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PubMed1984

Early bypass grafting following intracoronary thrombolysis with streptokinase.

Early bypass grafting following intracoronary thrombolysis with streptokinase may be indicated in patients with acute coronary artery thrombosis and severe coronary disease. To evaluate this approach, we prospectively studied 41 patients (32 men and nine women, mean age 53 years) with acute infarction. Emergency cardiac catheterization was performed within 18 hours after onset of chest pain and intracoronary streptokinase was given. All patients underwent bypass 3 to 10 days later (mean 7 days). Serial gated radionuclide left ventricular angiograms to determine ejection fraction were obtained on hospital admission, preoperatively, and 3 to 6 months later. Thirty-four patients had complete occlusion of the artery supplying the infarcted segment. In 30 patients (88%) reperfusion was not successful. In seven patients the artery was not totally thrombosed. Thirty-two patients (78%) had multivessel disease. An average of 2.8 grafts per patient were placed with an operative mortality of 2% (one patient). Serial measurements of ejection fraction were obtained in 23 patients in whom the admission ejection fraction was less than 50%. There was a significant increase in ejection fraction from admission (33% +/- 11%) to the preoperative measurement (41% +/- 9%, p less than 0.001), and this improvement persisted at follow-up (40% +/- 14%). Intracoronary streptokinase has been shown to restore blood flow to infarcting myocardium and to improve left ventricular performance. In patients with significant organic stenosis, the risk of bypass grafting 3 to 10 days after intracoronary streptokinase infusion appears to be no different from the risk of elective operation performed at a time remote from an acute infarction.

Adult↗

PubMed1983

The international registry to support approval of intracoronary streptokinase thrombolysis in the treatment of myocardial infarction. Assessment of safety and efficacy.

The data from 224 cases of acute myocardial infarction treated with intracoronary streptokinase plus standard coronary care unit management and 178 cases of acute myocardial infarction treated solely with standard coronary care unit management were reviewed to assess the efficacy and safety of the intracoronary administration of streptokinase during evolving myocardial infarction. Successful recanalization of the occluded infarct-related coronary artery was achieved in 176 of 224 streptokinase-treated cases (79%). The incidence of in-hospital postinfarction complications was lower and the mean left ventricular ejection fraction was improved in the successfully reperfused group. The in-hospital cardiac mortality in the reperfused patients was 4.5%. The intervention with coronary angiography and intracoronary streptokinase was generally well tolerated. Adverse reactions were relatively infrequent and were controlled with standard treatment.

Cardiac Catheterization↗

PubMed1981

[Reabsorption of standardised intramuscular haematomas in rabbits treated with streptokinase per os (author's transl)].

Standardised i.m. haematomas in rabbits were studied with and without oral administration of Varidase (containing streptokinase and streptodornase). 125I-fibrinogen was mixed with 2 ml of rabbit blood and reinjected i.m. The standardised haematomas were reabsorbed after 12 to 14 days. During the 3-day administration period of streptokinase the counts measured over the haematoma were even higher than in control animals. As during the therapy a high fibrinolytic activity was found, additional spontaneous bleeding into the haematomas may be suspected. When oral administration of streptokinase was stopped the decrease of counts detected in those animals was significantly accelerated as compared to non-treated animals. This indicates an accelerated reabsorption of those haematomas treated with streptokinase in a low concentration. These results were confirmed by microscopic findings.

Absorption↗

PubMed1980

[Effectiveness and the methods of using streptokinase in myocardial infarct and preinfarct stenocardia].

The effectiveness of streptokinase treatment of patients with myocardial infarction as compared to the control group and patients given anticoagulants is analysed. It is shown that the frequency of recurrent myocardial infarctions, congestive circulatory insufficiency, shock, and thromboembolic complications is lower in the group of patients treated with streptokinase than in the control group. Streptokinase improves the course of the disease and the prognosis in patients with preinfarction angina pectoris. The effect of streptokinase is higher in the first 3--6 hours after the development of myocardial infarction and in individuals under the age of 65. The effectiveness of the treatment does not diminish when the drug is injected for a short time and in small doses (300,000--750,000 U).

