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PubMed1987

[Action of streptokinase on the hemostatic indices of rabbits with a toxic lesion of the liver due to carbon tetrachloride].

The rabbits with CCl4-induced hepatic failure have revealed changes in hemostasis responses to streptokinase administration. The main distinction of hepatic dystrophy was the depression of plasma fibrinolytic activity accompanying the decrease in fibrinogen and antiplasmin concentrations. Streptokinase administration to rabbits with productive inflammatory liver disorders produced changes in hemostasis identical to those observed in intact rabbits, fibrinogen levels, however, remained unchanged. The common feature of all the toxic liver disorders is the increase of antithrombin III levels after streptokinase administration, whereas the antithrombin levels in the control animals were decreased.

Animals↗
PubMed1985

Local intra-arterial streptokinase therapy for acute peripheral arterial occlusions. Should thrombolytic therapy replace embolectomy?

Locally administered low-dose streptokinase was used in 13 patients with acute arterial occlusions. Systemic fibrinolytic effects were noted in each of 11 patients in whom some effective thrombolysis was demonstrated. In the two patients with no angiographically demonstrable thrombolysis, a systemic lytic effect was absent. Bleeding complications were frequent (31%). Three patients required amputations and one patient died. The systemic lytic effects of streptokinase appear to be necessary for complete clot lysis. Locally administered streptokinase appears to have no significant benefit compared to high-dose systemic administration. Occlusions accessible to balloon embolectomy should probably be treated surgically, reserving fibrinolytic therapy for inaccessible lesions. More research is needed to clarify the specific indications, as well as to determine optimal methods of administration and dosage.

Acute Disease↗
PubMed1985

[Streptokinase and streptodecase--new inhibitors of gluconeogenesis].

The influence of immobilized streptokinase-streptodecase preparation on the rate of gluconeogenesis in perfused liver of normal and infarcted rats was studied. The preparations were administered in a single dose on the basis of estimated appropriate clinical dosage. It was shown that perfused liver of normal rats can produce glucose from endogenous non-carbohydrate compounds. Polysaccharide dextran carrier, a streptodecase component, leads to the growth of glucose quantity in the perfusate. At the same time, streptokinase and streptodecase suppress sufficiently the rate of gluconeogenesis in normal and infarcted rats. The streptodecase effect is particularly marked and may be connected with the inhibition of endogenous substrate induction of glucogenesis as well as the inhibition of key enzymes. Catabolic activity of streptodecase appears to be weaker than that of streptokinase. It is supposed that streptodecase may be used for the treatment of various other pathologic states apart from myocardial infarction.

Animals↗
PubMed1985

[The conformation properties and conformation stability of streptokinase and its polymer derivative].

The properties and conformational stability of the proteinaceous activator of fibrinolysis--native streptokinase--and its derivative obtained by modification with a linear hydrophilic copolymer based on N-vinylpyrrolidone, were studied by the circular dichroism method. It was shown that polymeric modification of streptokinase had no effect on the secondary structure, while the conformational stability of the modified protein to urea was higher than that of the native one. Studies on thermal stability of both native and modified forms of streptokinase showed that the inactivation rate was lower in the modified form as compared to the native one.

Amino Acid Sequence↗
PubMed1978

Problems of resistant thrombolysis and early recurrent thrombosis in streptokinase therapy.

Problems of resistant thrombolysis and early rethrombosis during and immediately after streptokinase therapy have been studied with sequential phlebography in 39 patients. Early rethrombosis and resistant thrombolysis were found to correlate with the behavior of plasminogen and fibrinogen to streptokinase. Anticoagulants given during streptokinase therapy do not seem to affect these problems in a dramatic way.

Anticoagulants↗
PubMed1983

Experience with streptokinase treatment of major pulmonary embolism.

