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PubMed1992

Lack of influence of pretreatment antistreptokinase antibody on efficacy in a multicenter patency comparison of intravenous streptokinase and anistreplase in acute myocardial infarction.

Antistreptokinase antibodies present in patients as a result of previous streptococcal infections might theoretically influence the thrombolytic response to streptokinase or anistreplase. The potential influence of antibody, measured as antigen binding to immunoglobulin G, was investigated in a randomized, double-blind, multicenter patency comparison of intravenous streptokinase (1.5 million units/60 minutes) and intravenous anistreplase (30 units/2 to 5 minutes) in patients with acute myocardial infarction. Antibody results were evaluated in 333 patients (from a total study population of 370 patients) less than 76 years of age with ECG evidence of ST segment elevation who could be treated within 4 hours of the onset of symptoms. Variations in pretreatment circulating levels of antibody did not influence angiographically defined early coronary patency rates (Thrombolysis in Myocardial Infarction grade 2 or 3 perfusion, measured at a mean of 140 minutes after therapy was begun) for either streptokinase or anistreplase. Similarly the lytic response represented by systemic plasminogen activation and measured as changes in plasma plasminogen and fibrinogen levels after dosing (at mean times of 90 minutes and 24 hours) was not correlated with baseline antibody levels. Furthermore, pretreatment antibody was not a risk factor for poor outcome in response to streptokinase or anistreplase (reocclusion within 24 hours, in-hospital death, or stroke) and did not correlate with hypotension or allergic-type reactions recorded as adverse events. In conclusion, within the population limits defined by the inclusion and exclusion criteria of the study (patients were excluded if they had received streptokinase or anistreplase within the previous 6 months), pretreatment antistreptokinase immunoglobulin G is not a significant determinant of the efficacy response to streptokinase or anistreplase.

Anistreplase↗

PubMed1991

Early beneficial effect of streptokinase on left ventricular function in acute myocardial infarction.

The effect of intravenous streptokinase therapy on the time course of functional recovery was investigated in a controlled study of 64 patients randomized within 3 hours after the onset of acute myocardial infarction (AMI). Contrast ventriculography was performed 1 to 4 days after AMI and repeated 5 weeks later. Wall motion was analyzed by the centerline method in the central infarct, peripheral infarct and noninfarct regions. In patients with ventriculographic data at the early catheterization, streptokinase-treated patients had less severe hypokinesia in the central infarct region than control patients (-2.9 +/- 0.9 [n = 29] vs -3.4 +/- 0.7 standard deviations below normal [n = 21], p less than 0.05). The benefit of streptokinase was more marked in the peripheral infarct region (-1.5 +/- 0.7 vs -2.1 +/- 0.6, p less than 0.001). As a result, the ejection fraction was slightly higher in treated versus control groups (46 +/- 10 vs 43 +/- 7%, respectively; difference not significant). At 5 weeks, function in the streptokinase and control groups had diverged further because of continued improvement in the streptokinase-treated patients. This study shows that streptokinase benefits left ventricular (LV) function by 1 to 4 days after AMI, earlier than previously reported. The benefit was not limited to the peripheral infarct region, where ischemia might have been less severe, but was also seen in the central infarct region. The implication is that thrombolytic therapy can improve LV function during the period of myocardial stunning, while myocardial function is still recovering.

Adult↗

PubMed1993

Occurrence of hypotension during streptokinase infusion in suspected acute myocardial infarction, and its relation to prognosis and metoprolol therapy.

