SEARCH · PubMed Health

Results for “STREPTOKINASE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources

PubMed1987

Quantitative and qualitative effects of intracoronary streptokinase in unstable angina and non-Q wave infarction.

Thrombolytic therapy has been shown to be effective in reopening totally occluded arteries in acute myocardial infarction. Coronary thrombus is also believed to play a role in the pathophysiology of unstable angina and non-Q wave infarction. However, few patients with these two acute coronary syndromes have been treated with intracoronary streptokinase. Therefore, 100,000 to 300,000 IU (mean 177,000 +/- 80,000 IU) of intracoronary streptokinase was infused into 36 consecutive catheterized patients who either presented with an acute episode of unstable angina or had had a recent non-Q wave infarction and in whom a less than 100% occluded ischemia-producing artery could be identified. Qualitative techniques utilizing vessel magnification and quantitative analysis with digital subtraction were performed on the ischemia-producing coronary lesion before and immediately after streptokinase therapy and 3 to 10 days later in 18 patients who were restudied at the time of transluminal coronary angioplasty. Before streptokinase treatment, 24 (67%) of 36 ischemia-producing arteries contained eccentric, irregular lesions. The percent diameter stenosis and percent area stenosis in all ischemia-producing arteries averaged 83.8 +/- 8.3% and 94.8 +/- 3.3%, respectively. After streptokinase treatment there were 23 arteries (64%) with eccentric irregular lesions. The percent diameter stenosis and percent area stenosis in all ischemia-producing arteries were similar to pre-streptokinase values (82.9 +/- 5.9% and 93.8 +/- 4.0%, respectively). At restudy, there were also no significant changes in any quantitative or qualitative variable. Five individual patients showed a significant reduction in percent stenosis after streptokinase. This improvement was independent of duration of symptoms, use of heparin before angiography, streptokinase dose or reduction of fibrinogen levels post-streptokinase. Two additional patients deteriorated clinically and developed total occlusion of the ischemia-producing artery within 12 hours of streptokinase infusion. These data suggest that intracoronary streptokinase may be of limited utility in either unstable angina or recent non-Q wave infarction with a less than 100% occluded ischemia-producing artery. In these syndromes, thrombus may be organized or short infusions may be given too late to be effective. In some cases, thrombus may even be absent. Whether longer infusion of streptokinase or other thrombolytic agents will be of benefit remains to be determined.

Adult↗

PubMed2003

Efficacy and safety of a new streptokinase regimen with enoxaparin in acute myocardial infarction.

OBJECTIVE: To compare a new streptokinase regimen combined with either enoxaparin or unfractionated heparin (UFH) and the traditional streptokinase regimen combined with UFH in patients with acute myocardial infarction (AMI). METHODS: 412 patients (<75 years), hospitalized within 6 hours of the onset of chest pain, were allocated thrombolytic therapy by the treating physician: streptokinase 0.75 MU/10 minutes, repeated if no coronary reperfusion after one dose, plus enoxaparin 40 mg intravenously followed by 1 mg/kg bodyweight subcutaneously at 12-hour intervals for 5-7 days (n = 102); the same streptokinase regimen plus UFH 1000 IU/60 minutes intravenously for 48-72 hours ( n = 106); or streptokinase 1.5 MU/60 minutes plus the same UFH regimen (n = 204). All patients received 250-325 mg aspirin/day. Coronary reperfusion rates, 30-day mortality and hemorrhagic complications were recorded. RESULTS: Coronary reperfusion rates with 0.75 streptokinase + enoxaparin (78.4%) and 0.75 streptokinase + UFH (74.5%) were significantly higher than those with 1.5 streptokinase + UFH (62.2%), but there was no significant difference between the groups receiving the new regimen. Overall 30-day mortality (6.3%) was significantly lower than with 1.5 streptokinase + UFH (12.7%) ( p = 0.037). The incidence of major and minor hemorrhagic events was similar in all groups. CONCLUSIONS: The accelerated streptokinase regimen was well tolerated and resulted in a significantly higher coronary reperfusion rate and significantly lower mortality compared with the traditional regimen. The 0.75 streptokinase + enoxaparin combination was at least as efficacious as the 0.75 streptokinase + UFH combination and is preferred because of its ease of administration and predictable anticoagulant effect.

