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PubMed1986

[Intravenous streptokinase versus heparin in recent acute myocardial infarction. Randomized multicenter study in the Franche-Comté].

A multicentre randomised therapeutic trial was undertaken in 8 hospitals in the Franche-Comté department of France (Belfort, Besançon, Dole, Lons-le-Saunier, Luxeuil, Montbéliard, Vesoul, Pontarlier) in which 101 patients with acute primary myocardial infarction were treated within 5 hours of onset of symptoms with either intravenous streptokinase (1,500,000 U in 30 mn) or conventional heparin therapy. The results were assessed on the clinical outcome, arterial patency in the necrosed territory and global and regional ejection fractions (EF) at the 3rd week. After randomisation, 51 patients were given heparin and 50 received streptokinase. Seven patients died in the heparin group and 4 in the streptokinase group (NS). At the third week, the artery in the necrosed zone was patent in 69% of the heparin group and in 68% of the streptokinase group (NS). The EF was significantly higher in the patients with patent arteries in the necrosed zone than in those with occluded arteries (0.49 +/- 0.12 vs 0.41 +/- 0.15, p less than 0.01). There was no significant difference in EF between the heparin and streptokinase groups. The EF was significantly higher in patients with anterior infarction who received streptokinase than in those who received heparin (0.40 +/- 0.10 vs 0.33 +/- 0.09 p less than 0.05). Segmental wall motion was significantly better at the apex and free wall. There was no significant difference between the two groups in posterior infarction. These results show that reestablishment or maintenance of arterial patency in the necrosed zone improves left ventricular function and that patients with anterior wall infarction are the ones most likely to benefit from streptokinase therapy.

Clinical Trials as Topic↗

PubMed1988

Effect of the thrombolytic agent, streptokinase, on the responses to endotoxemia in conscious rats.

The potential role of coagulation defects as a pathologic mediator in septic shock is well documented, especially as it relates to increased thromboxane formation, thrombocytopenia, and disseminated intravascular coagulation. The present study was designed to determine the effect of the thrombolytic agent streptokinase on the sequelae of endotoxemia in the rat. Conscious male Sprague-Dawley rats were given a bolus intravenous dose of Salmonella enteritidis endotoxin (20 mg/kg; LD90 dose) 5 min after the intravenous administration of streptokinase (10,000 U/kg bolus + 1,000 U/kg/hr infusion), or heparin (100 U/kg bolus + 30 U/kg/hr infusion). The effects of streptokinase or heparin on blood clotting were determined by measuring ex vivo clot formation 1 hr after the administration of endotoxin. In naive and endotoxemic animals, both agents significantly reduced clot formation (P less than 0.05). In endotoxemic animals, streptokinase or heparin improved survival to 70%, compared to 8% survival in the endotoxin + vehicle group (P less than 0.05). The improvement in survival with streptokinase was dose-dependent. Neither streptokinase nor heparin prevented the thrombocytopenia or hemoconcentration which developed in endotoxemic animals. These results demonstrate the potential utility of streptokinase for improving survival in endotoxemia and further confirm the deleterious contribution of coagulation disorders in endotoxic mortality.

Animals↗

PubMed1987

Influence of vessel involvement and early streptokinase therapy on regional and global left ventricular function in acute myocardial infarction.

150 consecutive patients with acute myocardial infarction received 750,000 units of intravenous streptokinase within four hours of pain onset. Angiography was performed on day 6, from which ejection fraction (EF), infarct-related ejection fraction (IREF), and non-infarct related ejection fraction (NREF) were calculated. 50% stenosis was considered to be significant. The streptokinase patients with patent infarct-related arteries who had no evidence of previous myocardial infarction were compared with 82 conventionally treated (without streptokinase) patients who had no evidence of previous myocardial infarction. Sub-group analysis based on vessel involvement, usage and timing of streptokinase was done. Streptokinase was associated with better left ventricular function in all sub-groups if given less than 2 hours after pain onset. In inferior myocardial infarction, streptokinase patients with single-vessel disease had normal EF (67 +/- 8), compared to significantly depressed EF in multi-vessel disease (56 +/- 12, p less than 0.05). This difference is accounted for more by the NREF than the IREF. In anterior infarction, patients with single-vessel disease did only slightly better than multi-vessel disease. In multi- and single-vessel anterior infarction, preservation of function by streptokinase appears to be due to the compensatory ability of the non-infarcted region as well as the residual function of the infarct-related region. region.

