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PubMed1991

The effect of streptokinase on chest pain in acute myocardial infarction.

Treatment with intravenous streptokinase is known to restore blood flow to the ischaemic myocardium in patients with acute myocardial infarction. However, little is known about its effect on chest pain. In a retrospective cohort study, 76 patients treated with streptokinase were compared to 76 patients not treated with streptokinase. All patients had acute myocardial infarction and less than 6 h of cardiac symptoms. Patients treated with streptokinase had a significantly lower need for nicomorphine (median 20 mg) than patients not treated with streptokinase (median 41 mg). Correspondingly, the median duration (3.5 h) of pain was reduced significantly in patients treated with streptokinase compared to patients not treated (24 h). We conclude that intravenous streptokinase given in the acute phase of myocardial infarction is effective in reducing the duration of cardiac chest pain.

Acute Disease↗

PubMed1988

Streptokinase-induced, antibody-mediated platelet aggregation: a potential cause of clot propagation in vivo.

The administration of intracoronary streptokinase to a patient with a prior history of rheumatic fever was associated with the retrograde propagation of thrombus from the left anterior descending coronary artery into the left main coronary artery with near catastrophic consequences. The addition of streptokinase to platelet-rich plasma from the patient initiated platelet aggregation and secretion in vitro. Platelet aggregation was also seen in 1 of 15 control subjects after the addition of streptokinase, and the addition of plasma or immunoglobulin G (IgG) from the index patient supported platelet aggregation in the presence of streptokinase in all of the previously nonreactive control subjects. This in vitro platelet aggregation was specific for streptokinase and not initiated by either urokinase or tissue plasminogen activator. Streptokinase-induced platelet aggregation was not inhibited by aprotinin, but was completely attenuated by the addition of an excess of antihuman IgG Fab. These findings suggest that streptokinase can initiate specific antibody-mediated platelet aggregation in vitro and may be more than coincidentally related to clot propagation or thromboembolism in vivo.

Antibodies, Viral↗

PubMed1992

Conformation ability test of human, rabbit and bovine plasminogens and their specific interaction with streptokinase.

Human, rabbit and bovine plasminogens, having different sensitivity to streptokinase-activating action, differ, according to spectrophotometric titration, tryptophan fluorescence and circular dichroism spectroscopy, in the state of tyrosine and tryptophan residues, and in secondary and tertiary structures. Human plasminogen-streptokinase equimolar complex formation (according to gel chromatography) is accompanied by a differential ultraviolet spectrum. Difference spectroscopy is a convenient and adequate means of studying the formation of the said complexes. Streptokinase-human plasminogen complex formation is not hindered by partial substitution of water (20%) with ethanol or dimethylsulphoxide or by addition of 0.001 M sodium dodecylsulphate. The complex is not formed in 6 M urea, in solution, at pH less than 2.0 or approximately 12.0-13.0, or with bovine plasminogen. Circular dichroism and tryptophan fluorescence spectral pattern changes during streptokinase-plasminogen complex formation enable us to conclude that streptokinase secondary and tertiary structures undergo certain rearrangements in the framework of the complex, while tryptophan-containing sites of the molecule are not drastically changed. The data obtained enable us to presuppose formation of streptokinase-rabbit plasminogen complexes which differ from human plasminogen complexes with streptokinase.

Animals↗

PubMed1983

Retrograde lysis of coronary artery thrombus by coronary venous streptokinase administration.