The efficacy of streptokinase was studied in an open trial on 30 consecutive patients with major pulmonary embolism, affecting at least three lobar arteries in pulmonary angiography. Streptokinase was started on average 26 hours from the onset of symptoms and usually given directly to the pulmonary artery. Conventional dosage was used and adjusted by thrombin time. The average treatment period was 32 hours. 26 patients (87%) survived and made a good clinical recovery. Improvement occurred early: signs of improved pulmonary perfusion appeared usually within four hours. Repeat angiograms in 20 patients showed remarkable increase in pulmonary perfusion and partial but not complete lysis of the emboli. Four patients (13%) died, three of them because of no response and one due to late cardiac arrhythmia. Bleeding requiring blood transfusion occurred in four patients, but caused no late sequelae. It is concluded that streptokinase treatment of major pulmonary embolism is effective and safe in rapidly restoring pulmonary perfusion.

Adult↗
PubMed1983

Controlled multicenter pilot study of urokinase- heparin and streptokinase in deep vein thrombosis.

Thirty-three patients with acute iliofemoral thrombosis were randomly assigned to three treatment groups in a pilot dose-ranging study of thrombolytic therapy in deep vein thrombosis. One group received tissue culture urokinase in a dose of 2,200 I.U./kg/hr, and a second group in a dose of 1,100 I.U./kg/hr following a loading dose of 4,400 I.U./kg given in ten min. Urokinase was administered for 12 hr periods, alternating with 12 hr periods of heparin. A third group received an initial dose of 250,000 I.U. of streptokinase in 20 min, followed by 100,000 I.U./hr. Treatment of all patients continued for three days. At the end of this period little improvement, evaluated by "blinded" interpretation of pre- and post-treatment phlebograms, was found in five out of ten of the higher-dose urokinase patients, seven out of eleven of lower-dosage urokinase patients, and six out of ten of streptokinase patients. Optional treatment for another three days showed little further improvement of urokinase-patients and moderate further improvement in the streptokinase-patients. Neither of the 2 dosage schemes at intermittent application of urokinase appeared to be advantageous. Urokinase treated patients experienced fewer adverse reactions.

Adolescent↗
PubMed1983

Enzyme-linked immunosorbent assay (ELISA) for streptokinase antibodies.

A micro plate Enzyme-linked immunosorbent assay (ELISA), developed for detection of antibodies to Streptokinase, was used to analyze 80 human sera. The aim was to provide a simple method for antibody screening that required neither sophisticated equipment nor a high degree of technological skill. Preliminary results show that ELISA is specific, reproducible and sensitive. Comparative evaluation of the ELISA and the coagulum lysis test for antibodies against streptokinase show excellent correlation. We also evaluated the anti-Streptolysin O titer either by conventional method or ELISA. The sensitivity of ELISA for detecting anti-Streptolysin O antibodies was 3-4-fold higher than that of the hemolytic test. The sensitivity of ELISA for detecting anti-streptokinase antibodies was 10-20-fold higher than that of the coagulum lysis. The Enzyme-linked immunosorbent assay seems to offer some advantages over the more commonly used coagulum lysis test as far as sensitivity is concerned and potentially it is suggested that this method could be usefully employed clinically in human streptococcal infections.

Adult↗
PubMed1983

[Hemopericardium after coronary recanalization with streptokinase in the acute phase of myocardial infarction. Drainage and early aortocoronary bypass on the 4th day].

A case of hemopericardium after coronary recanalisation with streptokinase during the acute phase of myocardial infarction is reported, emphasising the value of routine daily echocardiography in all cases of intracoronary thrombolysis. The patient was a 48 year old man with a primary antero-lateral infarct in whom coronary angiography was performed at the 4th hour, showing total proximal obstruction of the left anterior descending artery. The streptokinase protocol of intracoronary thrombolysis was performed, resulting in recanalisation of the left anterior descending artery at the 30th minute. Improved left ventricular function and persistance of coronary patency were confirmed 14 hours after recanalisation. In the following days the patient showed signs of right ventricular failure with successive echocardiogrammes demonstrating an increasing pericardial effusion. On the 4th day, 600 ml of blood were drained surgically and aorto-coronary bypass carried out on the left anterior descending artery. This procedure maintained coronary patency and the improvement in left ventricular function. Several studies have shown that the hemorrhage of reperfusion only occurs in the zones of necrosis, and thrombolytics, especially streptokinase, may aggravate this condition.