Cardiac Output↗

PubMed1971

Streptokinase in recent myocardial infarction: a controlled multicentre trial. European working party.

In this controlled multicentre trial treatment with either streptokinase or heparin was allocated at random to patients suffering from myocardial infarction of less than 24 hours' duration. Treatment with either drug was standardized and lasted for 24 hours. A total of 764 patients entered the trial; 34 patient charts were rejected (including all 28 charts from one centre) because of data failure. On retrospective analysis of the 730 remaining patients the two groups were found to have been comparable at the start.The total hospital mortality was 18.5% of 373 patients allotted to streptokinase treatment and 26.3% of 357 given herapin. The mortality after infusion (24 hours) was 10.6% of 340 patients treated with streptokinase and 17.8% of 320 given herapin (P=0.011). Reinfarction in hospital after the 24-hour period of infusion occurred significantly less often in patients treated with streptokinase (P=0.036). Bleeding from puncture sites and pyrexia occurred more frequently during streptokinase treatment.After exclusion of those patients whose diagnosis was unconfirmed on retrospective assessment, the total hospital mortality rate was 19.0% of 357 patients treated with streptokinase and 27.4% of 339 treated with heparin (P=0.011). These results indicate that in recent myocardial infarction streptokinase was superior to heparin in reducing mortality and reinfarction rate during an average period of six weeks in hospital.

Age Factors↗

PubMed1984

In vitro effects of the acylated streptokinase-plasminogen activator complex BRL 33 575 incubated with normal human plasma.

Thrombolysis with acylated streptokinase-plasminogen complexes is aimed to achieve fibrinolysis without systemic fibrinogenolysis. The p-aminobenzoyl-streptokinase-(Lys)-plasminogen-complex (BRL 33 575) should be particularly useful due to its slow deacylation rate. Unexpectedly, repeated doses of 10 mg of BRL 33 575 (corresponding to 310'000 streptokinase equivalent units) induced systemic effects in patients though less than streptokinase alone. In vitro incubation of normal human plasma with BRL 33 575 at concentrations used in patients resulted in nearly complete consumption of alpha 2-antiplasmin and plasminogen and significant fibrinogenolysis within 3 hr. This demonstrates that - despite of slow deacylation of BRL 33 575 - the small amounts of activator generated are highly efficacious in activating plasma plasminogen under conditions in which no physiological clearance of the free activator takes place. Simulating the calculated activator release from BRL 33 575 by infusing equivalent amounts of streptokinase into plasma resulted in less pronounced effects. This is probably explained by anti-streptokinase antibodies which will neutralize the initially infused streptokinase but will be bound by BRL 33 575. Our in vitro experiments indicate that further clinical studies should be done with lower doses of BRL 33 575 or prolonged dosage intervals.

Fibrinogen↗

PubMed1994

[Actilyse (a recombinant tissue-type plasminogen activator] in the treatment of acute myocardial infarct. Comparison of the effects of Actilyse and streptokinase].