This study examined whether an occlusive thrombus within a coronary artery can be lysed by streptokinase retroperfusion into the associated regional coronary vein. Experimental coronary artery thrombosis was induced in 15 closed chest dogs by placing a small copper coil at a proximal site of the left anterior descending coronary artery. Total thrombotic obstruction of this artery was verified within 10 to 60 minutes (38.0 +/- 15.8, mean +/- standard deviation) and streptokinase was administered within 94.0 +/- 17.4 minutes from coil insertion at an average rate of 42 IU/kg per minute by one of three modes: 1) intermittent 10 minute direct coronary venous retroinfusion (five dogs); 2) continuous infusion into the pumping circuit of synchronized phased retroperfusion of the great cardiac vein with arterial blood (five dogs); and 3) for comparison, streptokinase administered intravenously (five dogs). The intracoronary thrombus was fully lysed and anterograde reperfusion established within 51.0 +/- 18.7 minutes by intermittent streptokinase retroinfusion, and in 50.0 +/- 6.1 minutes by streptokinase supplemented synchronized retroperfusion (50.5 +/- 13.2 minutes for pooled retrograde coronary venous delivery). Lysis was also induced by systemic streptokinase, but the time to lysis was significantly longer and more variable (131.6 +/- 60.6 minutes) than with retrograde administration (p less than 0.01). The retroperfusion modality appears the preferable technique because it provides early thrombolysis and, at the same time, improves cardiac function and maintains myocardial viability of the jeopardized ischemic zone pending achievement of full reflow. Thus, streptokinase retroperfusion, if promptly instituted, may be a useful complemental nonsurgical treatment of evolving acute myocardial infarction after thrombotic coronary artery occlusion.

Animals↗

PubMed1985

High dose intravenous streptokinase for acute myocardial infarction: preliminary results of a multicenter trial.

To assess the efficacy of intravenous streptokinase in patients with acute myocardial infarction, 40 patients (30 men and 10 women, mean age 54 years) with acute myocardial infarction were given 1.5 million U of streptokinase intravenously in 1 hour, and coronary arteriography was performed repeatedly to assess reperfusion. Streptokinase treatment was begun 270 +/- 86 (mean +/- SD) minutes after the onset of chest pain. Of the 40 patients, 34 had total or near total coronary occlusion before streptokinase administration. In 14 (41%) of these 34 patients, some reperfusion occurred during the 90 minutes after the administration of streptokinase, but in only 11 of the 14 was reperfusion present at 90 minutes. After streptokinase administration, all patients received heparin for 8 to 10 days; they were subsequently administered aspirin and dipyridamole. Clinical evidence of reocclusion during the first 24 hours of heparin therapy occurred in one patient. Thus, when given to patients with acute myocardial infarction and total coronary occlusion an average of 4 1/2 hours after the onset of chest pain, high dose intravenous streptokinase achieves reperfusion in only about 40% and results in sustained reperfusion in only about 30%.

Adult↗

PubMed1987

A prospective placebo-controlled double-blind multicenter trial of intravenous streptokinase in acute myocardial infarction (ISAM): long-term mortality and morbidity.

Long-term mortality and morbidity of 1,741 patients with acute myocardial infarction, treated with intravenous streptokinase (1.5 million IU/h) or placebo, was assessed in a double-blind placebo-controlled trial (ISAM). At the 7 month follow-up, 94 (10.9%) of the 859 patients in the streptokinase group and 98 (11.1%) of the 882 patients in the placebo group had died; at an average follow-up of 21 months, 14.4% of the streptokinase group and 16.1% of the placebo group had died. The differences were not statistically significant. Long-term mortality was slightly higher in patients with anterior myocardial infarction and streptokinase treatment (20.1 versus 18.4%) and lower in patients with inferior myocardial infarction (10.2 versus 14.2%). Patients with previous myocardial infarction had a higher long-term mortality rate with streptokinase (34.9 versus 21.5% with placebo, p = 0.03). At 7 months, there were significantly more cases of reinfarction in the streptokinase group (7.2 versus 4.5%, p = 0.02). It is concluded that despite a significant limitation of infarct size by intravenous streptokinase, long-term mortality is only slightly reduced and reinfarction is significantly more frequent. Both findings suggest the need for complementary therapy such as revascularization procedures after thrombolysis.

Clinical Trials as Topic↗

PubMed1987

Effect of intravenous streptokinase on left ventricular function and early survival after acute myocardial infarction.