Coronary Artery Bypass↗
PubMed1980

[Control of blood coagulation and complications in long-term streptokinase therapy].

Streptokinase was infused for 103 +/- 25 hrs. in 27 patients (6 with deep vein thrombosis of the leg, 7 with thrombosis of Vv. axillaris and subclavia, 9 with acute massive pulmonary embolism, 3 with chronic artery occlusion, 2 with thrombosis of the retinal vein). Blood coagulation studies were performed repeatedly. Anticoagulation (prolongation of thrombin time to 1 1/2-2 1/2 of normal) could be achieved without additional heparin by reduction of streptokinase to doses as low as 20 000 U/h. Reptilase time correlated significantly with thrombin times. Following 24 hrs. of infusion, PTT was less than 50 sec. and Quick test less than 50% of normal in most instances. No correlation was found between PTT or Quick test and factor II, V, VI, X activities during streptokinase infusion. Bleeding was observed in 18 patients. The infusion was stopped because of bleeding in 3 cases. None of the coagulation tests performed in this study correlated with the incidence of bleeding. Hemoglobin concentration decreased 2,6 +/- 1,6 gr% and this decrease could no be explained by blood lesses.

Female↗
PubMed1980

[Deep venous thrombosis: streptokinase treatment with adaptation of the maintenance dosage].

Prolonged infusion of streptokinase at the customary dose of 100 000 u/h results in undesired plasminogen depletion in many patients. This can be avoided by adaptation of the streptokinase maintenance dose to the presumed rate of plasminogen synthesis of each individual patient. The practicability of this approach was tested in 52 patients who had streptokinase therapy of 3 to 9 days duration for deep vein thrombosis. Twice daily measurements of thrombin time and fibrinogen concentration were performed for immediate clinical surveyance and dosage adjustments. These led to a change from the original 100 000 u/h in most patients: in 65% the dose was reduced and in 10% it was increased. By this measure excessive plasminogen depletion was avoided in 88% of the patients. In them the final maintenance dose ranged from 40 000 to 150 000 u/h. Side effects were similar to those reported for the standard dosage scheme, and clinical results were good with a phlebographic success rate of 91% in recent and 65% in subacute or chronic deep vein thrombosis.

Adult↗
PubMed1976

Streptokinase and urokinase in the treatment of pulmonary thromboemboli; from a national cooperative study.

In Phase I of this study of 160 patients with pulmonary embolism, it was demonstrated that of 12 hours of urokinase accelerated the resolution of pulmonary thromboemboli compared to heparin alone. Phase II compared 12 hours of urokinase, 24 hours of urokinase and 24 hours of streptokinase in 167 patients. All patients had a clinical history and angiographic diagnosis of pulmonary embolism. Patients were randomly allocated to treatment. All physicians making patient observations were unaware of drug assignment. Resolution of the thromboembolism 24-30 hours after therapy had been instituted was determined by pulmonary angiography, lung perfusion scans and cardiopulmonary hemodynamics. Twenty-four hours of urokinase did not demonstrate greater clot resolution than 12 hours of urokinase. Twenty-four hours of urokinase resulted in greater improvement than streptokinase in lung perfusion scans, but not in angiograms. In patients with massive embolism, this difference was statistically significant. Hemodynamic differences varied. Bleeding complications and morbidity due to allergic reactions with streptokinase and urokinase were minimal. There was no statistically significant difference in mortality in the three threatment groups. From the Phase I and Phase II data it is reasonable to conclude that all three regimens of thrombolytic therapy are more effective than heparin alone in accelerating resolution of pulmonary emboli. Thrombolytic therapy offers the clinician an alternative to pulmonary embolectomy.