Aged↗

PubMed1992

Prevalence and mechanism of streptokinase-induced platelet stimulation. Effect of acetylsalicylic acid.

It was recently shown that streptokinase may induce clot formation in vivo by immunoglobulin G mediated platelet stimulation. We evaluated the in vitro effect of streptokinase on platelet function in 103 subjects, of whom 52 were < or = 30 years and 51 were > or = 50 years old. Although streptokinase inhibited platelet aggregation in the majority of cases, in nine the threshold concentration of ADP required to induce irreversible aggregation decreased with streptokinase (1 million Units. l-1) by 30% or more. This observation was confirmed in five of the nine by repeated measurements indicating reproducible streptokinase-induced platelet stimulation. Among the five, two were < or = 30, and three were > or = 50 years old. In none of the five subjects did the radio allergo sorbent test detect type E immunoglobulins directed against streptokinase in the serum. In contrast, in four of the five subjects, streptokinase-induced platelet hyperaggregability was suppressed by addition of goat antibodies against human immunoglobulin G, or F(ab')2-fragments of such antibodies. Acetylsalicylic acid did not prevent streptokinase-induced platelet stimulation, but in three of five cases, led to an increase in the control threshold concentration for ADP, so that after the decrease induced by streptokinase the threshold concentration for ADP was in the same range as before acetylsalicylic acid and streptokinase administration. Thus, streptokinase led to an inhibition of platelet aggregation in the majority of subjects evaluated. In a minority of five out of 103, however, streptokinase reproducibly caused platelet stimulation, presumably mediated by immunoglobulin G.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Why do patients develop reactions to streptokinase?

Minor reactions to streptokinase are not uncommon, although the etiology is unknown. It is widely presumed, however, that these, like the more serious immune reactions, are antibody-mediated. We measured specific anti-streptokinase IgG, subclasses IgG1, IgG2, IgG3, IgG4 and IgE by ELISAs, haemagglutination, indirect Coombs' test and immunoblotting in six patients who developed reactions to streptokinase. Evidence of complement activation by streptokinase was sought by a haemolytic complement assay and by measurement of C3, C4 and C3d. The patients who reacted to streptokinase presented with low titres of anti-streptokinase IgG (median = 5; range 0-32) and IgG1 (median = 3; range 0-14). No evidence of any other IgG subclass was found, nor of specific anti-streptokinase IgE. Anti-streptokinase IgG1 was found to fix complement; patients who reacted to streptokinase were found to have low levels of total complement 1 year post reaction. Probable aggregates and fragments of human albumin (added stabilizer) were found in the streptokinase preparation and proved to be antigenic in some patients, but were not found to be related to the development of reactions. The findings suggest that patients who develop reactions to streptokinase cannot be predicted on the basis of antibody titres at presentation. Minor reactions to streptokinase would not appear to be antibody-mediated, although complement activation may be involved.

Aged↗

PubMedDate not supplied

[Effect of streptokinase on the interaction of alpha-2-antiplasmin with different sites of plasmin molecule].

Interaction of streptokinase and alpha-2-antiplasmin with plasmin and plasminogen fragments was compared. Binding sites on the enzyme become half-saturated, streptokinase and alpha-2-antiplasmin concentration being 8.5 and 30 nM, respectively. 6-Aminohexanoic acid in concentration of 20 mM reduces the adsorption of streptokinase and and alpha-2-antiplasmin by 20 and 60%, respectively. From all the investigated fragments, streptokinase shows the greatest affinity for mini-plasminogen and alpha-2-antiplasmin for kringles 1-3. Both proteins in the presence of 20 mM 6-aminohexanoic acid do not bind with kringle domains. Arginine dose 0.1 M does not influence streptokinase adsorption on mini-plasminogen and decreases the value of alpha-2-antiplasmin binding with mini-plasminogen by 50%. The data obtained indicate that plasminogen molecule has the sites of the highest affinity for streptokinase on the serine-proteinase domain, however for alpha-2-antiplasmin it is in the kringles 1-3. Streptokinase with equimolar quantity in respect of alpha-2-antiplasmin inhibits the adsorption of alpha-2-antiplasmin on the plasmin by 70% and in the presence of 6-aminohexanoic acid it is inhibited completely. Addition of streptokinase also increases the influence of increasing concentration of the acid. Inhibiting influence of streptokinase decreases, and that of 6-aminohexanoic acid increases, when plasmin is modified with diisopropylfluorophosphate in its active centre. At the same time maximum inhibition of streptokinase adsorption on the plasmin at different concentrations of alpha-2-antiplasmin and 6-aminohexanoic acid accounts for only 20%. We suppose that in the process of complex formation streptokinase competes with alpha-2-antiplasmin for the binding sites on the catalytic domain of the plasmin. Partial or complete blocking of the plasmin active centre contact zone by streptokinase effectively protects it from inhibition by alpha-2-antiplasmin.

