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 487 records · Page 27Linked to original sources

PubMed1986

Active streptokinase from the cloned gene in Streptococcus sanguis is without the carboxyl-terminal 32 residues.

The streptokinase expressed by the cloned gene in Streptococcus sanguis has a molecular weight of about 44 000 [Malke, H., Gerlach, D., Kohler, W., & Ferretti, J.J. (1984) MGG, Mol. Gen. Genet. 196, 360-365] while the molecular weight of the native streptokinase is 47 000. The structural and activity differences of the cloned streptokinase (cSK) as expressed by S. sanguis and the native streptokinase (nSK) were investigated. From a partially purified cSK, two active fractions were obtained by reversed-phase HPLC. The minor fraction cSKL was nearly as active as SK in plasminogen activation. The major fraction cSKs had only about one-fourth of the specific activity. The structures of cSKL and cSKs were studied and compared to the known amino acid sequence of SK [Jackson, K. W., & Tang, J. (1982) Biochemistry 21, 6620-6625]. From the NH2- and COOH-terminal sequences and amino acid composition of the cyanogen bromide (CNBr) fragments, it could be deduced that cSKL and cSKs are without 31 and 32 residues, respectively, from the COOH-terminal end of SK. Since the cloned gene contained the full SK structure, the missing structures must have been due to posttranslational proteolysis. An SK fragment similar in size to cSK was observed from a chymotryptic digest of SK.

Amino Acids↗

PubMed1982

Enhancement of the streptokinase-catalyzed activation of human plasminogen by human fibrinogen and its plasminolysis products.

The effects of human fibrinogen, and several plasmin-derived fragments of fibrinogen, on the streptokinase-induced activation of human plasminogen (Pg) have been investigated. Fibrinogen stimulates the rate of activation of human Glu1-Pg, Lys77-Pg, and Val442-Pg. The cofactor activity of fibrinogen appears to reside mainly in the D-domain region, since purified fragment D is active in this system. Fibrinogen fragment E was not active in this regard. The cofactor activity of fragment D was partially dependent on the presence of Ca2+. This effect of Ca2+ was likely due to its stabilizing influence on fragment D, as revealed by studied employing differential scanning calorimetry. Conversion of fragment D1 to fragments D2--5 did not alter the cofactor activity. Steady-state kinetic analysis of the activation of Val442-Pg by the streptokinase-Val442-plasmin complex demonstrated that the Km decreased approximately 2-fold, in the presence of fragment D1. Very little change in the steady-state kinetic parameters for Glu1-Pg and Lys77-Pg, when activated by the streptokinase-Lys77-plasmin complex, was noted in the presence of fragment D1. It was also found that both fibrinogen and fibrinogen fragment D1 increased the rate of formation of the active site in the streptokinase-plasminogen complex, of all forms of plasminogen, and that this effect was sufficient to explain the overall stimulation of the activation of plasminogen by fibrinogen and fibrinogen fragment D1.

Calcium↗

PubMed1989

Kinetics of the reaction of streptokinase-plasmin complex with purified human and mouse alpha 2-macroglobulin. Implications for mechanism.

Streptokinase-human plasmin complex (Sk-hPm) reacted rapidly with purified mouse alpha 2-macroglobulin (m alpha 2M) in vitro at 37 degrees C. Approx. 98% of the plasmin in Sk-hPm bound covalently to at least one m alpha 2M subunit. Most of the streptokinase dissociated (95%). The rate of Sk-hPm inactivation clearly depended on the m alpha 2M concentration. With 1.2 microM-m alpha 2M, 50% of the Sk-hPm (0.02 microM) reacted in less than 50 s. A double-reciprocal plot comparing pseudo-first-order rate constants (kapp.) and m alpha 2M concentration yielded a second-order rate constant of 2.3 x 10(4) M-1.s-1 (r = 0.97). This value is an approximation, since Sk-hPm preparations are heterogeneous. Sk-hPm reacted with human alpha 2M (h alpha 2M), forming alpha 2M-plasmin complex (98% covalent). More than 99% of the streptokinase dissociated. The rate of reaction of Sk-hPm with h alpha 2M did not clearly depend on inhibitor concentration. The kapp. values determined with 0.6-1.2 microM-h alpha 2M were decreased 10-20-fold compared with m alpha 2M. In order to study the effect of Sk-hPm heterogeneity on the reaction with alpha 2M, the proteinase was incubated for various amounts of time at 37 degrees C before addition of inhibitor. The enzyme amidase activity was maximal within 5 min; however, reaction of Sk-hPm with m alpha 2M or h alpha 2M was most extensive after 20 min and 2 h respectively. After incubation for more than 1 h, Sk-hPm acquired fibrinogenolytic activity, suggesting plasmin dissociation. Therefore the enhanced reaction of h alpha 2M with 'older' Sk-hPm preparations may have resulted in part from dissociated plasmin or 'plasmin-like' species. By contrast, the reaction of Sk-hPm with m alpha 2M was most rapid when the proteinase preparation was free of plasmin, indicating direct reaction of Sk-hPm with m alpha 2M as the only major mechanism. Finally, streptokinase-cat plasminogen complex reacted more extensively with m alpha 2M than with h alpha 2M, suggesting that m alpha 2M may be a superior inhibitor with this class of plasminogen activators in general.

