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PubMed2001

High dose and short-term streptokinase infusion in patients with pulmonary embolism: prospective with seven-year follow-up trial.

BACKGROUND: High dose and short-term streptokinase infusion has proved to improve survival among few patients with pulmonary embolism and cardiogenic shock, without increasing hemorrhagic complications. However its efficacy and safety in terms of long follow-up and in major number of patients requires to be established. METHODS: Patients with pulmonary embolism proved through high probability V/Q lung scan, suggestive echocardiogram, or deep venous thrombosis were enrolled. All were assigned to receive 1,500,000 IU in one-hour streptokinase infusion. The primary end point was efficacy and safety of streptokinase regimen in terms of pulmonary arterial hypertension, right ventricular dysfunction, perfusion abnormalities, recurrence, mortality and hemorrhagic complications. In long-term follow-up, we assessed functional class, recurrence, chronic pulmonary arterial hypertension, postthrombotic-syndrome and mortality. RESULTS: A total of 40 consecutive patients (47.3+/-15.3 years of age) with large or massive pulmonary embolism were enrolled. In 35 patients high dose and short-term streptokinase regimen reversed acute pulmonary arterial hypertension, clinical and echocardiographic evidence of right ventricular dysfunction and improved pulmonary perfusion without increasing hemorrhagic complications. In acute phase 5 patients died, necropsy study performed in 4 patients showed massive pulmonary embolism and right ventricular myocardial infarction, without significant coronary arterial obstruction. Risk factors for mortality and recurrence were: right ventricular global hypokinesis (p<0.0001), 6 hours or over between onset symptoms and streptokinase regimen (p=0.02), severe systolic pulmonary arterial hypertension (p=0.001) right ventricular hypokinesis (p=0.001), hypoxemia (p=0.02) and right ventricular acute myocardial infarction (p<0.0001). Right ventricular hypokinesis (p=0.02) was the only independent risk factor for recurrence. In a seven-year follow-up of the original 35 patients who survived in acute phase, 2 patients were lost and 33 are alive, in functional class I, without recurrence or chronic pulmonary arterial hypertension. CONCLUSIONS: Our report indicates that among properly selected high-risk PE patients, short-term streptokinase infusion is effective and safe.

Adult↗

PubMed1984

Effects of intracoronary streptokinase and intracoronary nitroglycerin infusion on coronary angiographic patterns and mortality in patients with acute myocardial infarction.

We randomly assigned patients with a clinical diagnosis of acute myocardial infarction to one of four treatment groups: intracoronary streptokinase, intracoronary nitroglycerin, intracoronary streptokinase and intracoronary nitroglycerin, or conventional therapy without initial angiography. Of 124 patients 122 sustained acute myocardial infarction. Initial angiography revealed total occlusion of the coronary artery responsible for infarction in 67 per cent (61 of 91). Acute recanalization occurred in 74 per cent (32 of 43) of patients receiving streptokinase but in only 6 per cent (1 of 18) of patients treated with nitroglycerin alone (P less than 0.01). At angiography of all four groups on Day 10 to 14 the vessel responsible for acute myocardial infarction was patent in 77 per cent (71 of 92) of patients; there was no difference among groups, indicating gradual, endogenous thrombolysis in patients not treated with streptokinase. Patients with subtotal obstruction initially had significant improvement in left ventricular function, significantly lower peak creatine kinase levels, and a trend toward lower mortality than patients with total occlusion initially. Mortality at six months in patients receiving streptokinase (21 per cent, 13 of 62) did not differ significantly from that in patients not treated with streptokinase (10 per cent, 6 of 61). Additional studies will be necessary to assess treatment effects in the angiographic subsets identified by this trial.

Angiography↗

PubMed1986

A prospective randomized clinical trial of intracoronary streptokinase versus coronary angioplasty for acute myocardial infarction.