In all patients who received streptokinase infusion for strongly suspected acute myocardial infarction in 1 hospital during 1989 to 1990, the occurrence of hypotension during infusion is described and related to prognosis. In 54% of patients, the beta blocker metoprolol was simultaneously administered intravenously. The median systolic blood pressure (BP) before infusion was 135 mm Hg, and the median value for the lowest systolic BP recorded during infusion was 100 mm Hg (p < 0.001). A positive correlation between systolic BP before streptokinase and the lowest systolic BP during infusion was found (r = 0.53; p < 0.001). Among patients administered streptokinase and metoprolol, 23% had systolic BP < 90 mm Hg, and 12% had < 80 mm Hg at any time during infusion; corresponding values for patients administered streptokinase only were 47 and 30%, respectively. Patients with the lowest systolic BP < 80 mm Hg during infusion had a mortality during the first 2 weeks of 22 vs 11% for those with between 80 and 100 mm Hg, and 8% for those with > 100 mm Hg (p < 0.001). However, in a multivariate analysis the systolic BP before infusion rather than the lowest systolic BP during infusion was independently associated with death. It is concluded that although patients with low systolic BP during streptokinase infusion have a high mortality, the level of systolic BP before infusion is more strongly associated with the outcome. Simultaneous use of intravenous beta blockade does not increase the occurrence of hypotension during streptokinase infusion.

Adult↗

PubMed1989

Site-specific alteration of Gly-24 in streptokinase: its effect on plasminogen activation.

Oligonucleotide-directed mutagenesis was carried out to replace glycine-24 of streptokinase with histidine, glutamic acid, or alanine. Substitutions with either histidine or glutamic acid resulted in almost complete loss of streptokinase activity but streptokinase replaced with alanine retained its activity. Although streptokinases with histidine-24 or glutamic acid-24 bound normally to human plasminogen, they were not able to generate active plasmin, whereas those with alanine-24 or glycine-24 (wild-type) could generate active plasmin. The results indicate that the small, uncharged alkyl group side-chain on the 24th amino acid residue of streptokinase is indispensable for the activity of the human plasminogen-streptokinase complex.

Alanine↗

PubMed1991

The leader sequence of streptokinase is responsible for its post-translational carboxyl-terminal cleavage.

When the expression of streptokinase from two tac promoter-controlled expression vectors, one of these deleted a putative leader sequence of streptokinase and the other not, was compared, both normal and degraded streptokinase were detected in proteins expressed from the leader-contained vector, but only normal streptokinase was detected from the leader-deleted vector. These findings indicate that the characteristic carboxyl-terminal cleavage of streptokinase is correlated with its leader sequence and occurs during the defective secretion. The homogeneous preparation of streptokinase was facilitated by expressing from this leader-deleted vector.

Base Sequence↗

PubMed1992

On the plasminogen-activating function of streptokinase.

1. Several hypotheses have been advanced to explain the activating function of streptokinase. The predominant hypothesis suggests a stable equimolar streptokinase-plasmin(ogen) complex, activating free plasminogen by an active centre, which is located in the plasmin(ogen) part of the complex. 2. This hypothesis cannot explain a number of phenomena and certain accumulated experimental data, for example: rabbit and bovine plasminogen activation by streptokinase, not forming stable complexes with these plasminogens; possible activation with pH less than or equal to 2, in the presence of urea, during modification of streptokinase tyrosine residues, i.e. when these two proteins cannot form a stable complex. 3. On the basis of acquired experimental data the following concept is suggested: the activating function of streptokinase is oxygen-dependent and is realised with the help of superoxide radical due to the O(2-.)-generating ability of plasminogen and the O(2-.)-converting ability of streptokinase.

Animals↗

PubMed1984

Intracoronary streptokinase in acute evolving myocardial infarction: you can, but should you?

