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PubMed1991

Non-Q- and Q-wave infarction after thrombolytic therapy with intravenous streptokinase for chest pain and anterior ST-segment elevation.

The clinical features of patients treated with streptokinase for chest pain and anterior ST-segment elevation who subsequently develop non-Q-wave infarction are unknown. Of the 75 consecutive patients who initially presented with chest pain and ST-segment elevation in the anterior leads (V1-V6, I, aVL) and were treated with intravenous streptokinase (time from symptoms to treatment averaged less than 3 hours), 32 (43%) developed a non-Q-wave and 43 (57%) a Q-wave myocardial infarction. Twenty seven of 32 patients (84%) from the non-Q-wave group and 39 of 43 (91%) from the Q-wave group were studied by angiography at 5.16 +/- 2.88 days after the onset of myocardial infarction. Left ventricular end-diastolic pressure was 13 +/- 6 vs 20 +/- 7 mm Hg (p less than 0.001), left ventricular ejection fraction was 60 +/- 8 vs 49 +/- 14% (p less than 0.001) and the infarct vessel patency rate was 85 vs 72% (p = 0.44) in patients with a non-Q versus a Q-wave infarction, respectively. In summary, when patients presenting with chest pain and ST-segment elevation are treated with streptokinase, a significant portion of these symptoms will evolve into a non-Q-wave infarction. Patients with a non-Q-wave infarction will have a better preserved left ventricular function than patients who develop a Q-wave infarction. This suggests the need for equal distribution of such patients in randomized trials of thrombolytic therapy for acute myocardial infarction to avoid misinterpreting data between groups.

Adult↗

PubMed1983

Complex formation of human Val354-plasminogen with streptokinase.

A controlled digestion of native human plasminogen (Glu1-plasminogen) from either carbohydrate variant 1 or 2 with pancreatic elastase yields, among others, an activatable fragment, designated Val354-plasminogen (Pgc). This species represents the smallest human plasminogen fragment (ca., 50,000 Mw) known to bind to Sepharose-lysine. Pgc forms a tight equimolar complex with streptokinase, as determined by sucrose density ultracentrifugation, whether formed from Val354-plasminogen or Val354-plasmin. The Val354-plasmin-streptokinase complex readily activates ovine plasminogen, which is normally insensitive to streptokinase, and this complex is essentially inactive toward casein, similar to the equimolar complexes formed with Lys77-plasmin and the elastase fragment, Val442-plasmin.

Animals↗

PubMed1987

Ancrod enhances the thrombolytic effect of streptokinase and urokinase.

Since thrombi continue to incorporate fibrin during lysis we tested the effect of pretreatment with ancrod, a defibrinating agent from Malaysian pit viper venom, on thrombolysis with urokinase and streptokinase. Thrombi were induced by copper-coils in the carotid arteries of the dogs, weighed after 1 hour and inserted into the femoral arteries of the same animals. They were then exposed for 15 min to iv boluses of streptokinase 10,000 U/kg, urokinase 10,000 U/kg and urokinase 25,000 U/kg with or without pretreatment with ancrod. Ancrod depleted fibrinogen within 5 min and enhanced the lytic effect of streptokinase from 25 +/- 8% to 59 +/- 13% (p less than .05), urokinase 10,000 U/kg from 16 +/- 11% to 66 +/- 18% (p less than .01) and urokinase 25,000 U/kg from 27 +/- 17% to 85 +/- 8% (p less than .001) of the initial thrombus weight. Ancrod itself did not activate plasminogen to plasmin. We conclude that ancrod enhances thrombolysis probably by depleting fibrinogen and preventing new fibrin incorporation into the thrombus during lysis.

Ancrod↗

PubMed1989

An anti-plasminogen antibody preparation that inhibits the activation of human plasminogen but enhances the activator activity of the B-chain-streptokinase complex.