We randomly assigned 56 patients who presented within 12 hours of their first symptoms of acute myocardial infarction to treatment with either intracoronary streptokinase or coronary angioplasty. The mean (+/- SD) duration of symptoms (3.0 +/- 1.2 hours in the group treated with angioplasty vs. 3.6 +/- 1.8 in the group treated with streptokinase; P not significant) and time to recanalization (4.1 +/- 1.4 hours vs. 4.8 +/- 1.7 hours; P not significant) were similar in both groups. Coronary recanalization was achieved in 83 percent of the patients treated with angioplasty and in 85 percent of those treated with streptokinase (P not significant). Residual luminal stenosis in the coronary artery was significantly decreased after angioplasty, as compared with streptokinase therapy (43 +/- 31 percent of patients vs. 83 +/- 17; P less than 0.001). Residual stenosis of 70 percent or more was present in 4 percent of the angioplasty-treated patients and in 83 percent of the streptokinase-treated patients (P less than 0.01). Ventricular function after therapy was assessed by serial contrast ventriculograms. Increases in both global ejection fraction (8 +/- 7 percent vs. 1 +/- 6; P less than 0.001) and regional wall motion (+1.32 +/- 1.32 SD vs. +0.59 +/- 0.79 SD; P less than 0.05) were greater for the angioplasty group. We conclude that angioplasty and streptokinase produce similar rates of early coronary reperfusion during evolving transmural myocardial infarction. However, angioplasty is significantly more effective in alleviating the underlying coronary stenoses, and this may result in more effective preservation of ventricular function after therapy.

Angiography↗

PubMed1986

A prospective trial of intravenous streptokinase in acute myocardial infarction (I.S.A.M.). Mortality, morbidity, and infarct size at 21 days.

Within six hours after the onset of symptoms of myocardial infarction, we randomly assigned 1741 patients up to 75 years of age to a one-hour intravenous infusion of 1.5 million IU of streptokinase or placebo. At 21 days mortality was 6.3 percent in the streptokinase group and 7.1 percent in the placebo group. Of those treated within three hours of the onset of symptoms, 5.2 percent died in the streptokinase group (n = 477), as compared with 6.5 percent in the placebo group (n = 463). These differences were not significant. The time to peak serum levels of creatine kinase of myocardial origin (CK-MB) after the onset of symptoms was significantly shorter (13.9 vs. 19.2 hours), and the integrated area under the CK-MB curve (CK-MB infarct size) was significantly smaller, in the streptokinase group (P less than 0.02). Angiograms obtained in 848 patients three to four weeks after infarction revealed that the streptokinase group had higher global ejection fractions (56.8 vs. 53.9 percent, P less than 0.005) and regional ejection fractions (all patients in group, P less than 0.005; patients with anterior or inferior infarctions, P less than 0.05). We conclude that beginning intravenous streptokinase infusion early after the onset of myocardial infarction limits the size of the infarct regardless of its localization. There was, however, only a trend toward reduced mortality at 21 days.

Aged↗

PubMed2000

Streptokinase does not activate the complement system.

Streptokinase is an extensively used thrombolytic agent. However, different preparations cause severe hypotension during therapy, partially related to the complement cascade activation. In four ischaemic stroke patients treated with Streptase, an increased level of soluble terminal complement complex (SC5b-9) was measured. In the sera of normal subjects, the increase in SC5b-9 induced by Streptase, Kabikinase and Calbiochem streptokinases was highly significant (P < 0.005). Sigma streptokinase did not activate the complement system. Sigma streptokinase analyzed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis showed a homogeneous band. The other three preparations were contaminated with albumin and other proteins. Based on our in vivo and in vitro data, we conclude that complement activation is related to contamination of different streptokinase products rather than the streptokinase itself.

Acute Disease↗

PubMed1989

Effect of thromboxane antagonism on recanalization during streptokinase-induced thrombolysis in anesthetized monkeys.