Intracoronary streptokinase infusion is an exciting new technique, it is feasible and relatively safe, and it can restore antegrade coronary flow in 80% of the patients with an evolving myocardial infarction. Current data indicate that successful reperfusion apparently is associated with improved left ventricular function. The ultimate benefit, a significant decrease in mortality, has not yet been established. Furthermore many questions have not been answered: what is the optimal dosage of streptokinase? How should it be administered: systemic, intracoronary or super selective? Which thrombolytic agent should we use? How can we prevent reocclusion? What is the role of PTCA or acute surgery? A major shortcoming of this technique is the impact on equipment and personnel together with the rather low percentage (25%) of patients with evolving myocardial infarction, in whom this technique is applicable. Of course, although not within the scope of this article, this i.c. streptokinase treatment will have to be compared with other interventions which may reduce morbidity and mortality in patients with acute myocardial infarction. Thus, antegrade flow with i.c. streptokinase can be restored in patients with an evolving myocardial infarction. The main question is: should you do so? Until now, management of patients with an acute myocardial infarction has been conservative and is directed to treatment of pain, arrhythmias and heart failure. At the moment this approach can be considered respectable. For those who propose active management and believe in i.c. streptokinase treatment, until now, insufficient scientific data are available to back this up. For those who have doubts, but like to be active, the best is to put their patients in a well-conducted randomized trial. This will eventually resolve the question: you can, but should you? However, even if i.c. streptokinase is proven to be beneficial to the patient, this technique will not receive widespread application because of its great impact on limited health resources.

Arrhythmias, Cardiac↗

PubMed1990

Intravenous streptokinase in the management of a subset of patients with unstable angina: a randomized controlled trial.

We report the results of a randomized controlled trial of intravenous streptokinase in a subset of patients with unstable angina. Seventy-six patients were admitted with prolonged (more than 20 minutes) angina at rest of less than 3 weeks onset. Fifty-two patients continued to have more than 3 episodes of prolonged angina in 48 hours on medical therapy with metoprolol, isosorbide dinitrate, nifedipine and intravenous nitroglycerin. Forty-eight patients consented to enter the study and were randomized into two groups. The first group, of 24 patients, received 1.5 million units of streptokinase infusion and the second group, also of 24 patients, received a placebo. Pain relief within 48 hours was achieved in 19/24 (79.1%) patients after streptokinase infusion as compared to 9/24 (37.5%) of the controls (P less than 0.05). Approximately 90% (17/19) of patients responding to streptokinase therapy were relieved of chest pain within the first six hours as against none in the controls. The incidence of acute myocardial infarction within six months was 12.5% (3/24) in those receiving streptokinase and 25% (6/24) in the controls. Mortality at six months stood at 8.33% (2/24) in the treated patients and 16.6% (4/24) in the controls. Intravenous streptokinase thus appears to be of benefit in patients with angina at rest of recent onset which does not respond to conventional medical therapy.

Angina Pectoris↗

PubMed1991

Anti-streptokinase levels in Indian patients.

Levels of anti-streptokinase antibodies were measured in 75 Indian patients who were divided into three groups. The first group consisted of 25 healthy blood donors; the second group of 25 patients with ischaemic heart disease with stable angina; and the third group of 25 patients with acute myocardial infarction. The mean level of anti-streptokinase for the entire group was 0.37 SD 0.20 million international units (IU) (range 0.09 to 1.15 million IU). There was no significant difference in the anti-streptokinase levels among the three groups. In order to neutralise the anti-streptokinase levels in 90% of the study population, 0.57 million IU of streptokinase was necessary. These levels are more than twice the current Western levels. In the light of this study, it may be necessary to reconsider the adequacy of the conventional dosage of streptokinase while treating acute infarctions in India and, possibly, other tropical countries where prevalence of prior streptococcal infection is high.

Adult↗

PubMed1990

Coronary lesion morphology in acute myocardial infarction: demonstration of early remodeling after streptokinase treatment.