Binding Sites↗

PubMed1987

The isolation and characterization of a ternary human plasmin B-chain-streptokinase-plasminogen complex.

A ternary equimolar human plasmin B-chain-streptokinase-plasminogen complex was isolated from a mixture of the plasmin B-chain-streptokinase complex and human plasminogen at 0 degrees C and 37 degrees C. A ternary complex which was shown to be species specific, was identified and characterized by ultracentrifugal, acrylamide gel electrophoretic, and agarose double diffusion analyses. When mixed at a 1:1 molar ratio at 0 degrees C, 39.9% of the preparation existed as a plasmin B-chain-streptokinase-plasminogen complex; when mixed at 37 degrees C, 86.4% existed as a complex, which was identified by electrophoretic analyses to be a plasmin B-chain-streptokinase-plasmin complex. Sedimentation velocity analyses gave s degrees 20,w values of 3.79 for the plasmin B-chain-streptokinase complex, 4.10 for Lys-plasmin, and 6.23 for the plasmin B-chain-streptokinase-plasmin complex. Sedimentation equilibrium analyses gave molecular weights of 73,900 for the plasmin B-chain-streptokinase complex, 82,900 for Lys-plasmin, and 153,100 for the plasmin B-chain-streptokinase-plasmin complex. The diisopropylphosphorofluoridate (DFP)-inhibited and the p-nitrophenyl-p-guanidino-benzoate (NPGB)-inhibited plasmin B-chain-streptokinase complexes both retained their ability to form a ternary complex with human plasminogen, but this complex did not convert to a plasmin B-chain-streptokinase-plasmin complex. Thus, the active site serine residue is essential for the activator activity of the plasmin B-chain-streptokinase complex, but it is not necessary for the binding of the plasmin B-chain-streptokinase complex to plasminogen to form a ternary complex.

Binding Sites↗

PubMedDate not supplied

Direct effects of streptokinase on the isolated rat myocardium.

The utilization of streptokinase as a thrombolytic agent is prevalent in the management of patients following a myocardial infarction. The present investigation was designed to assess the direct effects of streptokinase infusion on the normal isolated rat heart and on the globally ischemic isolated rat heart. The effects of streptokinase on the mechanical function of the hearts were monitored, as well as the effects on the membrane integrity of the cells, as indicated by enzyme release. The normal hearts were infused with either buffer or streptokinase. Both the normal and streptokinase-treated normal hearts exhibited a decrease in function during the course of each experiment. Under these conditions, there were no significant differences in the values for mechanical function in either group. The release of lactate dehydrogenase (LDH) and creatine kinase (CK) into the coronary effluents was not significantly increased during the infusion of streptokinase. There was a significant increase in the release of nucleosides during the streptokinase infusion period compared with the buffer infusion period. The infusion of either buffer or streptokinase was compared in the preischemic and postischemic rat heart. The values obtained during preischemic infusion with buffer or streptokinase were comparable to the values obtained in the normal and streptokinase-treated normal hearts. There were no significant differences in the values for mechanical function measured during buffer infusion following ischemia compared with those measured during streptokinase infusion following ischemia. In the postischemic hearts, there was a sixfold increase in the release of nucleosides during buffer infusion, whereas only a twofold increase was observed in the postischemic hearts during streptokinase infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1998

Preparation of a novel streptokinase mutant with improved stability.