Angina Pectoris↗

PubMed1993

Thrombin generation induced by the intrinsic or extrinsic coagulation pathway is accelerated by streptokinase, independently of plasminogen.

Thrombolytic therapy paradoxically induces the formation of fibrinopeptide A, fibrin degradation products and thrombin-antithrombin complexes, indicating thrombin generation. Part of the mechanism of this thrombin generation under the influence of thrombolytic agents was unraveled in this study. We measured thrombin with a chromogenic substrate at several time intervals after recalcification of citrated plasma which had been preincubated with urokinase, streptokinase, recombinant tissue plasminogen activator (rt-PA) or recombinant single-chain urokinase-type plasminogen activator (rscu-PA). Thrombin generation induced by the addition of thromboplastin together with calcium (extrinsic pathway) was greatly accelerated in the presence of streptokinase (from about 7 to 2 min), and to a lesser extent in the presence of urokinase, rt-PA or rscu-PA. Similar effects were seen after the addition of calcium to the plasma containing the thrombolytic agent and preincubated with partial thromboplastin (intrinsic pathway). Hirudin quenched the conversion of the chromogenic substrate completely, confirming that thrombin was the active enzyme. Aprotinine did not affect the results, and the effect of streptokinase was also observed in plasminogen-depleted plasma. We conclude that streptokinase, and to a lesser extent other thrombolytic agents, activate the prothrombinase complex directly or indirectly through a calcium-dependent mechanism, independently of plasminogen, with a resulting acceleration of thrombin generation.

Blood Coagulation↗

PubMed1993

[Assessment of outcome in treatment of cardiac shock after myocardial infarction with intravenous streptokinase].

In 1986 a prospective randomized study coordinated by the Institute of Cardiology in Warsaw was started in 10 teaching cardiology hospitals in Poland for assessment of the results of treatment with intravenous streptokinase infusion in acute myocardial infarction. The studied population comprised 927 patients admitted to intensive treatment units within 6 hours after the onset of infarction pain. For the groups treated with streptokinase or heparin 752 patients were selected at random. In 175 cases the administration of streptokinase was contraindicated. These patients received conventional treatment and served as controls. The age of the patients was from 38 to 70 years, mean age 57.6 +/- 9.3 years. In 105 out of 927 cases cardiac shock was diagnosed. In the groups of early shock during hospitalization the death rate was 82%. No statistically significant difference was found in the death rates between patients with cardiac shock treated with heparin or with streptokinase.

Adult↗

PubMed1993

Intra-arterial streptokinase in acute ischaemic stroke. A pilot study.

AIMS: To assess the safety and efficacy of the intra-arterial administration of streptokinase within 24 hours of acute ischaemic stroke. METHODS: Patients who presented to the Austin Hospital casualty department between 3 and 22 hours after an acute stroke were considered for the study. Eligible patients had pretreatment non-contrast computed tomographic scans of the brain to exclude haemorrhage. Streptokinase (250,000 units) was administered directly into the common carotid artery or the cervical portion of the internal carotid artery. MAIN OUTCOME MEASURES: The incidence of symptomatic and asymptomatic cerebral haemorrhage, haemorrhagic transformation of infarction, angiographic reperfusion, clinical outcome at seven to 10 days and the frequency of other complications. RESULTS: Thirteen patients were treated over a 16-month period. Major clinical improvement occurred in five patients (39%) at 48 hours. This was associated with angiographically demonstrated recanalisation of a middle cerebral artery occlusion in two patients and partial recanalisation in two others. Significant hypotension in two patients required therapy to be stopped. In five other cases mild hypotension developed but the streptokinase infusion was completed. Haemorrhagic transformation of the infarct occurred in four patients without clinical deterioration. CONCLUSION: Intra-arterial administration of streptokinase is safe in selected patients with acute ischaemic stroke. The theoretical benefit of an increased local thrombolytic effect and reduced systemic complications, compared with the use of higher intravenous doses, justifies a randomised clinical trial. If therapies such as this are to be successful, rapid referral to an appropriate centre is necessary.

Aged↗

PubMed1993

[Myocardial infarction treated within 4 hrs: comparison of the cost-benefit ratio of 3 thrombolytic treatments: APSAC, rt-PA and streptokinase in 270 patients].