Coronary lesion morphology was analyzed in 72 patients 1 to 8 days after streptokinase treatment for acute myocardial infarction and compared with lesion morphology in a control group of 24 patients with stable angina. In the streptokinase group the infarct-related artery was patent in 55 patients (76%). Compared with stenoses in the stable angina group, there were no differences in the stenosis length, severity, calcification or in the proportion located at an acute bend or at a branch point. However, lesions in the streptokinase group were more often irregular (p less than 0.005) and eccentric (p less than 0.01), had a shoulder (p less than 0.0001), globular filling defects (p less than 0.01), linear filling defects (p less than 0.00005) and contrast staining (p less than 0.05). Plaque ulceration index was higher in the streptokinase than in the stable angina group (6.2 +/- 7.9 versus 3.5 +/- 3.4, p less than 0.001). Of the 72 streptokinase-treated patients, 35 were maintained on heparin infusion until angioplasty 2 to 10 days later. At repeat angiography before angioplasty, globular lesion filling defects seen in eight patients had disappeared, whereas linear filling defects persisted in 7 of 14 cases. Fewer lesions were irregular (p less than 0.0001) and the ulceration index decreased from 7.4 +/- 10.4 to 3.0 +/- 1.6 (p less than 0.001). These data show that the lesion in the infarct-related artery after streptokinase treatment is irregular and often associated with filling defects, perhaps corresponding to plaque fissuring and intraluminal thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗

PubMed1991

Intravenous streptokinase in acute myocardial infarction (I.S.A.M.) trial: serial evaluation of left ventricular function up to 3 years after infarction estimated by radionuclide ventriculography. I.S.A.M. Study Group.

The Intravenous Streptokinase in Acute Myocardial Infarction (I.S.A.M.) trial was a prospective, placebo-controlled, double-blind multicenter trial of high-dose short-term intravenous streptokinase in acute myocardial infarction administered within 6 h after the onset of symptoms. Global and regional left ventricular ejection fractions were determined by radionuclide ventriculography in a subset of 120 patients 3 days, 4 weeks, 7 months, 18 months and 3 years after acute myocardial infarction. In patients with anterior myocardial infarction, left ventricular ejection fraction was higher in the streptokinase than in the placebo group 3 days after acute infarction (49 +/- 14% vs. 40 +/- 11%, p = 0.02). This difference of about 10% units in ejection fraction persisted during the 3 year follow-up period. Among streptokinase-treated patients, regional left ventricular ejection fraction was higher within the infarct zone as well as in remote myocardium throughout the follow-up period. Among patients with inferior infarction, no significant differences between the treatment and control groups were demonstrable with respect to global and regional left ventricular ejection fraction. Thus, intravenous administration of streptokinase within 6 h after the onset of symptoms of acute myocardial infarction preserves left ventricular function over a period of greater than or equal to 3 years in patients with acute anterior myocardial infarction. It improves regional myocardial function within the infarct zone as well as in remote areas. In patients with acute inferior myocardial infarction, benefit from intravenous streptokinase is of only minor degree.

Creatine Kinase↗

PubMed1994

Failure of fixed dose intravenous heparin to suppress increases in thrombin activity after coronary thrombolysis with streptokinase.