The novel mutant streptokinase, SK-K59E, can activate human plasminogen as efficiently as the purified commercially available streptokinase. Several peptide bonds including Lys59-Ser60 in native streptokinase were hydrolyzed in reaction with plasmin and peptides of small molecular masses were generated. The plasminogen activator activity of native streptokinase in reaction with human plasmin declined to 25% of the original activity in a 120-min incubation. On the other hand, the NH2-terminal peptide of SK-K59E remained intact in reaction with plasmin and the activator activity of streptokinase decreased to 75% of the original activity in 120 min. The major degraded peptide fragments of native streptokinase in reaction with plasmin had molecular masses of 36 and 30 kDa. However, two major peptide fragments of 42 and 34 kDa were observed in the reaction of SK-K59E with human plasmin. The 42 kDa peptide fragment, which contained NH2-terminal of streptokinase, could activate human plasminogen as efficiently as the native streptokinase. SK-K59E can induce greater degree of caseinolysis and fibrinolysis than the native streptokinase. In conclusion, the results demonstrate that the prevention of cleavage at Lys59 of streptokinase prolongs the half-life of streptokinase in complex with plasmin and that the NH2-terminal of streptokinase (Ile1-Lys59) plays an important role in maintaining its stability.

Enzyme Stability↗

PubMed1959

The streptokinase-plasminogen system. I. Its effect on the pathogenicity of streptococci and other organisms for mice.

Human plasminogen, plasma, or serum increased the pathogenicity of six streptokinase-positive streptococcal strains for mice. Combinations of commercial streptokinase and plasminogen or streptokinase and plasma did not usually increase mouse mortality to a greater degree than did plasminogen or plasma alone, suggesting that the maximal effective amount of streptokinase was produced by the organisms. The pathogenicity of Salmonella paratyphi (fibrinolysin variable) and a Group D streptococcus (streptokinase-negative) was not increased by plasminogen, plasma, or streptokinase, whereas a combination of streptokinase and plasminogen, or streptokinase and plasma did significantly increase mouse mortality resulting from these organisms. Combinations of certain concentrations of streptokinase and plasminogen increased the pathogenicity of a fibrinolysin-negative staphylococcal strain for mice to a greater extent than did either substance alone. The observed results provide evidence that streptokinase, by an interaction with plasminogen, contributes to the pathogenicity of streptokinase-positive streptococci.

Animals↗

PubMed1975

[The technique of quantitative determination of streptokinase in the patient's plasma (author's transl)].

A method of a quantitative determination of plasma streptokinase concentrations in patients undergoing streptokinase infusion is described. The principle of this method is based on the clot lysis time recorded by the thromboelastograph. The test clot constituents were bovine fibrin, bovine plasminogen, human euglobulin, EDTA, human plasma (of unknown streptokinase quantity) and thrombin. As rather high concentrations (fixed excess) of plasminogen (euglobulin) and fibrinogen were present in the test coagulum, no interference with changing plasminogen and fibrinogen levels of the patient's plasma was observed. Furthermore, due to high EDTA concentrations, no interaction with platelet functions and coagulation factors took place. The standard deviation in measuring 2 u streptokinase in 1 ml human plasma was determined as s = +/- 0.19 u/ml, of 5 u streptokinase at s = +/- 0.47 u/ml and of 20 u streptokinase at s = +/- 2.5 u in 1 ml of human plasma. Plasma samples of patients undergoing fibrinolytic treatment were investigated with regard to their streptokinase content. Streptokinase concentration values varied between 0.7 u and 15 u/ml plasma. The average half life of streptokinase in the organism was 18 min. The decay of streptokinase in plasma at different temperatures and over various periods of time was also determined. A considerable loss of streptokinase in the plasma during storage at room temperature could be observed. Therefore, the determination procedures should be carried out without delay.

Animals↗

PubMed1982

Streptokinase-dependent delayed activation of horse plasminogen.

Complete activation of purified horse plasminogen to plasmin was obtained with a 1:10 molar ratio of streptokinase to plasminogen after 5 min of incubation at 37 degrees C. At a 1:1 molar ratio, maximal activity did not appear until 15-30 min, while at a ratio of 6:1 complete activation was delayed for 120-180 min. Gel filtration studies of isotopically labeled streptokinase and horse plasminogen suggest that the delay was due to impaired formation of a streptokinase-plasminogen complex. The predominant streptokinase moiety within the streptokinase-plasmin complex which forms from the streptokinase-plasminogen complex had a molecular weight of about 25000. The streptokinase-horse plasmin complex activated bovine plasminogen and was relatively stable. Native streptokinase was rapidly modified by horse plasmin predominantly to a fragment with a molecular weight comparable to that of the streptokinase moiety within the horse streptokinase-plasmin complex, about 25000 daltons. Partial characterization of horse plasminogen revealed no striking differences from human plasminogen in terms of molecular weight, N-terminal analysis and amino acid composition. However, horse plasminogen did not react with antibodies to human plasminogen, and its isoenzymes were more acidic than those of the human. Further characterization of horse plasminogen will be required to ascertain whether activation by streptokinase can serve as a model for the altered kinetics which have recently been described for the activation of aberrant types of human plasminogen.

