored arterial inflow to the graft, but surgery was needed to revise partially obstructed venous outflow. It is concluded that selective streptokinase infusion, with or without transluminal angioplasty and operation, is often effective in the treatment of acutely thrombosed vascular access fistulas.

Adult↗

PubMed1981

Orally and rectally administered streptokinase. Investigation of its absorption and activity.

The absorption and activity of orally and rectally administered streptokinase was investigated. No difference was found between the levels of plasminogen activators and antistreptokinase antibodies before and after oral or rectal administration of streptokinase-streptodornase (Varidase), nor was there any difference in the hematoma resorption times between patients treated with oral streptokinase and a control group. We found no evidence of streptokinase absorption or increased fibrinolytic activity in plasma after oral or rectal administration in our patients.

Administration, Oral↗

PubMed1988

Early prediction of left ventricular function in streptokinase-treated acute myocardial infarction.

We administered 750,000 units of intravenous streptokinase to 121 consecutive patients experiencing their first acute myocardial infarction within 4 h of pain onset. The following information was collected: hours between pain onset and streptokinase administration (TS), hours of pain after streptokinase administration (DP), initial and peak creatine phosphokinase levels (ICK and PCK), time to peak creatine phosphokinase, time to electrocardiographic ST segment resolution. Six days after the infarction, catheterization was performed to calculate ejection fraction, infarct-related regional ejection fraction, and dysfunction index. Data was analyzed using stepwise multiple regression. In patients experiencing anterior infarctions, the following equation was obtained predicting the ejection fraction (EF) with a correlation coefficient of 0.86: EF = 69 - 0.0050(PCK) - 3.7(TS) - 1.8(DP). In anterior infarctions the infarct-related ejection fraction and dysfunction index were similarly predictable. We were slightly less accurate in forecasting the outcome of inferior infarctions. The outcome of intravenous streptokinase therapy can be predicted early in the evolution of acute myocardial infarction using routinely available information.

Adult↗

PubMed1999

Platelet function during and after thrombolytic therapy for acute myocardial infarction with reteplase, alteplase, or streptokinase.

BACKGROUND: Changes in platelet aggregation (PA) and platelet surface receptor expression induced by thrombolytic therapy for acute myocardial infarction may influence the rate of initial reperfusion and early reocclusion. METHODS AND RESULTS: In the RAPID-1 (Reteplase Angiographic Phase II International Dose-finding study), RAPID-2 (Reteplase vs Alteplase Patency Investigation During myocardial infarction), INJECT (INternational Joint Efficacy Comparison of Thrombolytics), and GUSTO-3 (Global Use of Strategies To Open occluded coronary arteries) trials, 126 patients were enrolled in a single center. Patients were treated with either conventional alteplase (100 mg/180 min; n=15), accelerated alteplase (100 mg/90 min; n=21), reteplase 10+10-U double bolus (n=50), reteplase 10+5-U double bolus (n=15), reteplase 15-U single bolus (n=15), or streptokinase (1.5 MU/60 min; n=10). PA (after stimulation with ADP), P-selectin expression and fibrinogen binding to glycoprotein (GP) IIb/IIIa (determined by flow cytometry with and without stimulation with ADP), and levels of soluble P-selectin, prothrombin fragments F1 and F2, thrombin-antithrombin complexes (TAT), and antithrombin III (ATIII) were determined. PA decreased significantly at 1 and 2 hours in patients treated by 10+10-U reteplase or by streptokinase. Fibrinogen binding to platelet GP IIb/IIIa followed a similar pattern. Significant thrombin generation and significantly elevated thrombin levels during thrombolysis were reflected by increased F1 and F2 fragments and TAT levels in all treatment groups. ATIII levels decreased significantly during thrombolytic therapy. CONCLUSIONS: A decrease in PA in patients treated by reteplase or streptokinase compared with alteplase could be observed in the early phase. Double bolus (10+10 U) reteplase and streptokinase resulted in lower PA at 1 and 2 hours than therapy with accelerated alteplase. Total fibrinogen and fibrinogen binding to GP IIb/IIIa tended to be lower during the first 2 hours after reteplase than after accelerated alteplase.

Double-Blind Method↗

PubMed1983

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.

Adult↗

PubMed1983

Fibrinolytic effects of intracoronary streptokinase administration in patients with acute myocardial infarction and coronary insufficiency.