Clinical Trials as Topic↗
PubMed1975

[Resistance test to streptokinase. Its value in the establishing of a thrombolytic treatment using this enzyme].

The reckoning of the rate of serous anti-streptokinase (ASK) evidenced that 8 p. 100 of the test-sample presented a distinct resistance to Streptokinase (SK), and that this percentage could be more important under certain pathological circumstances. On account of this fact and also because SK injectable preparations may offer a variation in activity, the writers advocate a "preliminary control in vitro" by means of the resistance test to streptokinase that enables one to make sure, for each patient, of the biological efficacy of the drug and to specify the starting posology.

Aged↗
PubMed1993

[Mechanical reperfusion in acute myocardial infarction after failure of thrombolysis with intravenous streptokinase].

AIM: to report the clinical evolution of four patients with acute myocardial infarction that were subjected to immediate coronary angioplasty due to the failure of reperfusion with streptokinase. BACKGROUND: the limitations for the use of thrombolytic agents, an accepted treatment of acute myocardial infarction, or their uncertain results in selected groups of patients has prompted the search for mechanical revascularization infarction subjected to thrombolytic therapy with streptokinase (1.500.000 U i.v.) after administration of hydrocortisone (100 mg i.v.) and acetyl salicylic acid (500 mg od). After 60 min thrombolytic therapy and due to hemodynamic depression with requirement of inotropic agents or the absence of clinical signs of reperfusion, the patients were subjected to coronary angiography. In view of a total occlusion or severe stenosis of the artery responsible for the infarction, an immediate transluminal angiography was performed to improve coronary flow. RESULTS: transluminal coronary angioplasty revascularized arteries with total occlusion or increased the lumen of those with severe residual stenosis. This was accompanied by reduction in pain and hemodynamic improvement. In one patient with complete AV block, conduction was improved and sinus rhythm was recovered. Echocardiographic controls showed preservation of ventricular function with persistence of segmental motility alterations. CONCLUSIONS: transluminal coronary angioplasty can be a revascularization alternative in patients with acute myocardial infarction and failure of reperfusion with systemic streptokinase.

Aged↗
PubMed1993

[Cardiac events after myocardial infarction treated with streptokinase. The prognostic value of symptom-limited ECG on day 7].

One hundred and forty-seven consecutive patients admitted with suspected acute myocardial infarction (AMI) were treated with streptokinase. On day 7 after AMI 107 patients performed a symptom-limited exercise test (bicycle ergometer). Thirty-four of the tested patients developed at least one cardiac event (reinfarction, cardiac death, decided myocardial revascularization) during follow-up (30 months). Exercise induced ST-depression was more frequent among patients with cardiac events than among those without cardiac events (chi 2-test, p < 0.05). With multiple logistic regression analysis (BMPD) the following variables were found to have independent prognostic value for the development of new cardiac events: low maximal heart-rate during the exercise test, long duration of acute symptoms before streptokinase treatment and male sex. Exercise-induced ST-depression had no prognostic value in the BMPD-analysis. Exercise testing can be carried out with safety and supplies prognostic information concerning future cardiac events in patients with streptokinase-treated AMI.

Adult↗
PubMedDate not supplied

[Rescue thrombolysis with repeated doses of streptokinase in acute myocardial infarct. A preliminary report].