Animals↗

PubMed2001

Successful clot lysis using low dose of streptokinase in 22 neonates with aortic thromboses.

OBJECTIVE: To determine whether intravenous infusion of low dose of streptokinase was effective in lysing umbilical arterial catheter (UAC)-associated aortic thrombi. METHOD: A prospective cohort study of 31 consecutive newborn infants with UAC-associated aortic thrombi which were detected by abdominal ultrasonography after removal of UAC. Twenty-two infants were treated with intravenous infusion of low dose (1000 U/h) streptokinase, while nine others were not treated due to various contra-indications. Thrombolysis occurred after a mean interval of 2.2 days (standard deviation (SD) = 1.8) in the treated infants. In the untreated infants, spontaneous thrombolysis occurred significantly later, after a mean interval of 16.9 days (SD = 14.7) (95% confidence intervals of difference between mean intervals - 26.0, - 3.4; P = 0.02). Only one treated infant developed mild bleeding directly attributed to streptokinase therapy. CONCLUSION: Low dose streptokinase infusion was effective and safe in thrombolysing UAC-associated aortic thrombi.

Aortic Diseases↗

PubMed1986

Treatment of pulmonary embolism with full-dose heparin, streptokinase or embolectomy--results and indications.

The results of treatment of pulmonary embolism with heparin (n = 34), streptokinase (n = 28) or embolectomy (n = 25) are presented. The treatment groups represented different degrees of embolization with acute embolic scores (possible maximum: 20, mean +/- SD): 5 +/- 4, 9 +/- 3 and 13 +/- 3, respectively (p less than 0.0001). The post-treatment embolic score (mean +/- SD) for patients with acute massive central emboli (score greater than or equal to 9) was: 6 +/- 4 (n = 7) and 3 +/- 2 (n = 15) in the streptokinase and embolectomy groups, respectively, (p less than 0.01). The hospital mortality was 6% (n = 2), 21% (n = 6) and 20% (n = 5) in the heparin, streptokinase and embolectomy groups, respectively (p less than 0.05). The 5-year cumulative survival (+/- SE) was 68% +/- 10, 64% +/- 10 and 80% +/- 8, respectively (p: NS). The relative survival (hospital and late deaths, observed/expected) stratified according to acute embolic score showed the best results in the embolectomy group. Systolic pulmonary artery pressure greater than 60 mmHg was found in cases with a duration of symptoms greater than 7 days and/or with greater than or equal to 25 anamnestic recurrent embolic episodes before diagnosis, indicative of a gradual increase in pulmonary artery pressure and of partly organized non-lyseable emboli. Embolectomy carried a low risk of complications (8% with cerebral reduction). Streptokinase treatment was associated with serious complications (18% with cerebral reduction/fatal hemorrhage). Pulmonary embolectomy should be recommended in all cases with emboli in the main branches of the pulmonary artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1980

[Intracoronary application of streptokinase in acute myocardial infarction and non-stable angina pectoris (author's transl)].