Two hundred and seventy patients under 71 years of age with myocardial infarction less than 4 hours old, defined by clinical and electrocardiographic criteria, were included in this trial and followed up for 1 year: two groups of 89 and 92 patients were randomised to receive APSAC (30 mg i.v. over 5 minutes) or rt-PA (10 mg bolus + 5000 IU of heparin as a bolus, followed by 90 mg rt-PA over 3 hours) and compared with a control series of 89 consecutive patients treated with streptokinase (1.5 MU in 1 hour). Heparin and aspirin (250 mg/day) were prescribed systematically. A score of efficacy was established from the following 4 parameters: patency of the infarct-related artery on coronary angiography at day 6 +/- 2 (N = 252), dyssynergic score on radiological ventriculography, infarct size on resting Thallium myocardial scintigraphy performed between day 15 and 21 (N = 242) and radionuclide ejection fraction performed at the same time. This score (0-24) was respectively 17.8 +/- 6.4 for rt-PA, 17.7 +/- 6.0 for APSAC and 18.1 +/- 6.0 for streptokinase (NS). The costs of hospital treatment were assessed by including: the cost of thrombolytic therapy (ranging from 1.7% of total cost for streptokinase to 16% for rt-PA), the cost of other treatments and biological investigations (10% of total cost); the cost of followed coronary angiography, in 33% of patients, by an angioplasty (21% of total cost), the cost of hospital stay averaging 17 days (49% of total cost in the rt-PA and APSAC groups and 56% in the streptokinase group NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Cost-Benefit Analysis↗

PubMed1996

A comparative study of intravenous accelerated streptokinase dose regimen with conventional dose regimen for coronary thrombolysis.

The aim of this study is to test the patency rate and safety of the accelerated streptokinase dose regimen for coronary thrombolysis compared with the conventional one. One hundred and four patients entering three hospitals up to 12 hours after the onset of definite acute myocardial infarction were randomizely treated with intravenous accelerated streptokinase dose regimen (1.5 million units/30 min) (group A, 47 cases) and conventional dose regimen (1.5 million units/60 min) (group B, 57 casese). The reperfusion rate of infarct-related arteries determined by clinical evidence of reperfusion was 76.6% (36/47) in group A VS 61.4% (35/57) in group B. There was significant difference in reperfusion rates among patients within 6 hours after the onset of chest pain: 87.9% (29/33) in group A VS 67.4 (29/43) in group B (P < 0.05). The incidence of mild bleeding, allergic reaction, hypotension was 12.8% (6/47), 4.3% (2/47), 12.8 (6/47) respectively in group A vs 21.1 (12/57), 3.5 (2/57), 17.5% (10/57) respectively in group B. Compared to conventional dose regimen, intravenous accelerated streptokinase dose regimen for coronary thrombolysis seems to improve reperfusion rate markedly without increasing adverse events such as bleeding, allergic reaction and hypotension. It suggests that accelerated streptokinase therapy deserves more extensive investigation.

Aged↗

PubMed1979

[The heterogeneity of streptokinases].

Purified streptokinases of some strains of different types of Strep. pyrogenes (group A) as well as streptokinases of a strain of group C or group G streptococci, resp., were studied in regard of their heterogeneity. Differences of the streptokinases were found in their amino acid compositions and in isoelectric points. Serological differences were detected by a quantitative precipitation reaction with fluorescein-coupled antistreptokinase antisera from the goat as well as by neutralization reactions of the activator activities of the streptokinases by antistreptokinase antisera obtained from guinea pigs.

Amino Acids↗

PubMed1979

[Animal experimental studies on fibrinolysis with streptokinase].

In contrast to rabbit blood plasma, in guinea pig and rat blood plasma activation of fibrinolysis by streptokinase is achieved after addition of human plasminogen or human plasma only. A simple experimental procedure for testing application forms of streptokinase in rats is described. Fibrinolysis in vivo is more effective after subsequent administration of human plasma and streptokinase in rats than after administration of a mixture of human plasma and streptokinase (activator).

Animals↗

PubMed1998

[The absence of a procoagulant effect after TNK-t-PA: a comparison with streptokinase and rt-PA].