Serial coagulation studies were obtained in 25 patients treated with intracoronary streptokinase infusion for myocardial infarction (23 patients) or coronary insufficiency (two patients) to determine the frequency of systemic fibrinolytic activity. Clotting studies were obtained before and after infusion and at 4-hour intervals until normalization. Intracoronary thrombolysis was successful in 20 of 23 patients (87%) with myocardial infarction. Streptokinase dosage in this study was 201,000 +/- 74,000 IU (+/- SD). Systemic fibrinolytic activity, defined as greater than 70% reduction of fibrinogen using a functional assay (Claus method), occurred in 22 of 25 patients (88%) and was present at a mean streptokinase dosage of 119,000 +/- 52,000 IU. Fibrinogen in the total population decreased from 342 +/- 80 to 87 +/- 94 mg% (p less than 0.0001). In patients with systemic effect, the mean fibrinogen level after infusion was 17% of baseline, increased to 43% at 24 hours, and returned to normal at 30 hours. Plasminogen decreased to 7% of baseline activity after infusion (p less than 0.0001), was 44% of baseline at 24 hours, and returned to normal at 48 hours. Intraprocedural sampling during infusion showed reduction of fibrinogen by 25% after 30,000 IU (p less than 0.0005) and by 71% at 120,000 IU (p less than 0.0001); plasminogen decreased by 50% after 30,000 IU (p less than 0.0001) and by 84% at 120,000 IU (p less than 0.0001). Prothrombin time increased from 11.5 +/- 0.8 seconds to 22.0 +/- 7.8 seconds after infusion (p less than 0.0001) and returned to normal at a mean of 18 +/- 11 hours after infusion. Partial thromboplastin time was markedly prolonged (greater than 100 seconds) after infusion, returned to less than or equal to 2 times control at 5 +/- 2 hours, and returned to normal at 9 +/- 4 hours after infusion. Fibrinogen degradation products were less than 10 micrograms/ml before infusion, increased to greater than 40 micrograms/ml after infusion, and remained greater than 40 micrograms/ml in 40% of patients at 24 hours after infusion. These data indicate that systemic fibrinolytic activity occurs in a high percentage of patients with "low-dose" intracoronary streptokinase infusion and that coagulation variables may be altered for 24-48 hours after infusion.

Adult↗

PubMed1983

Effects of spontaneous and streptokinase-induced recanalization on left ventricular function after myocardial infarction.

The effect of recanalization of the "infarct vessel" on left ventricular (LV) function was assessed 6-8 weeks after acute myocardial infarction (MI) in two groups: patients who had streptokinase-induced recanalization during the acute phase and control patients who had spontaneous recanalization. The ejection fraction and severity of LV wall motion abnormalities in 100 patients with recanalization were compared with those in 78 patients with persistent occlusion of the infarct vessel. Among patients with inferior MI, LV function was significantly better in those with spontaneous (n = 41, p less than 0.05) and streptokinase-induced recanalization (n = 15, p less than 0.02) than in those with persistent occlusion of the infarct vessel (n = 40) in the control group. The LV function was equally good in patients with spontaneous and streptokinase-induced recanalization. Among anterior MI patients, LV function was significantly better in those with streptokinase-induced recanalization (n = 10) than in those with spontaneous recanalization (n = 34, p less than 0.01) or persistent occlusion in the control group (n = 28, p less than 0.001). We conclude that recanalization has a beneficial effect on LV function in patients with MI.

Aged↗

PubMed1983

Electrocardiographic changes after streptokinase-induced recanalization in patients with acute left anterior descending artery obstruction.

ECG changes were assessed in 15 patients in whom intracoronary streptokinase recanalized a totally occluded left anterior descending artery during acute myocardial infarction. These results were compared retrospectively with those in 22 comparable conventionally treated patients who underwent catheterization during the acute stage of infarction. Before angiography no significant differences were found in the sum of ST elevation (sigma ST increase V1-V6), the sum of R waves (sigma RV1-V6), or the number of Q waves (nQV1-V6) in leads V1 through V6. sigma ST increase V1-V6 was significantly lower in the streptokinase group than in control patients at all times after angiography. sigma RV1-V6 declined and nQV1-V6 increased in both groups during the first 12 hr, but there was no further change in the control group, whereas in the streptokinase group a significant increase in sigma RV1-V6 and decrease in nQV1-V6 followed. There was a significant correlation between long-term electrocardiographic (sigma RV1-V6; nQV1-V6) and angiographic findings (ejection fraction, akinetic segment length). Thus, the Q wave regression and increase in sigma RV1-V6 after streptokinase suggest, in accordance with angiographic findings, that jeopardized myocardium was salvaged by reperfusion.

Aged↗