An anti-Glu-plasminogen (GLU-PLG) polyclonal antibody antiserum was prepared in the goat, and specific IgG anti-GLU-PLG antibodies were purified by affinity chromatography using a sepharose-GLU-PLG column. In chromogenic assay studies, the anti-GLU-PLG antibody preparation was found to be an effective inhibitor of the activation of PLG, and it produced different inhibition curves with four different PLG activators. 80% inhibition of streptokinase (SK) activation of GLU-PLG occurred with an anti-GLU-PLG antibody/GLU-PLG molar ratio of 1:1, whereas at this ratio only 28% and 36% inhibition of the plasmin-streptokinase (PLN-SK) and the B-chain-streptokinase (B-SK) complexes occurred. At a 1:1 molar ratio of antibody to PLN, no inhibition of PLN activity occurred. When the anti-GLU-PLG antibody preparation was incubated with each PLG activator, an enhancement in the activator activity of the B-SK complex, but not the other activators was observed with mini-plasminogen (MINI-PLG). Enhancement occurred at a molar ratio of 1:1 and reached a peak of 97% enhancement at a molar ratio of 10:1. Enhanced activator activity of the B-SK complex of 49% occurred at a molar ratio of 1:1 when GLU-PLG was the substrate. At higher molar ratios inhibition of activator activity on GLU-PLG was observed, but not on MINI-PLG. These results indicate that there are multiple activator binding sites on PLG, that these four activators all bind differently to GLU-PLG and MINI-PLG, that some antibody populations that are specific for the PLN B-chain can stimulate activator activity, while other antibody populations that are specific for either the PLN A-chain or the B-chain are inhibitory.

Animals↗

PubMed1982

Segmental renal artery emboli treated with low-dose intra-arterial streptokinase.

Herein we describe a sixty-one-year-old man with unilateral segmental renal artery emboli treated with renal intra-arterial streptokinase infusion. The initial infusion rate was 9,000 units/hr. which was decreased to 5,000 units/hr. over the next six hours. Periodic arteriography demonstrated progressive lysis and virtual complete resolution after fifty-two hours of infusion. Intravenous pyelogram (IVP) six weeks later showed almost complete return of functional compared with IVP obtained six years earlier. We have demonstrated successful clot lysis at an infusion rate of 5,000 units/hr., compared with reported rates of 25,000 units/hr. and without the frequently utilized initial large intravenous bolus. Such low-dose streptokinase infusion should, theoretically, limit the incidence of recognized dose-related complications and permit its use in clinical settings where higher dosages are contraindicated. Intra-arterial streptokinase therapy seems particularly suitable for the high surgical risk patient and in arterial lesions not amenable to surgery. The availability of this potentially efficacious therapy suggests that aggressive diagnostic studies be pursued early in patients suspected of having an acute renal arterial embolus.

Embolism↗

PubMed1987

A canine model of thrombin-induced coronary artery thrombosis: effects of intracoronary streptokinase on regional myocardial blood flow, contractile function, and infarct size.

The present investigation was undertaken to produce and to validate a canine model of experimental coronary artery thrombosis. In anesthetized, open-chest dogs, thrombin (150-200 U) was injected through an intracoronary catheter proximal to a brief (1 min) left anterior descending coronary artery occlusion. After 1 min, the mechanical occlusion was released, but no reperfusion occurred. Intracoronary thrombus was limited to the large coronary artery proximal to the site of mechanical occlusion. In two groups of dogs (n = 8), 15 min following thrombosis, vehicle (saline) or streptokinase (20,000 IU) was administered as an intracoronary bolus followed by an intracoronary infusion for 1 hr. None of the vehicle-treated dogs demonstrated antegrade coronary flow for up to 4 hr following intracoronary thrombin, whereas seven of eight had return of antegrade flow among streptokinase-treated dogs. Following streptokinase, thrombus size was reduced from control (25.1 +/- 5.3 mg versus 1.8 +/- 1.3 mg), perfusion to the subepicardium, midmyocardium, and subendocardium was increased, and infarct size was reduced. The results of the present study indicate the usefulness and reproducibility of this model in evaluating the beneficial actions of thrombolytic therapy.

Animals↗

PubMed1988

Reduced incidence of left ventricular thrombi with intravenous streptokinase in acute anterior myocardial infarction: prospective evaluation by cross-sectional echocardiography.