OBJECTIVES: This study was designed to define the extent of inhibition of thrombin activity achieved with conjunctive fixed dose intravenous sodium heparin compared with fixed dose subcutaneous calcium heparin in patients receiving intravenous streptokinase for acute myocardial infarction. BACKGROUND: The role of heparin therapy during coronary thrombolysis with streptokinase is controversial, in part because the efficacy of different conjunctive heparin regimens in inhibiting early increases of thrombin activity is not known. METHODS: Twenty-eight patients treated with 1.5 million U of streptokinase and 165 mg of aspirin for acute myocardial infarction were randomly assigned to receive fixed dose subcutaneous heparin therapy (12,500 U every 12 h delayed until 4 h after the end of streptokinase therapy [n = 14]) or fixed dose intravenous heparin (5,000-U bolus followed by 1,000-U/h infusion [n = 14]). Anticoagulation was assessed with serial measurements of activated partial thromboplastin time, and thrombin activity by measuring fibrinopeptide A and thrombin-antithrombin III complex levels. Plasma concentrations of creatine kinase (CK) MM isoforms were measured for 3 h to determine recanalization (increase in activity > 0.18%/min). RESULTS: Recanalization occurred in 27%, 64% and 79% of patients given subcutaneous heparin versus 43%, 76% and 86% of those given intravenous heparin at 1, 2 and 3 h, respectively (p = 0.6). Concentrations of fibrinopeptide A (mean +/- SEM) at 1 h were higher in patients without (n = 5) than in those with (n = 23) CK-MM isoform criteria for recanalization (76.4 +/- 25.7 vs. 25.2 +/- 5.2 nmol/liter, p = 0.02), and at 1, 2 and 3 h were significantly lower with fixed dose intravenous heparin (18.4 +/- 4.8 vs. 46.7 +/- 10.2 nmol/liter at 1 h, p = 0.004) than without heparin. After fixed dose subcutaneous heparin at 4 h, fibrinopeptide A levels were similar in both groups despite lower activated partial thromboplastin times in patients who received fixed dose subcutaneous heparin. However, fibrinopeptide A was not consistently suppressed in either group (fixed dose subcutaneous heparin 8.7 +/- 1.8 nmol/liter vs. fixed dose intravenous heparin 11.8 +/- 5.2 nmol/liter) at 48 h (p = 0.4). No significant changes in the concentration of thrombin-antithrombin III complexes were found between the two groups. CONCLUSIONS: Fixed dose intravenous heparin attenuates increases in fibrinopeptide A early after streptokinase. Subsequent fixed dose intravenous and subcutaneous heparin have similar effects but are relatively ineffective in suppressing thrombin activity, suggesting a role for more potent antithrombin agents during coronary thrombolysis with streptokinase.

Aged↗

PubMed2005

Use of intrapleural streptokinase in experimental minimal clotted hemothorax.

OBJECTIVE: In clotted hemothorax, both thoracocentesis and closed tube thoracostomy will not be able to evacuate the pleural cavity especially if it is minimal. The aim of this study was to assess the effectiveness of intrapleural administered streptokinase on minimal clotted hemothorax without drainage, in order to accelerate the spontaneous resolution and absorption in blunt thoracic trauma. METHODS: Thirteen adult ewes were used for this experiment. The animals were divided into two groups. First group served as the control group (Group C) (n=5) and did not receive any intrapleural fibrinolytic treatment. In both groups, 200 ml of blood was taken from the left jugular vein and injected into the pleural cavity with a serum line through the scope after pleural abrasion. Streptokinase (150.000 U) was diluted in 100 ml of saline and applied to the second group (Group S) (n=5) in second postoperative day. One ewe in each group was sacrificed with a lethal dose of sodium thiopental in postoperative 2nd, 4th, 6th, 8th, and 10th weeks, respectively. When a left posterolateral thoracotomy was performed, pleural thickening and adhesion were evaluated. The lung and pleural tissue samples were taken for histopathologic examination. The slides were examined in a blinded manner. RESULTS: Thoracentesis was performed in all ewes in the second postoperative day and no fluid was detected. There was no allergic reaction in group S after the injection of streptokinase into the pleural cavity. During postmortem macroscopic evaluation, we observed clot in one of the ewes in group C in second postoperative week. A statistically significant difference was found between Group C and S regarding pleural thickening and adhesion (P=0.05). The ewes of Group S had less pleural thickening and adhesion compared to those of Group C. These results were confirmed with histopathological examination. CONCLUSION: We conclude that intrapleural streptokinase increases resolution of clot in the pleural space and decreases pleural thickening and adhesion in experimental minimal clotted hemothorax in ewes. This study has also demonstrated that intrapleural streptokinase can be used without drainage. Use of intrapleural streptokinase without drainage can be a novel therapeutic option for trauma patients with minimal clotted hemothorax after haemorrhage of other organs was excluded.