The effect of a selective thromboxane A2 (TxA2) receptor antagonist, SQ 30,741, on streptokinase-induced thrombolysis was examined in pentobarbital-anesthetized cynomolgus monkeys. The intimal surface of a stenosed carotid artery was stimulated with 100 microA anodal current to produce an occlusive thrombus. After 45 min of zero blood flow, a 1-h intraarterial (i.a.) infusion of streptokinase (680 U/min) was injected proximal to the thrombus. Five minutes before streptokinase (SK) intravenous (i.v.) infusions of heparin (200 U/kg + 120 U/h) and either SQ 30,741 (2 mg/kg + 2 mg/kg/min, n = 8) or vehicle (1 ml/h saline, n = 7) were started and maintained for 3 h. In four monkeys not given streptokinase or heparin, no recanalization was detected and occlusive thrombi were observed after 3 h. All animals receiving streptokinase were recanalized. SQ 30,741 had no effect on return of flow during streptokinase infusion, but increased average reflows during the second (60%, p less than 0.05) and third hours (159%, p less than 0.01). Average blood flows were decreased from the second to third hours with vehicle (p less than 0.001) and remained stable with SQ 30,741. Thromboxane antagonism also increased minimal blood flows during the third hour (438%, p less than 0.01) and decreased the total time reoccluded by 73% (p less than 0.05). However, SQ 30,741 had no effect on the time to recanalization, the maximum reflow, and both number of animals reoccluded and average number of reocclusions. Fibrinogen levels were equivalently diminished (8%, p less than 0.05), and platelet counts were unaffected in both treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Primary coronary angioplasty versus intravenous streptokinase in acute myocardial infarction: differences in outcome during a mean follow-up of 18 months.

BACKGROUND: Intravenous streptokinase and primary coronary angioplasty are both considered to be effective treatment strategies for patients with acute myocardial infarction. Although primary coronary angioplasty is associated with a high patency rate and a well-preserved left ventricular function, it is not known whether it results in a more favorable clinical outcome in randomized comparisons. METHODS: Clinical data were obtained after a mean follow-up of 18 months (range 6-36 months) after random allocation of 301 patients either to intravenous streptokinase (n = 149) or to primary angioplasty (n = 152). The primary endpoint includes death from cardiac causes and non-fatal reinfarction. The secondary endpoint is a weighted unsatisfactory outcome, one that includes death, stroke, heart failure, shock, ejection fraction lower than 30%, reinfarction, reocclusion and bleeding complications. The need for revascularization procedures was recorded. RESULTS: The relative risk of death from cardiac causes and non-fatal reinfarction in the streptokinase group was 6.1 (95% confidence interval 2.9-12.7) compared with the angioplasty group. There was a lower weighted unsatisfactory outcome score of 0.13 +/- 0.29 in patients randomly assigned to angioplasty compared with 0.34 +/- 0.33 in patients randomly assigned to streptokinase (P < 0.001). Coronary angioplasty or coronary artery bypass grafting, or both, were performed more often in the streptokinase group, with a relative risk of 2.1 compared with patients randomly assigned to angioplasty (95% confidence interval 1.5-3.2). CONCLUSION: Clinical outcome in patients with acute myocardial infarction after a mean follow-up of 18 months was more favorable in patients randomly assigned to primary angioplasty compared with those receiving intravenous streptokinase.

Aged↗

PubMed1993

Streptokinase, but not tissue plasminogen activator, attenuates platelet aggregation in patients with acute myocardial infarction.

OBJECTIVES: To investigate if tissue plasminogen activator (tPA) and streptokinase given during acute myocardial infarction (AMI) have different effects on platelet aggregation which could contribute to the higher reocclusion rate observed after tPA. DESIGN: Open labelled on consecutive patients. SETTING: Coronary care unit. SUBJECTS: Twenty patients with chest pain and ST elevations on an electrocardiogram suggestive of AMI. INTERVENTIONS: Ten patients were treated with tPA (100 mg 3 h-1), 10 patients with streptokinase (1.5 x 10(6) IU 1 h-1). MAIN OUTCOME MEASURES: Before, immediately after and 24 h after fibrinolytic therapy, platelet aggregation was estimated with filtragometry and whole blood aggregometry. Fibrinogen, beta-thromboglobulin, elastase and the fibrinogen-derived peptide B beta 30-43 were also measured. RESULTS: The groups were comparable at baseline. Directly after treatment, streptokinase prolonged aggregation time in filtragometry with 112 +/- 140 s (P < 0.03) and reduced conductance in whole blood aggregometry by 6.2 +/- 6.1 omega (P < 0.03), both tests indicating inhibited platelet function. Fibrinogen decreased 2.5 +/- 1.0 g l-1 (P < 0.02). In the tPA-treated group corresponding changes were 68 +/- 225 s (NS) and 2.5 +/- 7 omega (NS) with no significant reduction in fibrinogen. After 24 h, at which time every patient was on acetylsalicylic acid, aggregation was inhibited in both groups as measured by aggregometry. Directly after fibrinolytic treatment, neutrophils were similarly activated in both groups with increments of elastase and B beta 30-43 by 26 +/- 46 micrograms l-1 (P < 0.03) and 280 +/- 381 pmol l-1 (P < 0.03) respectively (streptokinase) and by 12 +/- 6 micrograms l-1 (P < 0.02) and 919 +/- 856 pmol l-1 (P < 0.02) respectively (tPA). CONCLUSIONS: Despite similar degrees of platelet and leucocyte activation, streptokinase but not tPA treatment appears to inhibit platelet aggregation. One possible reason could be a streptokinase-induced pronounced decrease of fibrinogen and increase of fibrinogen split products. Therefore, further development of adjuvant antiplatelet therapy could be of clinical importance.