The preparation Actilyse--a tissue plasminogen activator prepared by recombination--is an effective fibrinolytic drug. The authors recorded in a group of 33 patients reperfusion in 91%, evaluated on the basis of indirect criteria. In a group of 18 patients treated with streptokinase reperfusion was achieved in 74%. Based on changes of CK and CK-MB values--an earlier rise of values following Actilyse administration and conversely their more marked increase during subsequent sampling after streptokinase administration--it may be assumed that earlier dissolution of the thrombus in the coronary artery occurs after Actilyse administration, as compared with streptokinase. It may be thus assumed that there is also a smaller necrotic focus after Actilyse treatment, as compared with streptokinase. Early re-occlusion--according to indirect indicators--occurred in 8.6% in the Actilyse treated groups, as compared with 5.9% in the streptokinase treated group. The fibrinogen values decline in the Actilyse group to 40% and in the streptokinase group to 28%. Later enhanced new formation of fibrinogen occurs and the fibrinogen values rise to 160% in the Actilyse treated group and to 250% of the initial value in the streptokinase treated group. The elevated fibrinogen value, as compared with the baseline value, persists for the 12 days of the follow-up. No severe spontaneous haemorrhage was recorded, haemorrhagic manifestations were associated with blood sampling and i.v. administration of drugs only. The necessity to administer blood was due to a complication during puncture of the subclavian vein in one patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1993

[Anaphylactic reaction in streptokinase therapy].

Streptokinase is used worldwide as thrombolytic agent. Indications are deep vein thrombosis, arterial thrombosis and embolism, arteriovenous cannula occlusions, acute coronary artery thrombosis, and acute renal vein thrombosis. The major drawback in comparison with other thrombolytic drugs is its antigenicity. Allergic reactions have been reported but the underlying mechanisms have not yet been fully elucidated. A 58 year-old man with acute myocardial infarction developed an anaphylactic reaction immediately after commencement of streptokinase infusion, although immunological laboratory findings were not affected. The patient had no history of prior exposure to streptokinase, infections with streptococci, or chronic allergic reactions. 2 months after streptokinase therapy increased plasma levels were detected of specific IgG antibodies to streptokinase. The levels of specific IgE antibodies to streptokinase and other anti-streptococcal antibodies were within the normal range. A prick test performed 4 months later with 100 I.U. streptokinase was unremarkable. The problems of such allergic reactions are discussed on the basis of this case report and a review of the literature.

Anaphylaxis↗

PubMed1996

[Results of the North Baden Venous Lysis--NBVL--Study. Prospective phlebographically controlled randomized multicenter evaluation of ultra high versus conventional dose streptokinase in acute thrombosis of the leg and pelvic veins].

BACKGROUND AND AIM: The Nordbaden Multicentre Study on lysis of venous thrombosis was prompted by a lack of randomized studies comparing ultra-high and conventional-dose streptokinase therapy in fresh iliac and leg vein thrombosis. The aim was to compare prospectively the phlebographically monitored results of three courses of ultra-high dosed with those of a 5-day course of conventionally dosed streptokinase treatment and to record any side-effects of fibrinolysis. PATIENTS AND METHOD: 77 patients were randomized to ultra-high-dose streptokinase (group A), and 79 to conventionally-dosed streptokinase (group B) therapy. In 13 patients of group A and 10 of group B, no monitoring phlebography was possible--in 15 patients (9.6%) who broke off treatment prematurely, and in 8 (5.1%) who failed to keep their phlebography appointment. RESULTS: Detailed analysis of the phlebographic findings (main target criterion) on the basis of the IFP score revealed a decrease in the score from 4.55 to 2.41 (47%) for the 64 group A patients after a mean of 2.7 +/- 0.6 courses of treatment with administration of 24 +/- 5.7 million IU streptokinase, and from 4.2 to 2.93 (30%) for the 69 group B patients after a mean of 3.7 +/- 1.2 days of treatment with administration of 8.6 +/- 3.3 million IU (p = 0.007). Of the 281 totally occluded vein segments in group A, 132 (47%) were rendered fully patent, while this was true of 81 (29%) of the 279 total occlusions in group B. Of the 21 incomplete occlusions in each group, 10 in group A and 16 in group B became fully patent. Analysis of subgroups and individual factors showed that the re-establishment of patency in the 45 men in group A was better (55%) than in the 47 group B men (30%); while the women showed no inter-group difference there was an overall difference vis-a-vis the men (p = 0.02). In group A, patients aged over 60 showed better results (61%) than those of the same age in group B (20%) (p = 0.003). The presumably older thrombi were just as readily lysable as fresher ones. Among the 77 group A patients, side-effects occurred significantly less frequently than among the 79 group B patients. For the most part, side-effects were haemorrhage overall (22.1% vs. 35.7%) and urogenital bleeding in particular (6.5% vs. 22.8%); there were no deaths. Women bled somewhat more often than men (35.2% vs. 26.5%), and bleeding was more commonly in patients older than 65 years. CONCLUSIONS: 1. Ultra-high-dose streptokinase treatment of deep venous thrombosis (iliac, femoral, popliteal veins) is more effective (at least in males) and produces less bleeding than conventional doses. 2. Presumably older thromboses (8 to 14 days) are no less responsive to ultra-high dose streptokinase. 3. In view of the higher risk of bleeding in over-65-year-olds, the indication for fibrinolytic therapy must be considered with care.