Animals↗

PubMed2001

There is synergism between high-intensity, low-frequency ultrasound and streptokinase but not with eptifibatide, heparin, and aspirin. Differential effects on fresh and aged blood clots. An in vitro study.

OBJECTIVE: Ultrasound is emerging as a promising modality for recanalization of acutely thrombosed blood vessels, especially when associated with fibrinolytics. We assessed the efficacy of ultrasound combined with saline, heparin, eptifibatide, aspirin, and streptokinase in disruption of fresh as well as aged human blood clots, using an in vitro model. METHODS: Blood clots from five donors, 2-4 or 48 hours old, were cut into 250-400 mg slices and immersed for 1, 15, or 30 min in 10 ml saline containing either heparin, eptifibatide, aspirin, streptokinase, or saline alone. Clots were then randomized to 10 s of 20 kHz ultrasound or immersion alone. After treatment, the percentage difference in weight was calculated. RESULTS: Immersion of fresh clots without ultrasound in eptifibatide and heparin resulted in significantly more clot lysis than immersion in saline, aspirin, and streptokinase. Immersion of aged thrombi without ultrasound in heparin, eptifibatide, and aspirin had no additive effect over immersion in saline. Ultrasound enhanced clot disruption in all five solutions, in each immersion time and both in fresh and aged clots. Heparin and aspirin had no additive effect, compared with saline, on ultrasound disruption of both fresh and aged clots, whereas eptifibatide was less effective than saline. In contrast, streptokinase greatly enhanced disruption of both fresh (P=.004) and aged (P<.001) thrombi by ultrasound. The combinations of ultrasound with saline, heparin, eptifibatide, and aspirin were less effective on aged than fresh thrombi, whereas the combination of ultrasound with streptokinase was equally effective on fresh and aged thrombi. CONCLUSIONS: Using a simple in vitro model, we found that the combination of streptokinase and low-frequency ultrasound had a synergistic effect on disruption of both fresh and aged blood clots. Further studies are needed to assess the role of heparin and antiplatelet agents in augmenting clot disruption by ultrasound in in vivo models of acute and subacute thrombosis.

Aspirin↗

PubMed1985

Randomised trial of intravenous recombinant tissue-type plasminogen activator versus intravenous streptokinase in acute myocardial infarction. Report from the European Cooperative Study Group for Recombinant Tissue-type Plasminogen Activator.

In a single-blind randomised trial in patients with acute myocardial infarction of less than 6 h duration, the frequency of coronary patency was found to be higher after intravenous administration of recombinant human tissue-type plasminogen activator (rt-PA) than after intravenous streptokinase. 64 patients were allocated to 0.75 mg rt-PA/kg over 90 min, and the infarct-related coronary artery was patent in 70% of 61 assessable coronary angiograms taken 75-90 min after the start of infusion; 65 patients were allocated to 1 500 000 IU streptokinase over 60 min, and the infarct-related vessel was patent in 55% of 62 assessable angiograms. The 95% confidence interval of the differences ranges from +/- 30 to -2% (p = 0.054). Bleeding episodes and other complications were less common in the rt-PA patients than in the streptokinase group. Hospital mortality was identical in the 2 treatment groups. At the end of the rt-PA infusion the circulating fibrinogen level was 61 +/- 35% of the starting value, as measured by a coagulation-rate assay, and 69 +/- 25% as measured by sodium sulphite precipitation. After streptokinase infusion, corresponding fibrinogen levels were 12 +/- 18% and 20 +/- 11%. In the rt-PA group only 4.5% of the fibrinogen was measured as incoagulable fibrinogen degradation products, compared with 30% in the streptokinase group. Activation of the systemic fibrinolytic system was far less pronounced with rt-PA than with streptokinase.

Adult↗

PubMed1986

Prevention of subsequent exercise-induced periinfarct ischemia by emergency coronary angioplasty in acute myocardial infarction: comparison with intracoronary streptokinase.