Aged↗

PubMed1976

Purification of group C streptococcal extracellular antigens detected with naturally occurring human antibodies: isolation of streptokinase and two previously undescribed antigens.

Twelve antigens were detected in crude group C streptococcal extracellular concentrates, using naturally occurring antibodies in normal human gamma globulin. These group C streptococcal antigens all appeared to be present in crude group A streptococcal extracellular concentrates, although the latter contained additional antigens reactive with the human antibodies. Systematic purification procedures were established for the isolation of the group C streptococcal antigens by a sequence of salting out, hydroxylapatite chromatography, Sephadex G-100 gel filtration, and isoelectric focusing. With such procedures, three of the group C streptococcal antigens were isolated in a relatively pure state. One of the purified antigens was identified as streptokinase on the basis of its fibrinolytic potency, its reaction of identity with two purified streptokinase fractions obtained from other sources, and its high titer in immunodiffusion assays. The most highly purified streptokinase fractions, derived from the 0.1 M sodium phosphate hydroxylapatite eluate, revealed a plasmin-inhibiting effect at high concentrations of streptokinase. This was not seen in the purified streptokinase of equivalent functional and immunological purity that was derived from the 0.2 M sodium phosphate hydroxylapatite peak. Two other streptococcal antigens were also isolated to a high degree during the course of the above study. These were designated antigens X and Y and were found to be unrelated immunologically to each other or to streptokinase. Their isoelectric points were 6.7 and 8.8, respectively, and both were present in group A streptococcal concentrates. Esterase activity was found to be widely distributed in almost all of the fractions obtained in the various purification steps, indicating a high degree of heterogeneity of the streptococcal enzyme. Histochemical staining techniques applied to the immune precipitates formed with human antibodies indicated that none of the antigens detected in crude group C and group A streptococcal concentrates possessed catalase, glucuronidase, glucosaminidase, acid or alkaline phosphatase, arylsulfatase, leucineaminopeptidase, or chymotrypsin enzymatic activities.

Antigen-Antibody Reactions↗

PubMed1991

Immunoglobulin response to intravenous streptokinase in acute myocardial infarction.

OBJECTIVE: To devise assays to assess and follow the specific antibody response in patients treated with streptokinase for acute myocardial infarction. DESIGN: Venous blood samples were collected before treatment with streptokinase started and subsequently at regular intervals over one year. Specific IgG and subclass IgG1 were assessed by an enzyme linked immunosorbent assay. SETTING: Coronary care unit in a general hospital. PATIENTS: 48 patients with acute myocardial infarction: 22 patients had venous blood samples taken at presentation only; serial blood samples were taken from 20 patients who then received thrombolytic therapy with streptokinase and six patients who were unsuitable for thrombolytic therapy. RESULTS: Titres of antibodies to streptokinase were low at presentation in 36 (75%) of the 48 patients. Serial measurements made in 20 patients showed the virtual disappearance of antibody within the first 24 hours. This was followed by a steady increase in the specific IgG1 titre, which peaked at day 14 before gradually declining. Values at one year remained significantly higher than baseline values. There was no evidence of an IgM response in the patients studied. CONCLUSION: Low titres of antibodies to streptokinase were widespread in the population. Antibody was consumed after treatment and the subsequent immunoglobulin rise suggested a secondary immune responses; the recently described neutralising capacity to streptokinase is probably related to this antibody.

Acute Disease↗

PubMed1995

Rescue thrombolysis: alteplase as adjuvant treatment after streptokinase in acute myocardial infarction.