In a double-blind trial of streptokinase for acute myocardial infarction, 219 consecutive patients presenting with infarction within four hours (mean, 3.0 +/- 0.8) of the onset of chest pain were randomly assigned to treatment with streptokinase (1.5 million units) or placebo, given intravenously over 30 minutes. The primary end point of the study was left ventricular function in patients with first infarctions. Patients who could undergo beta-blockade also received intravenous propranolol. Heparin (for 48 hours) and a combination of low-dose aspirin and dipyridamole were administered to both groups until cineangiography was performed at three weeks. In the patients with first infarctions treated with streptokinase, the left ventricular ejection fraction was 6 percentage points higher (streptokinase vs. placebo, 59 +/- 10.5 vs. 53 +/- 13.5 percent; P less than 0.005), with benefit to patients with either anterior infarction (57 +/- 11.9 vs. 49 +/- 15.9 percent; P less than 0.05) or inferior infarction (60 +/- 9.1 vs. 55 +/- 11.3 percent; P less than 0.05). Left ventricular function was improved regardless of whether concomitant propranolol was given. Survival (at 30 days) was improved with streptokinase: 2 deaths occurred among 79 patients who received this drug, as compared with 12 deaths among 93 patients who received placebo (2.5 vs. 12.9 percent, P = 0.012). Rates of reinfarction (streptokinase vs. placebo, 3 vs. 1 percent) and requirements for surgery or angioplasty (7 vs. 5 percent) were similar in the two groups. We conclude that administration of intravenous streptokinase (1.5 million units) to patients with a first myocardial infarction results in improved left ventricular function and short-term survival.

Adrenergic beta-Antagonists↗

PubMed1989

Effect of intravenous streptokinase as compared with that of tissue plasminogen activator on left ventricular function after first myocardial infarction.

In a double-blind trial comparing two thrombolytic agents as treatment for acute myocardial infarction, we randomized 270 consecutive patients an average (+/- SD) of 2.5 +/- 0.6 hours after the onset of chest pain from a first myocardial infarction--135 to receive intravenous streptokinase (1.5 million units over 30 minutes) and 135 to receive intravenous recombinant tissue plasminogen activator (rt-PA) (100 mg over three hours). The primary end point was left ventricular function as assessed by cineangiography performed three weeks after infarction. The effects of the two agents on left ventricular function were similar. The ejection fraction was identical (58 +/- 12 percent) in both groups. The end-systolic volume was 61 +/- 29 ml in the streptokinase group and 66 +/- 31 ml in the rt-PA group (P not significant). Patency rates at three weeks for the infarct-related artery were also similar (75 percent in the streptokinase group and 76 percent in the rt-PA group). Reinfarction rates at 30 days were the same (5 percent) in both groups. One patient had a fatal intracerebral hemorrhage 13 hours after receiving rt-PA, and another had a fatal cerebellar hemorrhage 21 hours after receiving rt-PA for reinfarction nine days after treatment with streptokinase. An intention-to-treat analysis revealed that mortality at 30 days was 3.7 percent in the rt-PA group as compared with 7.4 percent in the streptokinase group (P greater than 0.2). Follow-up for a mean of 9.0 months revealed no significant difference in survival; we observed 12 deaths (8.9 percent) in the streptokinase group and 8 deaths (5.9 percent) in the rt-PA group (P = 0.34). We conclude that rt-PA and streptokinase, in the doses given, have similar effects on left ventricular function after a first myocardial infarction. Because of the small number of deaths, it is not possible to determine whether their effects on mortality are similar.

Double-Blind Method↗

PubMed1988

Discrepant changes in plasminogen by two different assays in patients receiving streptokinase.

The fluorogenic synthetic substrate and radial immunodiffusion assays of plasma plasminogen were compared before and after administration of intravenous streptokinase in differing doses to 57 patients being treated for acute myocardial infarction. There was a moderate correlation (r = 0.73, slope = 0.221, intercept = 1.005, n = 57 pairs) in the two assays of plasma plasminogen before the administration of streptokinase. After streptokinase, however, the correlation of the two assays was poor (r = 0.28, slope = 0.03, y-intercept = 0.003, n = 57 pairs). The decrease in plasma plasminogen by the fluorogenic synthetic substrate assay after streptokinase averaged 95 +/- 5%, with little variation between doses. In contrast, the percentage decrease in plasma plasminogen after streptokinase by the radial immunodiffusion assay averaged only 30 +/- 11%. The percentage change in plasma plasminogen by the two assays is significantly different (P = 0.001). The discrepancy in the percentage change in plasma plasminogen after streptokinase as measured by the fluorogenic synthetic substrate assay and the radial immunodiffusion assay can be explained by a lack of specificity for the antibody to plasminogen in the radial immunodiffusion kit. Antigen-antibody precipitin rings were observed after incubation of antibody with a mixture presumed to contain plasmin, plasmin-alpha 2 antiplasmin complexes, and plasmin-fibrin/fibrinogen degradation products. Based on these data, the fluorogenic synthetic substrate assay for plasma plasminogen is a superior means of following plasminogen depletion in response to thrombolytic therapy after streptokinase treatment for acute myocardial infarction.