Adult↗

PubMed1997

[Anti-streptokinase antibodies].

The use of thrombolytics has significantly improved the management of patients with acute myocardial infarction but available molecules remains imperfect: restoration of normal coronary patency in about half the cases, risks of reocclusion, risk of bleeding. Streptokinase (SK), which is the least expensive agent, has disadvantages as do the other thrombolytics. SK, an immunogenic bacterial protein, has another feature: administration of SK leads to an immunitory response with the production of specific anti-streptokinase antibodies. These anti-streptokinase antibodies may interfere with the future administration of a compound containing SK either by inducing an allergic response or by neutralising the SK and making it ineffective. Moreover, anti-streptokinase antibodies, the result of previous streptococcal infections, are present in the circulation. Although the prevalence of anti-streptokinase antibodies in the general population, especially coronary patients at risk of myocardial infarction, is not well known and their potentially harmful effects are even less well known. In particular, the platelet aggregant effect in vitro of these antibodies in the presence of SK was not taken into account in the trials studying the influence of anti-streptokinase antibodies in the results of thrombolysis by SK. The anti-lytic effect of anti-streptokinase antibodies is well documented. For this reason, it is not recommended to readminister SK in patients who have previously been thrombolysed with a product containing SK.

Antibodies, Bacterial↗

PubMed2000

The in vitro efficacy of varidase versus streptokinase or urokinase for liquefying thick purulent exudative material from loculated empyema.

Patients with loculated parapneumonic effusion or empyema are sometimes treated with streptokinase or urokinase in an attempt to facilitate pleural fluid drainage by liquefying the pleural exudate and destroying the fibrin membranes producing the loculation. This study evaluated the effectiveness of streptokinase, urokinase, and Varidase (the combination of streptokinase and streptodornase) in liquefying gummy, purulent, exudative material from loculated empyemas. An empyema was created by injecting 10(8) Pasteurella multocida bacteria into the pleural space of New Zealand white rabbits. Twenty specimens, each containing 0.5 g of purulent material obtained 5 days after empyema induction, were placed in test tubes. Streptokinase (15,000 IU), urokinase (10,000 IU), Varidase (4,000-15,000 IU streptodornase + 15,000 IU streptokinase) or saline was added to five sets of four test tubes each. The amount of nonliquefied material that remained after incubation with the fibrinolytic agents was quantitated. Over the 6-h incubation period, the amount of nonliquefied material decreased from 0.5 g to 0.02 g in the Varidase group but never decreased to less than 0.4 g in any of the other three treatment groups. Liquefaction of thick pleural exudates from rabbits with empyema can be achieved with Varidase but not with streptokinase or urokinase.

Animals↗

PubMed1984

Intravenous versus intracoronary streptokinase for acute transmural myocardial infarction.