Amino Acids↗

PubMed1993

Serum cholesterol concentration before and after streptokinase in acute myocardial infarction.

OBJECTIVE: To determine if serum cholesterol concentration should be measured before or after streptokinase therapy within the first 24 h of myocardial infarction. DESIGN: Prospective study of patients receiving streptokinase therapy for acute myocardial infarction (AMI). SETTING: Coronary care unit of a district general hospital. SUBJECTS: Thirty-one patients (26 men aged 38-74 years, mean 60 years) admitted with a definite diagnosis of myocardial infarction. INTERVENTION: Streptokinase therapy given intravenously at a mean of 5 h (range 1.5-15 h) after the onset of chest pain. MAIN OUTCOME MEASURES: Serum cholesterol concentration just prior to, and 11.5 h (range 4-20.5 h) after streptokinase administration. RESULTS: There was a significant mean fall of 0.4 mmol l-1 (P = 0.002, 95% CI = 0.2-0.6) in serum cholesterol concentration from a pre-streptokinase concentration of 7.0 (range 5.3-9.9) to a post-streptokinase concentration of 6.6 (range 4.9-9.9). In the patients who showed a fall in cholesterol concentration, the magnitude of fall correlated with the baseline cholesterol concentration (r = 0.66, P < 0.01) but not with peak cardiac enzyme activities (r = 0.05, P > 0.2 for aspartate aminotransferase; r = 0.10, P > 0.2 for lactate dehydrogenase), time from onset of chest pain to post-streptokinase measurement (r = 0.27, P > 0.2) or time from streptokinase administration to post-streptokinase measurement (r = 0.01, P > 0.2). CONCLUSION: Serum cholesterol concentration may be underestimated when measured after streptokinase therapy, particularly when the true basal value is high. Further management of this risk factor may be based more accurately on its measurement before than after streptokinase therapy within the first 24 h of AMI.

Adult↗

PubMed2000

Streptokinase in acute ischemic stroke: an individual patient data meta-analysis : The Thrombolysis in Acute Stroke Pooling Project.

BACKGROUND AND PURPOSE: Three major randomized controlled trials of streptokinase in acute ischemic stroke were curtailed because of safety concerns. The prospective Thrombolysis in Acute Stroke Pooling Project (TAS-PP) was established to examine the aggregate data to identify factors influencing the effect of streptokinase. METHODS: Individual patient data from the Australian Streptokinase Trial (ASK), Multicentre Acute Stroke Trial-Europe (MAST-E), Multicentre Acute Stroke Trial-Italy (MAST-I), and Glasgow Trial (Glasgow) were pooled. Multivariate modeling determined the interaction between treatment effect and delay from symptom onset to treatment, predicted baseline risk, age, concomitant aspirin or heparin use, and the presence of early CT signs on the outcomes of 10-day death, death and disability, or death alone at 3 or 6 months. RESULTS: Patients' records were pooled (total 1292 patients; streptokinase, n=653, no streptokinase n=639). The subgroup analysis of treatment effect according to delay from symptoms to inclusion shows only a trend toward a better treatment effect with shorter delay, which is not statistically significant for any outcome. Heavier patients in MAST-E may have had a lower (non significant) risk from the fixed dose of 1.5 million units of streptokinase. Concomitant aspirin increased the excess mortality rates in streptokinase-treated patients (17% without aspirin versus 91% with aspirin, P=0.005). The presence of early CT scan signs did not increase the detrimental effect of streptokinase. CONCLUSIONS: Few factors influenced the response to streptokinase. However, earlier administration, lower doses of streptokinase, and avoidance of concomitant aspirin should be considered if further streptokinase trials in acute stroke are planned.

Acute Disease↗

PubMed1989

Combination of the thromboxane receptor antagonist, sulotroban (BM 13.177; SK&F 95587), with streptokinase: demonstration of thrombolytic synergy.