Forty-five consecutive patients with transmural anterior acute myocardial infarction were prospectively studied to determine the effect of intravenous streptokinase on the incidence of left ventricular thrombi. Three patients died. The remaining patients were divided into 2 groups. Group 1 patients (n = 22) received 750,000 units of intravenous streptokinase within 6 hours of onset of symptoms. Neither thrombolytic therapy or anticoagulants were administered to 18 patients in group 2. Cross-sectional echocardiography was performed 8 to 10 days following acute myocardial infarction to detect left ventricular thrombus. Technically satisfactory echocardiography was not possible in 2 patients. Apical akinesia or dyskinesia was observed in all patients. No patient in the treated group developed left ventricular thrombus compared with 8 of 18 (44.4%) in group 2 (P less than 0.05). One patient in the control group sustained an embolic cerebrovascular accident. Thus intravenous streptokinase significantly reduces the incidence of left ventricular thrombus formation in patients of transmural anterior acute myocardial infarction.

Aged↗

PubMed1995

Pro- and antifibrinolytic effects of ultrasound on streptokinase-induced thrombolysis.

We have earlier documented that ultrasound can enhance the fibrinolytic effect of streptokinase and shorten the reperfusion time under experimental conditions. The present study concerns the magnitude of the effect in relation to ultrasound frequency, intensity and exposure time. The effect of ultrasound on the structural properties of the fibrin network was evaluated by scanning electron microscopy. Whole blood clots were created and exposed to streptokinase (5000 U/mL). In paired experiments, one clot was also exposed to pulsed ultrasound. Lysis is expressed as the percentage decrease in clot weight. Clot lysis was equally affected by ultrasound in the range of 0.5 to 2.3 MHz. Below 0.5 W/cm2 no enhancing effect was observed, while intensities between 0.5 and 1.5 W/cm2 resulted in a significant enhancement of clot lysis. Intensities above 4 W/cm2 inhibited the fibrinolytic effect of streptokinase but not of rt-PA. From scanning electron microscopy there was no evidence that ultrasound disrupted the clot surface or damaged the fibrin structure.

Analysis of Variance↗

PubMed1990

Duplication of the streptokinase gene in the chromosome of Streptococcus equisimilis H46A.

The erythromycin resistance plasmid pSM752 carrying the cloned streptokinase gene, skc, was introduced by protoplast transformation into Streptococcus equisimilis H46A from which skc was originally cloned. Cells transiently supporting the replication of pSM752 gave rise to an erythromycin-resistant clone designated H46SM which was plasmid free and produced streptokinase at levels approximately twice as high as the wild type. Southern hybridization of total cell DNA with an skc-containing probe provided evidence for the duplication of the skc gene in the H46SM chromosome. The results, which have some bearing on industrial streptokinase production, can be best explained by a single cross-over event between the chromosome and the plasmid in the region of shared homology leading to the integration of pSM752 in a Campbell-like manner.

Blotting, Southern↗

PubMed1985

Nucleotide sequence of the streptokinase gene from Streptococcus equisimilis H46A.

The entire nucleotide sequence of a cloned 2568-bp PstI fragment from the genome of Streptococcus equisimilis H46A encoding the streptokinase gene (skc) has been determined. The longest open reading frame comprises 1320 bp which code for streptokinase. The protein is synthesized with a 26-amino acid residue N-terminal extension having properties characteristic of a signal peptide. Comparison of the deduced amino acid sequence with the available amino acid sequence of a commercial streptokinase reveals minor primary structure differences. The nucleotide sequencing of skc does not support the hypothesis that the gene has evolved by duplication and fusion, as suggested by internal twofold amino acid homologies of its product. Furthermore, the skc gene sequence shows no extended regions homologous to the staphylokinase gene. Upstream from the skc gene, the putative skc promoter and the ribosome-binding site sequence have been identified; downstream from the coding region, inverted repeat sequences thought to function as transcription terminators have been detected.

Amino Acid Sequence↗

PubMed1988

Ventricular function and infarct size: the Western Washington Intravenous Streptokinase in Myocardial Infarction Trial.