In order to compare the thrombolytic efficacy of selective versus systemic administration of streptokinase, we gave this drug by either the intracoronary or intravenous routes to 25 patients during the first 6 hours of acute myocardial infarction. All patients had total occlusion of the infarct-related vessel, unresponsive to intracoronary nitroglycerin. Twelve patients received intravenous streptokinase and 13 received intracoronary administration of the drug. Angiograms were taken prior to and during streptokinase administration. Reopening was achieved in 11 of 13 intracoronary patients and 8 of 12 intravenous patients (P = Ns). Time to reopening was longer (54 minutes) in the intravenous patients than in the intracoronary patients (26 minutes) (P less than 0.05). In this study, intravenous streptokinase reopened infarct-related vessels nearly as often as intracoronary streptokinase, but it took longer. Given the limited access and time to prepare for intracoronary infusion and the ease of intravenous administration, further study of intravenous streptokinase is justified.

Adult↗

PubMed1994

Streptokinase inhibits pulmonary tumor seeding in an animal experimental model.

One aspect of the metastatic process involves entrapment of tumor cells within the microcirculation of organs in a "fibrin-platelet mesh." We postulate that destruction of this mesh by fibrinolysis might discourage tumor seeding, thereby inhibiting metastasis. To study this hypothesis, the effect of intravenous streptokinase on pulmonary tumor seeding was examined in a rodent model. In vitro experiments demonstrated that streptokinase had no cytotoxic or cytostatic effect on the Mtln3 cell line. Pharmacokinetic studies showed that at 30,000 U/kg, streptokinase caused systemic fibrinolysis in the Fischer rat, as demonstrated by the thrombin time and fibrin plate lysis assay. Streptokinase administered at this dose, 30 min after tumor cell injection, caused a significant decrease in pulmonary tumor seeding (median 23.0 in the streptokinase-treated group vs. 67.5 in untreated controls, P < 0.0001, Mann-Whitney U-test). Analysis of fibrin degradation products in the streptokinase-treated group suggested that this effect might be secondary to fibrinolysis. The implications of these findings are discussed.

Adenocarcinoma↗

PubMed1984

Expression of a streptokinase gene from Streptococcus equisimilis in Streptococcus sanguis.

Using recombinant DNA techniques, we introduced a previously cloned streptokinase gene from Streptococcus equisimilis into the Challis strain of S. sanguis (group H). The gene was expressed in the new host under the control of its own promoter and the gene product had biological properties identical to authentic streptokinase. However, the molecular weight of cloned streptokinase (42 K) as expressed by S. sanguis was substantially lower than that of authentic streptokinase (47 K). Since the cloned streptokinase gene encoded a 47 K mature protein, the lowered molecular weight of S. sanguis streptokinase may reflect posttranslational proteolytic cleavage, which leaves the biological activity of the gene product and its serological reactivity unimpaired.

Cloning, Molecular↗

PubMedDate not supplied

Mechanism of the stimulatory effect of 6-aminohexanoic acid on plasminogen activation by streptokinase or tissue plasminogen activator: the role of chloride.

Studies were conducted on the mechanism of the stimulatory effect of 6-aminohexanoic acid (6-AH) during the in vitro activation of human glutamic plasminogen (Glu-Plg) by streptokinase or by tissue plasminogen activator (t-PA) and the possible role of the addition of physiological concentrations of NaCl to the buffer solution. Enhancement by 6-AH was investigated by measuring the rate of plasmin generation using chromogenic substrate H-D-glu-phe-lys-pNA (S-2403). Control studies using plasmin showed that the addition of 6-AH at concentrations below 20 mM did not significantly affect the initial rate of the amidolytic activity of plasmin with or without the addition of NaCl to 0.05 M Tris buffer (pH 7.4). On the other hand, addition of NaCl to the buffer slowed down the initial rate of activation of Glu-Plg by streptokinase or by t-PA while increasing the percent enhancement by 6-AH when compared with the controls. The ratios of the initial rates of plasmin generation in the presence or in the absence of 6-AH were plotted against the inverse of the volume fraction of Glu-Plg, streptokinase or t-PA after serial dilutions. The results showed that when the activation reactions were performed in 50 mM of Tris buffer (pH 7.4), the enhancements by 6-AH were related to its interaction with streptokinase or t-PA, while using the same Tris buffer containing 0.6 % NaCl, the enhancements by 6-AH were related to its interaction with both Glu-Plg and streptokinase or t-PA. However, upon increasing the NaCl to 0.9%, the results showed that the enhancements by 6-AH of the activation of Glu-Plg by streptokinase or t-PA were related to its interaction with Glu-Plg. The results suggested that changes in the concentrations of NaCl play a regulatory role during the activation process.