To compare the efficacy of emergency percutaneous transluminal coronary angioplasty and intracoronary streptokinase in preventing exercise-induced periinfarct ischemia, 28 patients presenting within 12 hours of the onset of symptoms of acute myocardial infarction were prospectively randomized. Of these, 14 patients were treated with emergency angioplasty and 14 patients received intracoronary streptokinase. Recatheterization and submaximal exercise thallium-201 single photon emission computed tomography were performed before hospital discharge. Periinfarct ischemia was defined as a reversible thallium defect adjacent to a fixed defect assessed qualitatively. Successful reperfusion was achieved in 86% of patients treated with emergency angioplasty and 86% of patients treated with intracoronary streptokinase (p = NS). Residual stenosis of the infarct-related coronary artery shown at predischarge angiography was 43.8 +/- 31.4% for the angioplasty group and 75.0 +/- 15.6% for the streptokinase group (p less than 0.05). Of the angioplasty group, 9% developed exercise-induced periinfarct ischemia compared with 60% of the streptokinase group (p less than 0.05). Thus, patients with acute myocardial infarction treated with emergency angioplasty had significantly less severe residual coronary stenosis and exercise-induced periinfarct ischemia than did those treated with intracoronary streptokinase. These results suggest further application of coronary angioplasty in the management of acute myocardial infarction.

Adult↗

PubMed1987

Streptokinase for the treatment of acute myocardial infarction: a brief review of randomized trials.

This is a review of the important randomized trials of intracoronary and intravenous streptokinase therapy for treatment of acute myocardial infarction. Trials carried out before 1980 failed to recognize the relations between early coronary reperfusion and myocardial salvage and therefore have not been included in this review. Seven studies on intracoronary streptokinase have been reviewed. The two largest of these studies, the Western Washington trial and the Netherlands trial, show a similar reduction in early mortality. Two other small studies demonstrated a trend toward a reduction in mortality with streptokinase therapy and the other three did not. One small and two large intravenous streptokinase trials are reviewed. Of these, the large GISSI trial in Italy demonstrated a 23% reduction in mortality in patients treated within 3 hours from the onset of symptoms and the Intracoronary Streptokinase in Acute Myocardial Infarction (ISAM) trial showed a similar trend toward reduced mortality. The small Western Washington trial showed an even greater trend toward reduced mortality but this benefit was limited to patients with anterior myocardial infarction who received early therapy. It is concluded that intracoronary and intravenous streptokinase therapy, when initiated within the first 6 hours of acute myocardial infarction, reduces mortality. The therapy is most beneficial for those patients with anterior myocardial infarction and those who can receive therapy within the first 2 to 3 hours from the onset of symptoms.

Clinical Trials as Topic↗

PubMed1982

Complete amino acid sequence of streptokinase and its homology with serine proteases.

The complete amino acid sequence of streptokinase has been determined by automated Edman degradation of its cyanogen bromide and proteolytic fragments. The protein consists of 415 amino acid residues. Sequence microheterogeneity was found at two positions. The NH2-terminal 245 residues of streptokinase are homologous to the sequences of several serine proteases including bovine trypsin and Streptomyces griseus proteases A and B. The sequence alignment suggests that the active-site histidine-57 has changed to a glycine in streptokinase. The other active-site residues, aspartyl-102 and serine-195, are, however, present at the expected positions. Streptokinase also contains internal sequence homology between the NH2-terminal 173 residues and a COOH-terminal 162-residue region between residues 254 and 415. Moderate homology in predicted secondary structures also exists between these two regions. Although streptokinase is not a protease, these observations suggest that it has evolved from a serine protease by gene duplication and fusion. A COOH-terminal region of about 80 residues is apparently deleted from the second half of the duplicated structures. These observations further suggest that the three-dimensional structure of streptokinase likely contains two independently folded domains, each homologous to serine proteases.

Amino Acid Sequence↗