The Western Washington Intravenous Streptokinase in Acute Myocardial Infarction Trial randomized 368 patients with symptoms and signs of acute myocardial infarction of less than 6 h duration to either conventional care or 1.5 million units of intravenous streptokinase. The mean time to randomization was 209 min and 52% of patients were randomized within 3 h of symptom onset. Quantitative, tomographic thallium-201 infarct size and radionuclide ejection fraction were measured at 8.2 +/- 7.5 weeks in 207 survivors who lived within a 100 mile radius of a centralized laboratory. Overall, infarct size as a percent of the left ventricle was 19 +/- 13% for control subjects and 15 +/- 13% for treatment patients (p = 0.03). For anterior infarction in patients entered within 3 h of symptom onset, infarct size was 28 +/- 13% in the control group versus 19 +/- 15% for the treatment group (p = 0.09). Left ventricular ejection fraction was 47 +/- 15% in the control versus 51 +/- 15% in the treatment group (p = 0.08). For anterior infarction of less than 3 h duration, the ejection fraction was 38 +/- 16% in the control versus 48 +/- 20% in the treatment group (p = 0.13). By statistical analysis incorporating the nonsurvivors, p values for all of these variables were less than or equal to 0.08. There was no benefit for patients with inferior infarction or for anterior infarction of greater than 3 h duration. It is concluded that intravenous streptokinase, when given within 3 h of symptom onset to patients with anterior infarction, reduces infarct size and improves ventricular function.

Clinical Trials as Topic↗

PubMed1989

A new thrombolytic regimen for acute myocardial infarction using combination half dose tissue-type plasminogen activator with full dose streptokinase: a pilot study. KAMIT Study Group.

Because a previous study utilizing a combination of recombinant tissue-type plasminogen activator (rt-PA) and urokinase demonstrated reduced reocclusion rates compared with rates obtained with rt-PA alone, this study was conducted to determine whether the combination of rt-PA and streptokinase might achieve similar results at reduced cost. Forty patients with acute myocardial infarction were treated with a 1 h infusion of rt-PA (50 mg) and streptokinase (1.5 million U) administered within 6 h (mean 3.6 +/- 1.2) of symptom onset. Emergency coronary arteriography revealed patency of the infarct-related artery in 30 (75%) of 40 patients. With the addition of coronary angioplasty in those who had unsuccessful thrombolytic reperfusion, the early patency rate was increased to 98%. In-hospital mortality rate (2.5%) and the incidence of significant bleeding requiring transfusion (15%) were low. Angiographically documented reocclusion of the infarct vessel occurred in 3 (8%) of 37 patients by day 7. Regional wall motion of the infarct zone improved by 0.9 +/- 0.9 SD/chord (p less than 0.0005), and ejection fraction increased 3.6 +/- 8% units (p less than 0.05) between immediate and day 7 studies. In contrast to the price of full dose rt-PA ($2,300) or rt-PA with urokinase ($3,500), the cost of this regimen was $1,230. This pilot study demonstrates that at half the cost, a combination of half dose rt-PA with full dose streptokinase offers high infarct vessel patency, recovery of ventricular function, a low rate of reocclusion and few bleeding complications.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1991

Comparison of the effects of streptokinase and tissue plasminogen activator on regional wall motion after first myocardial infarction: analysis by the centerline method with correction for area at risk.

In a trial of streptokinase versus recombinant tissue-type plasminogen activator (rt-PA) for a first myocardial infarction, 270 patients were randomized. Regional left ventricular function was assessed in 214 patients at 3 weeks. The infarct-related artery was the left anterior descending artery in 78 patients, the right coronary artery in 122 and a dominant left circumflex artery in 14. Analysis was by the centerline method with a novel correction for the area of myocardium at risk, whereby the search region was determined by the anatomic distribution of the infarct-related artery. Infarct-artery patency at 3 weeks was 73% in the streptokinase group and 71% in the rt-PA group. Global left ventricular function did not differ between the two groups. Mean chord motion (+/- SD) in the most hypokinetic half of the defined search region was similar in the streptokinase and rt-PA groups (-2.4 +/- 1.5 versus -2.3 +/- 1.3, p = 0.63). There were no differences in hyperkinesia of the noninfarct zone. Compared with conventional centerline analysis, regional wall motion in the defined area at risk was significantly more abnormal. The two methods correlated strongly, however (r = 0.99, p less than 0.0001), and both methods produced similar overall results. Patients with a patent infarct-related artery and those with an occluded artery at the time of catheterization had similar levels of global function (ejection fraction 58 +/- 12% versus 57 +/- 12%, p = 0.58).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Catheterization↗

PubMed1993

Randomized trial of direct coronary angioplasty versus intravenous streptokinase in acute myocardial infarction.