Streptokinase, 1000-2000 U/h, was administered into the coronary artery via catheter over 15-60 minutes to 12 patients. Six of them had an infarct in the early stage (A), two a fresh re-infarction (B) and four nonstable angina (C). Nitroglycerine had been injected at a dose of 0.1-0.45 mg into the coronary artery before infusion of streptokinase. Nitroglycerine induced angiographic demonstrably better filling of the infarcted vessel in two patients of group A. After intracoronary injection of streptokinase the occluded artery re-opened or, if there had been subtotal stenosis, significantly widened in all patients of group A. But there was no complete disappearance of the narrowing. In the patients of group B and C there was no angiographic evidence of change, neither after nitroglycerine nor after streptokinase. There was no marked change in systemic clotting function. The findings indicate that after acute, first-time infarction a fresh coronary thrombus forms on the basis of atheromatous narrowing. The thrombus can be quickly removed by selective lysis via coronary catheter. Fresh thrombotic deposition is less likely on re-infarction or in nonstable angina. These results must be confirmed by observation on a larger group of patients.

Adult↗

PubMed1985

The western Washington randomized trial of intracoronary streptokinase in acute myocardial infarction. A 12-month follow-up report.

After cardiac catheterization and coronary arteriography, 134 patients who had had an acute myocardial infarction were randomly assigned to treatment with intracoronary streptokinase (4000 U per minute, begun approximately 4 1/2 hours after the onset of symptoms, for a total of 286,000 +/- 77,800 U over 72 +/- 24 minutes); 116 control patients received standard care after they returned to the coronary care unit, immediately after angiography. Preliminary results of this trial have been published in the Journal (1983; 309:1477-81). During the first 30 days, 5 deaths occurred in the streptokinase group and 13 occurred in the control group (3.7 vs 11.2 per cent, P = 0.02); during the first year, the corresponding figures were 11 and 17 deaths (8.2 vs. 14.7 per cent, P = 0.10). However, when a minor imbalance in the ejection fraction and infarct location between the two groups was adjusted by logistic regression, the difference in one-year mortality became significant (P = 0.03). In the streptokinase group, 2 of the 80 patients in whom perfusion was reestablished (2.5 per cent) had died by one year, whereas 3 of the 13 with partial reperfusion (23.1 per cent) and 6 of the 41 with no reperfusion (14.6 per cent) had died (P = 0.008). Mortality among patients with partial reperfusion was not significantly different from that among those without reperfusion (P greater than 0.90). No base-line clinical, angiographic, or hemodynamic variable was predictive of successful reperfusion, according to univariate and multivariate analyses. We conclude that intracoronary streptokinase reduces one-year mortality among patients with acute myocardial infarction, but this improvement occurs only among those in whom thrombolysis results in coronary artery reperfusion.

Coronary Angiography↗

PubMed1993

The effects of tissue plasminogen activator, streptokinase, or both on coronary-artery patency, ventricular function, and survival after acute myocardial infarction.

BACKGROUND: Although it is known that thrombolytic therapy improves survival after acute myocardial infarction, it has been debated whether the speed with which coronary-artery patency is restored after the initiation of therapy further affects outcome. METHODS: To study this question, we randomly assigned 2431 patients to one of four treatment strategies for reperfusion: streptokinase with subcutaneous heparin; streptokinase with intravenous heparin; accelerated-dose tissue plasminogen activator (t-PA) with intravenous heparin; or a combination of both activators plus intravenous heparin. Patients were also randomly assigned to cardiac angiography at one of four times after the initiation of thrombolytic therapy: 90 minutes, 180 minutes, 24 hours, or 5 to 7 days. The group that underwent angiography at 90 minutes underwent it again after 5 to 7 days. RESULTS: The rate of patency of the infarct-related artery at 90 minutes was highest in the group given accelerated-dose t-PA and heparin (81 percent), as compared with the group given streptokinase and subcutaneous heparin (54 percent, P < 0.001), the group given streptokinase and intravenous heparin (60 percent, P < 0.001), and the group given combination therapy (73 percent, P = 0.032). Flow through the infarct-related artery at 90 minutes was normal in 54 percent of the group given t-PA and heparin but in less than 40 percent in the three other groups (P < 0.001). By 180 minutes, the patency rates were the same in the four treatment groups. Reocclusion was infrequent and was similar in all four groups (range, 4.9 to 6.4 percent). Measures of left ventricular function paralleled the rate of patency at 90 minutes; ventricular function was best in the group given t-PA with heparin and in patients with normal flow through the infarct-related artery irrespective of treatment group. Mortality at 30 days was lowest (4.4 percent) among patients with normal coronary flow at 90 minutes and highest (8.9 percent) among patients with no flow (P = 0.009). CONCLUSIONS: This study supports the hypothesis that more rapid and complete restoration of coronary flow through the infarct-related artery results in improved ventricular performance and lower mortality among patients with myocardial infarction. This would appear to be the mechanism by which accelerated t-PA therapy produced the most favorable outcome in the GUSTO trial.