BACKGROUND: In acute myocardial infarction patients who do not reperfuse their infarct arteries shortly after thrombolytic treatment have a high morbidity and mortality. Management of this high risk group remains problematic, especially in centres without access to interventional cardiology. Additional thrombolytic treatment may result in reperfusion and improved left ventricular function. METHODS: Failure of reperfusion was assessed non-invasively as less than 25% reduction of ST elevation in the electrocardiographic lead with maximum ST shift on a pretreatment electrocardiogram. 37 patients with acute myocardial infarction who showed electrocardiographic evidence of failed reperfusion 30 minutes after 1.5 MU streptokinase over 60 minutes were randomly allocated to receive either alteplase (tissue type plasminogen activator (rt-PA) 100 mg over three hours) (19 patients) or placebo (18 patients). 43 patients with electrocardiographic evidence of reperfusion after streptokinase acted as controls. Outcome was assessed from the Selvester Q wave score of a predischarge electrocardiogram and a nuclear gated scan for left ventricular ejection fraction 4-6 weeks after discharge. RESULTS: Among patients in whom ST segment elevation was not reduced after streptokinase, alteplase treatment resulted in a significantly smaller electrocardiographic infarct size (14% (8%) v 20% (9%), P = 0.03) and improved left ventricular ejection fraction (44 (10%) v 34% (16%), P = 0.04) compared with placebo. This benefit was confined to patients who failed fibrinogenolysis after streptokinase (fibrinogen > 1 g/l). In patients in whom ST segment elevation was reduced after streptokinase, infarct size and left ventricular ejection fraction were not significantly different from those in patients treated with additional alteplase. CONCLUSION: Patients without electrocardiographic evidence of reperfusion after streptokinase may benefit from further thrombolysis with alteplase.

Drug Therapy, Combination↗

PubMed1988

Marked platelet activation in vivo after intravenous streptokinase in patients with acute myocardial infarction.

We assessed thromboxane biosynthesis as an index of platelet activation in 6 patients with acute myocardial infarction receiving intravenous streptokinase. Urinary 2,3-dinor-thromboxane B2 and plasma 11-dehydro-thromboxane B2, major enzymatic metabolites of thromboxane A2, were markedly increased after intravenous streptokinase (11,063 +/- 2758 pg/mg creatinine and 33 +/- 10 pg/ml, respectively) compared with levels in patients not receiving thrombolytic therapy (502 +/- 89 pg/mg creatinine and 3 +/- 0.7 pg/ml). Prostacyclin biosynthesis also increased markedly after streptokinase coincident with the increase in thromboxane A2 formation. Administration of aspirin between the time of onset of coronary thrombosis and reperfusion both in man and in a canine preparation demonstrated that this reflected thromboxane biosynthesis de novo and not metabolism of preformed inactive thromboxane B2 washed out from the coronary circulation. Since the platelet is the major source of thromboxane A2, these findings suggest that there is marked platelet activation after coronary thrombolysis with streptokinase. Studies in vitro demonstrated that streptokinase enhanced platelet activation in a dose-dependent manner, resulting in the secondary release of thromboxane A2. The increase in platelet activation and thromboxane A2 biosynthesis may limit the therapeutic effect of intravenous streptokinase in acute myocardial infarction.

Aspirin↗

PubMed1990

Bleeding time prolongation with streptokinase and its reduction with 1-desamino-8-D-arginine vasopressin.

The mechanism by which treatment with thrombolytic agents causes bleeding is not known. Recently, frequency of bleeding events has been shown to correlate with bleeding time, particularly in individuals treated with aspirin. We examined the effects of streptokinase (20,000-60,000 IU/kg) on bleeding time in 40 rabbits pretreated with aspirin, a model for fibrinolytic therapy. We then tested the effects of 1-desamino-8-D-arginine vasopressin (DDAVP) (0.3 microgram/kg), an agent known to reduce bleeding time in a variety of bleeding disorders, in 20 rabbits and compared the results with those of a control group of rabbits receiving normal saline placebo. Aspirin increased the bleeding time from a baseline mean +/- SEM value of 119 +/- 15 to 191 +/- 34 seconds in the control group and from 114 +/- 6 to 188 +/- 18 seconds in the experimental group. The addition of streptokinase increased the bleeding time to 592 +/- 119 seconds in the control group and 810 +/- 114 seconds in the experimental group (p = NS). Subsequent infusion of DDAVP decreased the bleeding time in the experimental group to 302 +/- 29 seconds (p less than 0.01 versus streptokinase) compared with 572 +/- 79 seconds (p = NS versus streptokinase) in the control animals given saline placebo. In a subset of rabbits receiving aspirin and streptokinase (40,000-60,000 IU/kg), samples were obtained for platelet aggregation (n = 16), von Willebrand factor antigen concentration (n = 17), and von Willebrand factor multimer distribution (n = 14). Maximal rates of ADP-induced platelet aggregation were not affected by DDAVP infusion, nor was the plasma concentration of von Willebrand factor antigen, quantified by an immunoradiometric assay, significantly affected by DDAVP infusion. Furthermore, the von Willebrand factor multimer ratio decreased with DDAVP administration. These findings indicate that aspirin and streptokinase combined result in a marked increase in bleeding time that can be reduced by DDAVP. This effect of DDAVP is not accompanied by an increase in platelet aggregation response, plasma von Willebrand factor antigen concentration, or von Willebrand factor multimer ratio.