We examined the ability of the prostaglandin endoperoxide/thromboxane A2 antagonist, sulotroban (BM 13.177; SK&F 95587) to enhance the thrombolytic efficacy of a minimally effective thrombolytic dose of streptokinase. A critical stenosis sufficient to just abolish the hyperemic response to a 20-sec total occlusion was placed on the left circumflex coronary artery of anesthetized open chest dogs using an adjustable screw occluder clamp. Thrombi were formed by applying a 150 microA anodal current to a wire placed within the lumen of the left circumflex just proximal to the screw occluder clamp. After thrombus formation, animals were given either streptokinase (20,000 I.U. bolus + 2,000 I.U./min x 180 min, N = 10), streptokinase + sulotroban (5 mg/kg bolus + 5 mg/kg/hr, N = 10), streptokinase + heparin (300 I.U./kg bolus + 100 I.U./kg/hr, N = 9) or streptokinase + heparin + sulotroban (N = 9). Plasma thromboxane A2 level (as measured by the metabolite, thromboxane B2) was not significantly reduced by any treatment, whereas the dose of sulotroban used completely abolished U46619-induced ex vivo platelet aggregation. Of 10 animals receiving streptokinase alone, only 1 reperfused at 55 min after the start of the streptokinase infusion. Conversely, 9 of 10 animals receiving streptokinase + sulotroban reperfused at 79.4 +/- 10.5 min poststreptokinase (P less than .05). When animals were treated with heparin before streptokinase administration, 8 of 9 animals receiving the streptokinase + heparin combination reperfused in an average of 66.8 +/- 8.6 min after the start of streptokinase infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group.

17,187 patients entering 417 hospitals up to 24 hours (median 5 hours) after the onset of suspected acute myocardial infarction were randomised, with placebo control, between: (i) a 1-hour intravenous infusion of 1.5 MU of streptokinase; (ii) one month of 160 mg/day enteric-coated aspirin; (iii) both active treatments; or (iv) neither. Streptokinase alone and aspirin alone each produced a highly significant reduction in 5-week vascular mortality: 791/8592 (9.2%) among patients allocated streptokinase infusion vs 1029/8595 (12.0%) among those allocated placebo infusion (odds reduction: 25% SD 4; 2p less than 0.00001); 804/8587 (9.4%) vascular deaths among patients allocated aspirin tablets vs 1016/8600 (11.8%) among those allocated placebo tablets (odds reduction: 23% SD 4; 2p less than 0.00001). The combination of streptokinase and aspirin was significantly (2p less than 0.0001) better than either agent alone. Their separate effects on vascular deaths appeared to be additive: 343/4292 (8.0%) among patients allocated both active agents vs 568/4300 (13.2%) among those allocated neither (odds reduction: 42% SD 5; 95% confidence limits 34-50%). There was evidence of benefit from each agent even for patients treated late after pain onset (odds reductions at 0-4, 5-12, and 13-24 hours: 35% SD 6, 16% SD 7, and 21% SD 12 for streptokinase alone; 25% SD 7, 21% SD 7, and 21% SD 12 for aspirin alone; and 53% SD 8, 32% SD 9, and 38% SD 15 for the combination of streptokinase and aspirin). Streptokinase was associated with an excess of bleeds requiring transfusion (0.5% vs 0.2%) and of confirmed cerebral haemorrhage (0.1% vs 0.0%), but with fewer other strokes (0.6% vs 0.8%). These "other" strokes may have included a few undiagnosed cerebral haemorrhages, but still there was no increase in total strokes (0.7% streptokinase vs 0.8% placebo infusion). Aspirin significantly reduced non-fatal reinfarction (1.0% vs 2.0%) and non-fatal stroke (0.3% vs 0.6%), and was not associated with any significant increase in cerebral haemorrhage or in bleeds requiring transfusion. An excess of non-fatal reinfarction was reported when streptokinase was used alone, but this appeared to be entirely avoided by the addition of aspirin. Those allocated the combination of streptokinase and aspirin had significantly fewer reinfarctions (1.8% vs 2.9%), strokes (0.6% vs 1.1%), and deaths (8.0% vs 13.2%) than those allocated neither. The differences in vascular and in all-cause mortality produced by streptokinase and by aspirin remain highly significant (2p less than 0.001 for each) after the median of 15 months of follow-up thus far available.