Dose-Response Relationship, Drug↗

PubMed2005

Comparative analysis of the activity and content of different streptokinase preparations.

AIMS: The dosage of fibrinolytic agents such as streptokinase must be controlled carefully to maximize therapeutic activity while avoiding adverse effects. Therefore, the integrity and activity of streptokinase products is likely to be clinically relevant. This study was conducted to compare the in vitro characteristics of different streptokinase preparations. METHODS AND RESULTS: Sixteen streptokinase preparations (three of which were recombinant) were compared in a chromogenic substrate activity assay by native, and reducing, sodium dodecyl sulphate (SDS)-polyacrylamide gel electrophoresis (PAGE), and N-terminal sequencing. Deficiencies in streptokinase activity were observed in most of the products: only three fulfilled the minimum requirements of the European Pharmacopoeia. These were Icikinase (ICI Pharm Ltd, India, only one of two batches tested), Kabikinase (Pharmacia Upjohn, Sweden), and Streptase (Aventis Behring GmbH, Germany). The remaining products exhibited activities ranging from 20.8 to 86.6% of the label claim. Differences in composition and purity were demonstrated by both native and reducing SDS-PAGE. N-terminal sequencing of the recombinant preparations showed differences compared with the native protein--indeed, for one product, the 15 N-terminal amino acids bore no resemblance to streptokinase. CONCLUSION: There are wide variations in the activity, purity, and composition of the available streptokinase preparations.

Electrophoresis, Polyacrylamide Gel↗

PubMed1990

More rapid thrombolysis with coronary venous retroinfusion of streptokinase compared with intravenous administration. An experimental study in canines.

The efficacy of coronary venous retroinfusion vs intravenous administration of streptokinase was compared in 20 closed chest dogs with copper coil induced thrombosis of the left anterior descending coronary artery. Streptokinase was continuously infused for 60 min (100 IU kg-1 min-1) starting 60 min after coronary artery occlusion. Time to clot lysis was determined by coronary angiography performed at 5 min intervals. Complete lysis occurred in eight out of 10 dogs receiving intravenous streptokinase and in all 10 dogs in the coronary venous group. Time to thrombolysis was significantly shorter with coronary venous retroinfusion (23 +/- 8 min) than after systemic infusion (62 +/- 26 min; P less than 0.001). Recovery of ischaemic zone left ventricular systolic function, studied by two-dimensional echocardiography, was significantly better in the animals that received retrograde streptokinase than in the group that received intravenous streptokinase (17 +/- 12% vs -2 +/- 16%; P less than 0.05). Myocardial necrosis expressed as a percentage of the risk area was 8 +/- 12% after retroinfusion of streptokinase compared with 32 +/- 25% (P less than 0.005) after intravenous administration. In conclusion, coronary venous administration of streptokinase was more effective than intravenous therapy as determined by more rapid clot lysis which resulted in improved functional recovery of the ischaemic myocardium and a significant reduction in myocardial necrosis.

Animals↗

PubMed2002

The effect of 6-aminohexanoic acid and fucoidan on the activation of glutamic plasminogen by streptokinase.

Studies were conducted on the effect of 6-aminohexanoic acid (6-AH) or fucoidan on the activation of glutamic plasminogen (glu-plg) by streptokinase using 0.05 mol/l Tris buffer containing a physiological concentration of NaCl. In contrast to the earlier reports where no NaCl was added to the buffer solution, addition of 6-AH enhanced the initial rate while the inhibition by fucoidan was not affected. Double reciprocal plots of the activation of glu-plg by streptokinase in the presence of 6-AH showed an increase in Vmax, but no change in Km. However, the addition of fucoidan showed a decrease in Vmax, but no change in Km. To determine whether the stimulatory effect of 6-AH was specifically directed towards glu-plg or streptokinase, the ratios of the initial rate of plasmin generation in the presence of 6-AH over the controls were plotted against the inverse of the volume fraction of glu-plg or streptokinase after serial dilutions. The results indicated that the dilutions of glu-plg, but not of streptokinase, influenced the ratios, suggesting an interaction of 6-AH with glu-plg. Similar experiments were conducted to determine the mechanism of inhibition of streptokinase by fucoidan. The results indicated that fucoidan was interacting with streptokinase, but not with glu-plg. Circular dichroism studies of glu-plg in the near-ultraviolet spectra (250-308 nm) showed that addition of 6-AH enhanced the spectra in the region around certain chromophores, which reflected conformational changes. On the contrary, the far-ultraviolet spectra were almost identical.