Animals↗

PubMed1996

One-year results from the Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries (GUSTO-I) trial. GUSTO-I Investigators.

BACKGROUND: In the randomized Global Utilization of t-PA and Streptokinase for Occluded Coronary Arteries (GUSTO-I) trial, 41021 patients received one of four thrombolytic regimens. Patients treated with accelerated tissue plasminogen activator (TPA) had a lower 30-day mortality rate (6.3%) than those treated with the other regimens (7.3%, combined streptokinase groups). METHODS AND RESULTS: Each patient who was alive at 30 days was sent a return postcard to ascertain vital status at 1 year. If the postcard was not returned, the patient (or an alternate specified at randomization) was contacted by telephone. A locator service was used in the United States for patients who could not be located by these methods. Final follow-up was 96% worldwide. One-year mortality rates remained in favor of accelerated TPA (9.1%) over streptokinase with subcutaneous heparin (10.1%, P = .011) and streptokinase with intravenous heparin (10.1%, P = .009). Combination therapy had an intermediate 1-year mortality (9.9%); this outcome was statistically indistinguishable from that with streptokinase (P = .47) but was marginally different from that with accelerated TPA (P = .05). CONCLUSIONS: The 1-year results demonstrated a saving of 10 lives per 1000 patients treated with accelerated TPA versus streptokinase and subcutaneous or intravenous heparin. Combination thrombolytic therapy had an intermediate benefit but offered no advantage over accelerated TPA treatment alone.

Aged↗

PubMed1998

Thrombolytic therapy in acute myocardial infarction: comparison of procoagulant effects of streptokinase and alteplase regimens with focus on the kallikrein system and plasmin.

BACKGROUND: Thrombolytic therapy in patients with acute myocardial infarction (AMI) is hampered by procoagulant effects. In vitro studies have indicated that plasmin stimulation activates the kallikrein-contact-phase system, resulting in thrombin activation. This prospective comparative study was designed to examine the procoagulant effects of streptokinase or alteplase in AMI. METHODS AND RESULTS: Sixty-one patients with AMI received 1.5 million U of streptokinase or front-loaded alteplase (up to 100 mg) and systemic heparin. Twenty-four patients with AMI and no thrombolytic therapy and 30 control subjects were examined for comparison. Molecular markers of thrombin, plasmin activation, and coagulation activities were determined before therapy and serially for up to 10 days. Moderate thrombin (initial thrombin-antithrombin [TAT] complex 18+/-5 versus 4+/-0.3 microg/L, P<0.05) and kallikrein (up to 45+/-4 versus 30+/-1 U/L at 3 hours, P<0.01) activation occurs in patients with AMI. D-Dimers are increased (P<0.01), and plasmin is stimulated (P<0.01). Streptokinase and alteplase increase TAT to 50+/-17 and 51+/-18 microg/L at 3 hours and to 50+/-17 and 33+/-14 microg/L at 6 hours, respectively (P<0.01). Kallikrein activity is elevated (P<0. 01) to 76+/-5 and 71+/-7 U/L at 3 hours and 64+/-6 and 47+/-5 U/L by streptokinase and alteplase, respectively, at 6 hours. Reductions in fibrinogen and increases in D-dimers and plasmin-antiplasmin complexes are more marked (P<0.05 and 0.01) after streptokinase versus alteplase. Correlations were found among TAT, kallikrein activity, and plasmin activation (P<0.01). CONCLUSIONS: The data indicate a more marked procoagulant action of the streptokinase regimen compared with front-loaded alteplase, thus supporting the hypothesis of a plasmin-mediated kallikrein activation with consecutive procoagulant action in vivo.