A limitation of current fibrinolytic drugs is the procoagulant activity induced by their administration. TNK is a mutant of tissue plasminogen activator (t-PA) with high fibrin specificity, resistance to plasminogen activator inhibitor-1 and slow plasma clearance, which is administered in a single intravenous bolus. In this study we investigated the procoagulant effect of TNK-t-PA compared to streptokinase, rt-PA or no thrombolysis. Twenty-nine patients with acute myocardial infarction, treated within 6 hours of symptom onset with 1.5 MU streptokinase over 1 hour (n = 12), 100 mg rt-PA in 1.5 hours (n = 12) or 30-40 mg TNK-t-PA in 15 s (n = 5), were studied and compared to 7 patients with contraindications to thrombolysis (control group). All patients received a similar i.v. heparin regimen for at least 24 hours. Blood samples were drawn before the start of treatment (time 0) and after 2 hours. Thrombin formation was assessed as plasma concentrations of thrombin-antithrombin complex (TAT). The four patient groups did not differ significantly in age, sex, time to treatment, infarct location, and TAT values at time 0 (mean value +/- standard error of the mean 9 +/- 2 micrograms/l). Mean TAT levels at 2 hours were 26 +/- 6 micrograms/l in streptokinase treated patients (p = 0.005 vs time 0), 21 +/- 4 micrograms/l in rt-PA treated patients (p < 0.05 vs time 0), 5 +/- 0.6 micrograms/l in TNK treated patients, and 4 +/- 0.4 micrograms/l in controls (NS vs time 0 for TNK and controls). In conclusion, our data suggest that, in patients with acute myocardial infarction, bolus TNK-t-PA, unlike streptokinase or rt-PA infusions, is devoid of procoagulant effects, evaluated 2 hours after its administration.

Aged↗

PubMed1995

Streptokinase and Heparin versus Heparin Alone in Massive Pulmonary Embolism: A Randomized Controlled Trial.

To test the efficacy of thrombolytic therapy in massive pulmonary embolism, we conducted a prospective randomized controlled trial. Eight patients were randomized to receive either 1,500,000 IU of streptokinase in 1 hour through a peripheral vein followed by heparin or heparin alone. All patients had major risk factors for deep vein thrombosis (DVT) and were considered to have high clinical suspicion for pulmonary embolism (PE). At baseline all patients had a similar degree of systemic arterial hypotension, pulmonary arterial hypertension, and right ventricular dysfunction. The time of onset of cardiogenic shock in both groups was comparable (2.25 +/- 0.5 hours in the streptokinase group and 1.75 +/- 0.96 hours in the heparin group). The four patients who were randomized to streptokinase improved in the first hour after treatment, survived, and in 2 years of follow-up are without pulmonary arterial hypertension. All four patients treated with heparin alone died from 1 to 3 hours after arrival at the emergency room (p = 0.02). Post-thrombolytic therapy the diagnosis of PE was sustained in the streptokinase group by high probability V/Q lung scans and proven DVT. A necropsy study performed in three patients in the heparin group showed massive pulmonary embolism and right ventricular myocardial infarction, without significant coronary arterial obstruction. The results indicate that thrombolytic therapy reduces the mortality rate of massive acute pulmonary embolism.

Journal Article↗

PubMed1995

Issues Regarding the Use of Heparin Following Streptokinase Therapy.

The success of thrombolytic therapy is dependent upon the balance of fibrinolytic activity and procoagulant activity. Streptokinase produces fibrin degradation products that have anticoagulant effects and may potentially protect against reocclusion. However, streptokinase also activates platelets and thrombin, and the prothrombotic effects may be more marked than after administration of recombinant tissue plasminogen activator (rt-PA). Administration of high-dose, delayed subcutaneous heparin after streptokinase and aspirin has been shown to have some benefits and some risks. The benefits and risks of adding intravenous heparin to aspirin and streptokinase have not been clearly defined.

Journal Article↗

PubMed1983

Spontaneous mediastinal hemorrhage. A complication of intracoronary streptokinase infusion for coronary thrombosis.