Aminocaproic Acid↗

PubMedDate not supplied

Beneficial effects of streptokinase on left ventricular function after myocardial reoxygenation and reperfusion following global ischemia in the isolated rabbit heart.

To determine the effect of streptokinase on the ischemic myocardium independent of its effects on the occluding thrombus, the isolated rabbit heart, perfused with Krebs-Henseleit solution, was subjected to a 45-min period of ischemia--83% reduction in myocardial (perfusion) flow--plus anoxia (95% N2 and 5% CO2), followed by restoration of perfusion and reoxygenation. Streptokinase, 75 or 150 IU/min, was infused starting 15 min before reperfusion and continuing for 30 min after reperfusion. Compared with the control group, streptokinase was associated during reperfusion with a significant dose-dependent greater restoration or smaller depression of ventricular function, dP/dt, and developed pressure. To determine if streptokinase effects were mediated during the ischemic or reperfusion phase, the high streptokinase dose was administered in either the last 30 min of the ischemia or the first 30 min of reperfusion. The improvement in recovery of left ventricular function was primarily in the group having streptokinase administered only during the ischemic period. Thus, streptokinase affects the ischemic myocardium so that there is an acceleration in the recovery of ventricular function or a reduction of the impairment in ventricular function during myocardial reperfusion.

Animals↗

PubMed2002

Roles of the plasminogen activator streptokinase and the plasminogen-associated M protein in an experimental model for streptococcal impetigo.

Primary infection by group A streptococci (GAS) takes place at either the throat or skin of the human host, often leading to pharyngitis or impetigo, respectively. Many GAS strains differ in their preference for throat and skin tissue sites. Previous epidemiological findings show that many of the strains displaying strong tropism for the skin have a high-affinity binding site for plasminogen, located within M protein (PAM), a prominent surface fibril. Plasminogen bound by PAM interacts with streptokinase, a plasminogen activator secreted by GAS, to yield bacterial-bound plasmin activity. In this study, PAM and streptokinase were tested for their roles in infection using an experimental model that closely mimics human impetigo. Inactivation of genes encoding either PAM or streptokinase led to a partial, but significant, loss of virulence in vivo, as measured by net growth of the bacteria and pathological alterations. The relative loss in virulence in vivo was greater for the streptokinase mutant than for the PAM mutant. However, the PAM mutant, but not the streptokinase mutant, displayed a partial loss in resistance to phagocytosis in vitro. The combined experimental and epidemiological data provide evidence that PAM and streptokinase play a key role in mediating skin-specific infection by GAS. In addition, secreted cysteine proteinase activity due to SpeB leads to degradation of streptokinase in stationary phase broth cultures. Since SpeB is also a determinant of tissue-specific GAS infection at the skin, direct interactions between these two proteolytic pathways may constitute an important pathogenic mechanism. An integrated model for superficial infection at the skin is presented.

Animals↗

PubMed1978

A controlled clinical trial of streptokinase and heparin in the treatment of major pulmonary embolism.

Treatment with streptokinase or heparin was allocated randomly to 20 patients with major pulmonary embolism verified by angiography. In addition, 4 patients treated with streptokinase and 1 patient treated with heparin were included in the trial prior to the start of treatment. Streptokinase of heparin was given for 72 hours and pulmonary angiography was repeated. The angiographic evidence of thrombolysis was significantly greater (p less than 0.01) in the 14 patients treated with streptokinase than in the 11 treated with heparin. In the heparin group, 1 patient died from massive embolism 15 hours after the start of treatment. In another patient who died 4 weeks later from cerebral glibolastoma, persistent massive embolism contributed to the fatal outcome. In the streptokinase group, 1 patient with a metastatic pulmonary carcinoma died 3 weeks after the start of treatment from gangrene of both legs following thrombotic occlusion of the inferior vena cava. Bleeding was more common after treatment with streptokinase than with heparin, but was not a serious problem in any patient. It is concluded that patients with life-threatening pulmonary embolism should be offered the benefits of streptokinase.