Acute Disease↗

PubMed1989

Enhanced streptokinase-induced thrombolysis using heparin in a rabbit model.

Heparin potentiation of clot lysis by streptokinase was studied in a rabbit model. Clot was initiated in the rabbit aorta with stasis and thrombin and allowed to naturally propagate proximally until stasis met flow. The clot was allowed to age for 1 h before assigning treatment. Fifteen rabbits (group I) were given streptokinase (10,000 IU/h) and 11 rabbits (group II) were given streptokinase (10,000 IU/h) plus sodium-heparin (120 IU/h). Thrombolytic therapy was continued for 5 h. Clot lysis averaged 30% in group I and 70% in group II. Ten of 11 rabbits in group II had more than 50% clot lysis, whereas only 4 of 15 in group I had this degree of lysis. One group II rabbit and four group I rabbits died prematurely; each was noted to have clot propagation at the time of death. While a trend for amelioration of hypofibrinogenemia was observed in the group receiving both streptokinase and heparin, this difference was not statistically significant. We conclude, in the animal model, that thrombolysis by a combination of heparin and streptokinase is more effective than streptokinase alone. Systemic effects are apparently no worse with the combination.

Animals↗

PubMed2006

[Usefulness of thrombolytic therapy with low doses of streptokinase in acute myocardial infarction].

BACKGROUND: The optimal dose of Streptokinase in the treatment of acute myocardial infarction is not well established. Apparently, the thrombolytic efficacy would not increase with doses over 750,000 units. AIM: To compare the effectiveness and safety of treatment with low doses of Streptokinase, ranging from 500,000 to 750,000 units, in patients with ST elevation acute myocardial infarction. PATIENTS AND METHODS: From September 1993 to September 1998, the GEMI register of patients with acute myocardial infarction, was carried out in 37 hospitals, incorporating 4,938 patients. Of these, 1,631 patients received streptokinase. According to the administered dose of Streptokinase, patients were divided in two groups: 1,465 patients who received 1.5 millions U in 60 minutes (classical therapy group), and 166 patients with ischemic chest discomfort and either ST-segment elevation or left bundle-branch block on the electrocardiogram, who received 500,000 to 750,000 U streptokinase administered in no more than 30 minutes, with heparin, within 0 to 6 hours of symptom onset. Successful reperfusion, mortality, complications, and hospital outcome was evaluated in both groups. RESULTS: The low dose group of patients had a better reperfusion criteria profile. No differences between groups were observed in patient evolution, mortality, maximum Killip classification, post myocardial infarction heart failure, ischemic complications, arrhythmias or mechanical complications. CONCLUSIONS: These results suggest that streptokinase in low doses is at least as effective as classical therapy, in the treatment of ST elevation acute myocardial infarction.

Aged↗

PubMedDate not supplied

[Plasminogen binding with decapeptide and polypeptide fragments of streptokinase].

The plasminogen binding with streptokinase decapeptides, modeling the primary structure of molecule, and chymotryptic fragments of streptokinase have been investigated. The immunoenzymatic assay has shown that plasminogen binds to all streptokinase fragments with the decreasing affinity in the set of fragments: 36 > 30 > 17 > 7 > 11 kDa. Location of the binding sites in streptokinase primary structure was performed using the immobilized decapeptides on plastic pins adopted to IEA. In the presence of 10 mM 6-aminohexanoic acid 11 sites for human Glu- and mini-plasminogens, pig and bovine plasminogens binding have been found. They were of the same location for human, bovine and pig plasminogens. 3 sites were located in plasminogen alpha-domain--T43-A72, N113-T126, Q133-V158, 5 sites in beta-domain--T163-L188, A203-S222, Q239-I264, Y275-L294, T315-L340, and 3 sites in gamma-domain--T361-R362, N377-E392, T397-N410. Participation of linear part of streptokinase polypeptide chain in plasminogen--streptokinase complex formation is suggested.

Amino Acid Sequence↗