In patients with persistent acute ischemia and early reocclusion after thrombolytic therapy, the available therapeutic options are optimum drug pharmacologic treatment or a mechanical revascularization. Recently, repeated doses of the same thrombolytic agent used (rescue thrombolysis) have been considered. We report our experience in seven patients with acute myocardial infarction treated with conventional streptokinase dose, within the first 6 hs after onset of the symptoms, and whom due to persistent myocardial ischemia or early reocclusion, hemodynamic instability, significative area of myocardium at risk, failure of maximal doses of conventional therapeutic and inaccessibility for performed mechanical revascularization, a second dose of streptokinase was successfully employed in the early (1:45 to 2:30 hs) and late (48 to 50:00 hs) phase, without hemorrhagic complications and without hypersensitivity effects. In every case rescue thrombolysis allowed to limit the time of ischemia and the extension of the myocardial infarction, demonstrated by indirect clinical criteria, improvement in hemodynamic instability and in the ventricular ejection fraction, that can be considered as a postinfarction myocardial function index, as well as by the reduced in-hospital mortality. These findings suggest that in patients with acute myocardial infarction treated with thrombolytic therapy, and persistent acute ischemia or early reocclusion, a second dose of streptokinase could be a safe and effective therapeutic option. Our successful results will lead to a prospective trial.

Aged↗
PubMed1996

Conjunctive administration of intravenous heparin attenuates cross-linked fibrin degradation in patients treated with streptokinase.

Increases in thrombin activity occur in patients treated with streptokinase, but conjunctive therapy with intravenous heparin does not appear to improve either the rate of early infarct artery patency or survival in patients with acute myocardial infarction. In a recent study we found that concentrations of fibrinopeptide A, a marker of thrombin-mediated fibrin formation, were lower in the first 3 h in patients treated with intravenous heparin (5000 U bolus followed by a fixed-dose 1000 U/h infusion, n = 14) compared with subcutaneous (12,500 U every 12 h, started 4 h after streptokinse, n = 14) administration, but were increased in both groups of patients, consistent with persistent thrombin activity. To determine whether the differential effects of the intensity of heparinization on thrombin formation were reflected in differences in fibrin degradation, we measured cross-linked fibrin degradation products (XL-FDP) before and 1, 2, 3, 8, 12, and 24 h after streptokinase in the same cohort of patients, with a new ELISA with a D-dimer-specific capture antibody (MAb 3B6) and a fibrin-specific tag antibody (MAb 1D2, Agen, Brisbane, Australia). The incidence of early coronary recanalization assessed by creatine-kinase MM isoforms (increase in activity > or = 0.18%/min), was similar in both groups (79 vs 86%). Concentrations of XL-FDP were similar in patients with and without recanalization, but were lower in patients treated with intravenous compared with subcutaneous heparin at 8 h, but the results did not reach statistical significance (627 +/- 151 ng/ml versus 1007 +/- 157 ng/ ml, p = 0.06), and were significantly lower at 12 h (327 +/- 72 versus 781 +/- 162 ng/ml, p = 0.03 at 12 h) (mean +/- SEM). Concentrations of cross-linked fibrin degradation products were also lower in patients in whom the activated partial thromboplastin time was greater than two times the control, compared with those with inadequate anticoagulation (498 +/- 105 versus 1084 +/- 179 ng/ml; p = 0.02) (mean +/- SEM). Thus, more effective inhibition of thrombin with conjunctive intravenous heparin therapy results in less cross-linked fibrin turnover in the first 12 h after thrombolysis with streptokinase. This probably reflects decreased fibrin formation with therapeutic anticoagulation.

Cohort Studies↗
PubMed1996

[Prognosis of return to work after streptokinase-treated acute myocardial infarction].

In order to assess the impact of thrombolytic therapy on return to work 18 months after a first myocardial infarction 32 patients treated with streptokinase were compared to 30 patients not treated with streptokinase. The study was designed as a historical cohort study. The patients in both groups had continuous chest pain of less than six hours prior to admission and electrocardiographic changes consistent with acute myocardial infarction. The two groups were comparable with respect to medical variables related to their myocardial infarction and to educational level. A total of 17 patients (53%) in the streptokinase group and 16 (53%) among controls had stopped working 18 months after their MI. An association between the treatment and the working status could not be found (relative risk = 1.0) nor could it be found if the figures were corrected for deaths and retirements because of age. In conclusion, this study could not demonstrate any beneficial effect of thrombolytic therapy on the return to work 18 months after an initial myocardial infarction.

Adult↗