Aminocaproic Acid↗

PubMed2005

Safety profile of the intravitreal streptokinase-plasmin complex as an adjunct to vitrectomy in the rabbit.

BACKGROUND: The generation of an atraumatic posterior vitreous detachment (PVD), a common goal in vitreoretinal surgery, is a challenge, particularly in children and young trauma patients. Plasmin has been proposed as an adjunct to vitrectomy to enzymatically generate a PVD. Low doses of streptokinase-activated plasmin were tested in human pilot studies. This dose-escalation study assesses the safety range of intravitreal human streptokinase-plasmin in rabbits. METHODS: Plasminogen was isolated from human plasma by affinity chromatography, followed by activation with streptokinase (1:1), to generate the streptokinase-plasmin complex. Enzyme doses from 0.1-7 activity units (AU, in 0.1 ml) were injected into the mid-vitreous of 35 eyes; six control eyes were injected with balanced salt solution (BSS, 0.1 ml). Thirty minutes after injection, a two-port vitrectomy was performed. Fundus and slit lamp examinations were performed on days 1 and 7. On days 2 and 7, bright flash electroretinography was performed and compared with preoperative recordings. Some animals receiving higher doses of streptokinase-plasmin (1-7 AU) were followed clinically and with electroretinography for up to 9 months. RESULTS: A mild-to-moderate inflammatory response was seen in both control and plasmin-treated eyes on day 1, but had disappeared completely by day 7 in most eyes. In the 7 AU group, inflammation was stronger and more protracted. Two of three eyes from this group developed wrinkling of the medullary rays; one of them showed discoloration and traction at the medullary rays in the late follow-up. Electroretinograms (ERGs) of vitrectomized control eyes showed the following changes from preoperative values: 48 h, a-wave -11.10% [no significant (n.s.)], b-wave -14.62% (P=0.046); 7 days, a-wave +9.18% (n.s.), b wave +11.69% (n.s.). For the enzyme-treated eyes: 48 h: a-wave -20.43% (P<0.001), b-wave -9.57% (p<0.001); 7 days: a wave -14.21% (P<0.001), b-wave +2.48% (P<0.001). There was no evidence of dose-dependent ERG changes in enzyme-treated eyes at doses up to 5 AU. Groups of up to 3 AU were investigated by light and transmission electron microscopy, without evidence of toxicity. CONCLUSION: Streptokinase-plasmin doses up to 3 AU were found to be safe when injected into rabbit eyes followed by vitrectomy.

Animals↗

PubMed1982

High-dose, brief intravenous streptokinase early in acute myocardial infarction.

An acute thrombus at the proximal border of a high-grade atherosclerotic obstruction is the usual cause of myocardial infarction. Although intracoronary thrombolysis is potentially an exciting new therapy for reducing the extent of myocardial infarction by lysing coronary clot, a number of major difficulties limit its widespread application. It is a complex procedure requiring intracoronary visualization and infusion within a few hours of onset of symptoms. Since intravenous streptokinase could be widely applied if effective, we and others have wondered whether high-dose, brief-duration intravenous streptokinase infusion given early in myocardial infarction would lyse coronary clots without bleeding. To date we have treated 13 patients within 6 hours of onset of symptoms and with ECG and angiographic evidence of typical myocardial infarction caused by coronary clot. Clot lysis and angiographically proved coronary reperfusion were achieved in 6 patients within 1 hour of starting a systemic intravenous infusion of 850,000 IU of streptokinase. Schroeder et al., in Berlin, West Germany, achieved angiographically proved coronary reperfusion in 11 of 21 patients with acute myocardial infarction following a 30-minute intravenous streptokinase infusion of 500,000 IU. Neuhaus et al., in Göttinen, West Germany, achieved angiographically proved coronary reperfusion in 24 of 39 similar patients within 48 minutes by intravenous infusion of 1,700,000 IU of streptokinase. In these three studies, no serious bleeding occured; left ventricular function was improved in patients who achieved coronary reperfusion. We conclude that rapid intracoronary clot lysis and coronary reperfusion can be achieved early in myocardial infarction by brief-duration systemic intravenous infusion of high-dose streptokinase without a high incidence of serious bleeding.