A 72-year-old man with a recent inferior-wall myocardial infarction complicated by continued ischemic cardiac pain underwent an intracoronary streptokinase infusion in an attempt to re-establish coronary perfusion. Although the cardiac catheterization and streptokinase infusion were technically uncomplicated, signs of an enlarging mediastinal mass associated with a drop in the hematocrit reading developed in the patient 12 hours after the procedure. Aortography showed no evidence of aortic dissection or laceration. The patient was believed to have a spontaneous mediastinal hemorrhage related to streptokinase infusion.

Aged↗

PubMed1984

Role of intra-arterial streptokinase in treatment of arterial thromboembolism.

We treated 27 cases of arterial thromboembolism, including nine thrombosed grafts, with intra-arterial (IA) streptokinase. Complete lysis without significant residual lesions was achieved in eight (30%) of the cases, and partial lysis with sustained improvement was achieved in an additional six cases (22%). Partial lysis revealing inaccessible residual disease in runoff vessels occurred in four (15%) of the cases, and nine (33%) were primary failures. Surgery was completely avoided in 11 (41%) of the patients, lesser amputations were possible in three (11%), and 18 (67%) avoided major amputation. Grafts lysed faster (35 v 62 hours) and more frequently (seven [78%] of nine v 11 [61%] of 18) than native vessels, but had a higher rethrombosis rate (four [71%] of seven v two [11%] of 11) and a lower late patency rate (two [22%] of nine v nine [50%] of 18). Significant bleeding occurred in one (3.7%) of the patients, and major thromboembolic complications occurred in four (13.8%). None occurred in those treated with concomitant heparin sodium. Better patency and fewer complications were also observed in limbs that were not acutely threatened, when IA streptokinase infusion was completed within 48 hours, and when the occluded segment and runoff vessels were rendered widely patent by IA streptokinase, with the aid of balloon angioplasty when necessary (five [36%] of 14).

Arteries↗

PubMed1986

Intra-arterial fibrinolytic therapy. Efficacy of streptokinase vs urokinase.

This study is a retrospective comparison of the results in 25 low-dose, intra-arterial streptokinase and 12 low-dose intra-arterial urokinase infusions for thromboembolic disease. Intra-arterial streptokinase was successful in 50% of infusions and was marked by significant abnormalities in the coagulation criteria. There was a high incidence of major and minor bleeding (48% overall), which could be attributed to systemic effects of the drug. Urokinase was successful in 100% of infusions, and showed no significant effects on systemic coagulation criteria. There were also fewer complications during urokinase infusion. The average pharmacy cost for a course of intra-arterial streptokinase was $165, while urokinase cost $1142. Despite the significant difference in expense, the increased efficacy and safety of urokinase make it the preferred agent for intra-arterial infusion. Theoretical reasons for the increased effectiveness of urokinase are discussed.

Adult↗

PubMed1989

Differential effects of low-dose tissue plasminogen activator and streptokinase on platelet aggregation.

Despite increasing success with low-dose intra-arterial thrombolysis, early rethrombosis still occurs. Platelet aggregation is thought to play a major part in this process. We have therefore investigated the effects of recombinant tissue plasminogen activator (rt-PA) and streptokinase on platelet function at doses currently used for peripheral arterial thrombolysis. Platelet-rich plasma was stirred at 37 degrees C, with either streptokinase (100, 300 or 1000 units ml-1) or rt-PA (10 (T10), 30 (T30) and 100 (T100) mg l-1), with immediate addition of an agonist for platelet aggregation (thrombin, collagen, adenosine diphosphate (ADP) or adrenaline) at a predetermined threshold dose. Significant inhibition of collagen-induced and adrenaline-induced platelet aggregation was produced with rt-PA at all doses used (P less than 0.05). With adrenaline as the agonist, T100 produced disaggregation to a mean (s.d.) level of 26 per cent. Thrombin-stimulated platelet aggregation was significantly reduced by T100 (P less than 0.001) and T30 (P less than 0.01) only, disaggregation being dose-dependent and complete with T100. Using ADP as the agonist, T100 produced a significant reduction in maximum platelet aggregation (P less than 0.01), and disaggregation was achieved to a mean (s.d.) level of 48(13) per cent. Streptokinase did not produce any significant changes in any parameter of aggregation.

Adenosine Diphosphate↗