Administration, Oral↗

PubMed1986

In vitro comparison of fibrinolytic activity of plasminogen activators using a thrombelastographic method: in vivo evaluation of the B-chain-streptokinase complex in the dog model using pre-titered doses.

Thrombelastography was used to quantitatively compare the clot-lysing efficiency of 6 different plasminogen activators, using human whole blood, pooled normal plasma, and platelet rich plasma. The activators compared were the B-chain-streptokinase complex, the plasmin-streptokinase complex, the mini-plasminogen-streptokinase complex, tissue plasminogen activator, streptokinase, and urokinase. The most efficient activator found was the B-chain-streptokinase complex. This complex was 4.0 times more effective than streptokinase, 3.0 times more effective than the plasmin-streptokinase complex, 1.3 times more effective than the mini-plasminogen-streptokinase complex, 2.3 times more effective than tissue plasminogen activator, and 16.0 times more effective than urokinase. Although there were differences in both the coagulation and fibrinolysis thrombelastographic patterns between plasma and whole blood, the comparative efficiencies of each activator were the same with either plasma or blood. The B-chain-streptokinase complex was evaluated as a thrombolytic agent in clot-lysis experiments in the jugular vein in the dog model, using a thrombelastographic method to determine the minimum dose of activator necessary for clot-lysis. With 6 dogs infused locally with 0.25 mg (8000 I.U.) of the plasmin-streptokinase complex, the cumulative clot-lysis was 18.0 +/- 3.0% with the first dose, 33.0 +/- 2.1% with the second dose, and 55.2 +/- 8.6% with the third dose. With 6 dogs infused locally with 0.03 mg (2000 I.U.) of the B-chain-streptokinase complex, the cumulative clot-lysis was 30.6 +/- 6.4% with the first dose, 54.4 +/- 9.6% with the second dose, and 80.2 +/- 9.0% with the third dose.

Animals↗

PubMed1986

Identification of patients at risk for anaphylaxis due to streptokinase.

To identify patients at risk for immediate-type allergic reactions to streptokinase, we performed streptokinase skin tests on patients immediately before planned administration of intravenous streptokinase for treatment of acute myocardial infarction. Forty-five patients had negative skin tests and received streptokinase without allergic reaction. One patient had a positive skin test and was given urokinase instead, without incident. Positive skin tests were also present in a patient who had recently had an anaphylactic reaction to streptokinase, and in two physician volunteers who had been sensitized to streptokinase during initial determination of the optimal skin testing dose. Immunoassays for IgE to streptokinase were performed on serum samples from skin-tested patients and volunteers, and on 16 other patients who had not been skin tested but had previously received streptokinase without allergic reactions. The skin test was a sensitive and specific indicator of elevated levels of IgE to streptokinase. We propose that skin testing immediately before streptokinase administration is a practical approach for identifying patients at risk for immediate-type allergic reactions to streptokinase, and its use may possibly prevent anaphylaxis and death.

Anaphylaxis↗

PubMed1983

Quantitative coronary angiography during intracoronary streptokinase in acute myocardial infarction: how long to continue thrombolytic therapy?

An intracoronary infusion of streptokinase is often administered in patients with acute myocardial infarction. To address the question of how long intracoronary streptokinase should be infused, we studied 13 patients with symptoms and electrocardiographic findings suggesting an evolving myocardial infarction. We used subselective catheterization techniques and made quantitative angiographic measurements of the percentage of reduction of coronary artery (CA) diameter before intracoronary streptokinase therapy, immediately after reperfusion was established, and at the completion of streptokinase infusion. Before intracoronary streptokinase and after intracoronary nitroglycerin, nine patients had 100% obstruction of the CA in the "infarct-related vessel." In seven patients reperfusion was established (25 +/- 21 min, mean +/- SD) at which time CA diameter was reduced by 77 +/- 22%. The streptokinase infusion was then continued until repeated films (every 10 to 15 min) suggested no further change at the site of CA obstruction (93 +/- 68 min). The percentage of CA diameter reduction when streptokinase infusion was discontinued was 55 +/- 32%; this value was less (P less than 0.05) than that observed early after reperfusion. These data show that after initial reperfusion was achieved by the use of intracoronary streptokinase, additional streptokinase lessened the reduction of CA diameter. Residual thrombus may be present at the narrowed CA site early after reperfusion, and further "cleanup" can be achieved by prolonging streptokinase infusion.

Adult↗