OBJECTIVES: The objective of this study was to obtain preliminary data on the relative clinical utility of direct coronary angioplasty compared with that of intravenous thrombolytic therapy for patients with acute myocardial infarction. BACKGROUND: The relative merits of intravenous thrombolytic therapy and direct coronary angioplasty as treatment for acute myocardial infarction are incompletely understood, and randomized trials of these treatments have been extremely limited. METHODS: One hundred patients with ST segment elevation presenting to a single high volume interventional center within 6 h of the onset of chest pain were randomized to receive either streptokinase (1.2 million U intravenously over 1 h) or immediate catheterization and direct coronary angioplasty. Patients were excluded for age > or = 75 years, prior bypass surgery, Q wave infarction in the region of ischemia or excessive risk of bleeding. All patients were then treated with aspirin (325 mg orally/day) and heparin (1,000 U intravenously/h) for 48 h until catheterization was performed to determine the primary study end point, namely, infarct-related artery patency at 48 h. Secondary end points were in-hospital death, left ventricular ejection fraction at 48 h and time to treatment. RESULTS: There was no difference in the baseline characteristics of the two treatment groups. Overall patient age was 56 +/- 10 years, 83% of patients were male, 11% had prior infarction, 40% had anterior infarction and 97% were in Killip class I or II. Although time to treatment was delayed in the angioplasty group (238 +/- 112 vs. 179 +/- 98 min, p = 0.005), there was no difference in 48-h infarct-related artery patency or left ventricular ejection fraction (patency 74% vs. 80%; ejection fraction 59 +/- 13% vs. 57 +/- 13%; angioplasty vs. streptokinase, p = NS for both). There were no major bleeding events, and the mortality rate with angioplasty (6%) and streptokinase (2%) did not differ (p = NS). CONCLUSIONS: These results suggest that intravenous thrombolytic therapy might be preferred over coronary angioplasty for most patients because of the often shorter time to treatment.

Aged↗

PubMed1995

Impairment of fibrinolysis by streptokinase, urokinase and recombinant tissue-type plasminogen activator in the presence of radiographic contrast agents.

OBJECTIVES: The purpose of this study was to determine whether an adverse interaction exists between radiographic contrast agents and thrombolytic drugs. BACKGROUND: Coronary thrombosis may occur in the setting of unstable angina and after coronary angioplasty. However, the use of thrombolytic drugs in the setting of unstable angina has not been beneficial and, in one large trial of angioplasty in patients with unstable angina, was associated with an increased incidence of ischemic complications and abrupt closure. The reasons for these results are not clear. Coronary arteriography was performed in many of these trials, and it is known that fibrin structure and assembly are altered by radiographic contrast agents. METHODS: Blood samples were obtained from patients before (n = 25) and after (n = 20) angiography using iohexol. Blood samples obtained before angiography were tested for response to streptokinase (10 and 100 IU/ml), urokinase (100, 200 and 500 IU/ml) and recombinant tissue-type plasminogen activator (rt-PA) (100 and 1,000 IU/ml) and the results measured. Iohexol, diatrizoate or ioxaglate (4% by volume) was added to separate aliquots of the baseline sample, and the test was repeated. Blood samples obtained after angiography were tested in a similar manner. RESULTS: The onset of lysis at baseline by rt-PA at 1,000 IU/ml occurred at 72 +/- 8.2 s (mean +/- SD) and was markedly delayed in the presence of diatrizoate (527 +/- 181.7 s, p < 0.001) or iohexol (460 +/- 197.0 s, p < 0.001) but not ioxaglate. At 100 IU/ml, there was no lysis detected with rt-PA after the addition of any contrast agent. The addition of a contrast agent caused similar delays in the onset of lysis by urokinase and streptokinase; similar to rt-PA, the effect was smaller at higher concentrations of drug. In vivo blood samples obtained from the patient after angiography showed delays in the onset of lysis by rt-PA and urokinase but not streptokinase. CONCLUSIONS: These data demonstrate that radiographic contrast agents impede fibrinolysis. This previously undescribed interaction was demonstrated using an in vitro test system, but these findings may have clinical relevance when thrombolytic drugs are used at the time of angiography.

Contrast Media↗

PubMed2004

Streptokinase--a clinically useful thrombolytic agent.