Adult↗

PubMed1988

A streptokinase dependent plasma factor (SKDF) induces leucocyte tissue factor activity.

Various inducers endow human leucocytes with a procoagulant activity of tissue factor type. We have observed a novel plasma factor which in combination with streptokinase induces powerful leucocyte procoagulant activity. This streptokinase dependent factor (SKDF) is present in normal plasma or serum albeit quantitatively different in individual donors. The generation of tissue factor activity as a function of streptokinase-plasma complex shows a specific and saturable sigmoidal dose-response curve. The Hill plot shows a straight line with Hill coefficient, H = 2.2, suggesting a strong positive cooperativity for the binding of this streptokinase-plasma complex to the leucocyte surface receptor for the signal transduction leading to the biosynthesis of tissue factor apoprotein. It also suggests that the leucocyte surface receptor for streptokinase-plasma complex differs from that for endotoxin lipopolysaccharides. SKDF is of apparent high molecular weight. It does not appear to be an antibody to streptokinase since its level does not correlate with the level of antibodies to streptokinase, and it does not correlate with the antistreptolysin titre. Furthermore, SKDF does not bind to protein A. It has a narrow pH range of stability, and is destroyed at 56 degrees C, or at freeze-drying, Urokinase, another plasminogen activator, or plasmin were unable to activate SKDF to induce the leucocyte procoagulant activity. SKDF may play a role in thrombolytic therapy.

Antibodies↗

PubMed1979

Kinetics of the reactions between streptokinase, plasmin and alpha 2-antiplasmin.

Streptokinase reacts very rapidly with human plasmin (rate constant 5.4 S 10(7) M-1 s-1) forming a 1:1 stoichiometric complex which has a dissociation constant of 5 X 10(-11) M. This plasmin-streptokinase complex is 10(5) times less reactive towards alpha 2-antiplasmin than plasmin, the inhibition rate constant being 1.4 X 10(2) M-1 s-1. The loss of reactivity of the streptokinase-plasmin complex towards alpha 2-antiplasmin is independent of the lysine binding sites in plasmin since low-Mr plasmin, which lacks these sites, and plasmin in which the sites have been blocked by 6-aminohexanoic acid, are both equally unreactive towards alpha 2-antiplasmin on reaction with streptokinase. The plasmin-streptokinase complex binds to Sepharose-lysine and Sepharose-fibrin monomer in the same fashion as free plasmin, showing that the lysine binding sites are fully exposed in the complex. Bovine plasmin is rapidly inhibited by human alpha 2-antiplasmin (k1 = 1.6 X 10(6) M-1 s-1) and similarly loses reactivity towards the inhibitor on complex formation with streptokinase (50% binding at 0.4 microM streptokinase).

Binding, Competitive↗

PubMed1994

Engineering and production of streptokinase in a Bacillus subtilis expression-secretion system.

Streptokinase is one of the major blood-clot-dissolving agents used in many medical treatments. With the cloned streptokinase gene (skc) available, production of the secreted streptokinase from various Bacillus subtilis strains was studied. The use of the six-extracellular-protease-deficient strain, WB600, greatly improved the production yield of the secreted streptokinase. A modified skc which has the original skc promoter and signal sequence replaced with the B. subtilis levansucrase promoter and signal sequence was also constructed. B. subtilis carrying either the wild-type or the modified skc produces streptokinase at a comparable level. Even with WB600 as the expression host, a C-terminally-processed streptokinase was also observed. Through region-specific combinatorial mutagenesis around the C-terminal processing sites, streptokinase derivatives resistant to C-terminal degradation were engineered. One of the derivatives showed a 2.5-fold increase in specific activity and would potentially be a better thrombolytic agent.

Amino Acid Sequence↗