Clinical Trials as Topic↗

PubMed1988

Short-term infarct vessel patency with aspirin and dipyridamole started 24 to 36 hours after intravenous streptokinase.

The duration of intravenous heparin therapy required to maintain patency of the infarct-related artery after intravenous streptokinase is uncertain. Twenty-eight patients were prospectively treated with 1.5 million units of intravenous streptokinase within 4 hours of onset of chest pain. Intravenous heparin was begun after the streptokinase infusion was complete and was discontinued within 36 hours. Aspirin, 325 mg daily, and dipyridamole, 75 mg three times a day, was begun before the heparin was discontinued. Coronary angiography was performed both at 2 hours after completion of the streptokinase infusion and again at a mean of 8.7 (+/- 3.2) days after the initial catheterization. One patient died after treatment with streptokinase but before early angiography. In 21 of 27 patients (78%), Thrombolysis in Myocardial Infarction trial (TIMI) grade 2 or 3 perfusion in the infarct vessel was observed on initial angiography. Repeat angiograms were available in 17 of the 21 patients with initially patent vessels. Continued patency (TIMI grade 2 or 3) was found in 15 of the 17 patients (88%). Two of the four patients who did not undergo repeat angiography died, and the remaining two patients required coronary artery bypass grafting for unstable angina. Bleeding complications occurred in 6 of 27 patients (22%), with two (7%) requiring surgical evacuation of a groin hematoma. There were no instances of intracerebral bleeding and only two patients required transfusions. Thus, the combination of aspirin and dipyridamole following 36 hours of systemic heparinization after intravenous streptokinase infusion is associated with a reocclusion rate comparable to that which has been reported for more prolonged systemic anticoagulation with fewer hemorrhagic complications.

Angiography↗

PubMed1990

ECG and enzymatic indicators of therapeutic success after intravenous streptokinase for acute myocardial infarction.

Thrombolytic therapy has been documented to result in reperfusion of jeopardized myocardium and reduction in the size of the acute myocardial infarction (AMI). The effect of intravenous streptokinase on a creatine kinase-MB (CK-MB) reperfusion index and an ECG estimate of myocardial salvage was therefore studied in 65 patients with a first AMI, randomized to treatment with streptokinase (n = 33) or placebo (control group, n = 32). Reperfusion was defined as a CK-MB appearance rate constant (k1) greater than 0.185. The final AMI size was first predicted from the admission standard ECG by previously developed formulas based on ST segment elevation. The final AMI size was estimated from the QRS score on the predischarge ECG. Myocardial salvage was defined as a greater than or equal to 20% decrease from predicted to final AMI size. The k1 value in the control group was significantly lower than that in the streptokinase group (median 0.157 versus 0.328; p = 0.0001). Accordingly the reperfusion rate was higher in the streptokinase group than in the control group (88% versus 34%; p = 0.0002). The difference in AMI size (final-predicted) was significantly greater in the streptokinase group than in the control group (median -7% versus +1%; p = 0.0001). Myocardial salvage occurred in 60% and 19%, respectively (p = 0.004). A significant correlation was found between CK-MB reperfusion and ECG salvage: 19 of 20 streptokinase-treated patients with salvage also had reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Creatine Kinase↗