A failure of hemostasis and consequent formation of blood clots in the circulatory system can produce severe outcomes such as stroke and myocardial infraction. Pathological development of blood clots requires clinical intervention with fibrinolytic agents such as urokinase, tissue plasminogen activator and streptokinase. This review deals with streptokinase as a clinically important and cost-effective plasminogen activator. The aspects discussed include: the mode of action; the structure and structure-function relationships; the structural modifications for improving functionality; recombinant streptokinase; microbial production; and recovery of this protein from crude broths.

Fibrinolysis↗

PubMed2004

Fibrinolytic treatment of complicated pediatric thoracic empyemas with intrapleural streptokinase.

OBJECTIVE: Proper antibiotic treatment and adequate pleural drainage is essential in successful management of pleural effusions. In complicated effusions the increased production of fibrin results in formation of loculations and septations within the thoracic cavity, leading ineffective chest tube drainage. Intrapleural fibrinolytic agents are employed to avoid thoracotomy in such complicated pleural effusions. Our study reviews the results of streptokinase treatment in children with pleural effusion. METHODS: Thirty-two patients with parapneumonic pleural effusions were admitted to our hospital. The patients beyond the exudative stage were divided into two groups according to the initial radiological findings and biochemical parameters of pleural fluid. Intrapleural streptokinase treatment was started in an average of 2 days following initial chest tube placement in both Group I (14 patients) in fibrino-purulent phase with pleural effusion and fluid volume estimated to be larger than one-third of the involved lung and Group II (18 patients) with additional findings in radiological examination regarding the presence of air-fluid levels, multiple loculations, necrotic debris and pleural thickening. The effectiveness of therapy was assessed by monitoring the volume of the fluid, the level of LDH, glucose, pH and by radiological imaging, pre- and post-instillation. RESULTS: There was statistically significant difference between two groups according to date of admission (6.8 vs 10.4 days), mean of total pleural fluid drainage before (106.9 vs 309.7 ml) and after (258.9 vs 511.2 ml) SK treatment, mean of total number of instillations (2.1 vs 3.6) required and total length of hospital stay (16.6 vs 22.4 days). There was a significant difference regarding pleural chemical analysis. Finally, surgical intervention was necessary in six intractable cases, all of which initially presented a significant small amount of pleural drainage in volume when compared to rest of the patients. The overall success rate of our treatment was calculated as 96% for G-I and 72.2% for G-II cases. CONCLUSIONS: Intrapleural streptokinase is an effective and safe adjunct in facilitating drainage in early and late stage II empyemas. A tendency of decreased rate of drainage besides persisting fever and respiratory symptoms, despite fibrinolytic treatment may be a clue for early surgical intervention.

Analysis of Variance↗

PubMed2005

Videothoracoscopy versus intrapleural streptokinase for management of post traumatic retained haemothorax: a retrospective study of 65 cases.

BACKGROUND: Post traumatic retained haemothorax (PRH) may cause pulmonary restrictions or septic pleural complications. Currently, minimally invasive procedures such as videothoracoscopy or intrapleural fibrinolysis have replaced open surgery in an effort to avoid these complications. OBJECTIVE: We have reviewed retrospectively our use of videothoracoscopy versus intrapleural streptokinase for the management of PRH over the last 10 years. PATIENTS AND METHOD: There were 56 males and nine females in the study. Thirty-one cases had been managed by intrapleural streptokinase (group I), and videothoracoscopy was performed on 34 cases (group II). Therapeutic results for both groups were determined by chest radiographs. RESULTS: In the population from which we drew our study group, retained haemothoraces occurred in 10.9% of 596 cases with traumatic haemothorax. In group I, 22 patients had radiological improvement; the others underwent thoracotomy. In this group, mean hospitalisation time was 14.5(+/-4.2) days, and three cases were complicated by empyema. In group II, all patients except four had complete radiological improvement; two of them required a decortication. In this group, mean hospital stay was 9.8(+/-3.7) days. There were no deaths in either group. The differences between group I and group II for length of hospital stay and number of thoracotomies was statistically significant. CONCLUSION: Videothoracoscopy is therefore a more effective procedure than intrapleural streptokinase for the management of PRH.

Adolescent↗