Cineangiography↗

PubMed1994

A decision analysis of streptokinase plus heparin as compared with heparin alone for deep-vein thrombosis.

BACKGROUND: It is uncertain whether patients with proximal deep-vein thrombosis should be treated with streptokinase followed by intravenous heparin or with intravenous heparin alone. Published reports indicate that streptokinase plus heparin increases the risk of bleeding, including central nervous system bleeding and death, but decreases the risk of postphlebitic syndrome. Previous recommendations regarding these treatments have not considered patients' preferences or the values they attach to the possible outcomes of therapy. METHODS: We used decision analysis to combine published estimates of the probabilities of various adverse outcomes of treatment (bleeding, pulmonary embolism, postphlebitic syndrome, and death) with the values patients placed on these outcomes. We questioned 36 patients about the values they attached to each outcome. Sixteen patients had had deep-vein thrombosis, and 20 had not. RESULTS: By the values they attached to the outcomes, all 36 patients indicated that they were unwilling to accept an increased risk of death to avoid postphlebitic syndrome. According to the decision analysis, heparin alone was the better treatment for all 36 patients. As compared with streptokinase plus heparin, heparin alone provided 29 days of additional life expectancy over the predicted life expectancy of 20 years. Although the difference between the two treatments was small, heparin alone remained the better treatment in sensitivity analyses that examined the reasonable ranges of probabilities of the clinical outcomes. CONCLUSIONS: The values patients placed on the outcomes of treatment for deep-vein thrombosis support the use of heparin alone over the combined use of streptokinase and heparin.

Cerebral Hemorrhage↗

PubMed1995

A role for fibrinogen in the streptokinase-dependent acquisition of plasmin(ogen) by group A streptococci.

Acquisition of plasmin(ogen) by group A streptococci occurs by two distinct pathways. In addition to the well-characterized direct interaction of plasmin with cell-surface receptors on group A streptococci, a second pathway dependent on streptokinase and a nonplasminogen factor(s) present in human plasma was identified. The role of streptokinase in the second pathway was not merely as a plasminogen activator, since substitution of the plasminogen activator urokinase did not result in the capture of plasmin(ogen) by bacteria in the presence of plasminogen-depleted plasma. However, if streptokinase was added to plasmin that had been generated by treatment of plasminogen with urokinase, the ability of the bacteria to capture plasmin in the presence of plasminogen-depleted plasma was restored. Fibrinogen present in human plasma was identified as the major factor required for streptokinase-dependent uptake of plasmin(ogen) by group A streptococci.

Fibrinogen↗

PubMed1992

Blood rheology in acute myocardial infarction: effects of high-dose i.v. streptokinase compared to placebo.

To compare the haemorheological effects of an i.v. infusion of 1.5 MU of streptokinase with placebo, we investigated the time course of plasma fibrinogen concentration and the haemorheologic parameters plasma viscosity, erythrocyte aggregation and whole blood viscosity at different shear rates during the early phase of acute myocardial infarction until week 3 in 38 unselected patients from the ISAM and ISIS-2 study. Within 3 h, streptokinase led to a near afibrinogenaemia lasting for more than 24 h. Concomitantly, with streptokinase we found a reduction of plasma viscosity, erythrocyte aggregation and whole blood viscosity, whereas with placebo, values showed a slight increase, resulting in significant differences between the groups within the first 2 days. Thereafter, both groups showed an increase in all parameters, values reaching a maximum after 1 week. The streptokinase-induced reduction in blood viscosity may lead to an improvement in microcirculation in the infarction area during the early phase, whereas the hyperviscosity observed independently of therapy after 1 week may lead to an impairment of microcirculation.

Adult↗

PubMed1995

Pre-hospital thrombolytic therapy with either alteplase or streptokinase. Practical applications, complications and long-term results in 529 patients.

OBJECTIVE: To assess the practical application, safety and long-term outcome of pre-hospital thrombolytic intervention with either alteplase or streptokinase in patients with extensive myocardial infarction. DESIGN: Prospective study. SUBJECTS: Patients with chest pain of more than 30 min duration, presenting within 6 h of symptom onset and with electrocardiographic evidence of extensive evolving myocardial infarction. METHODS: Eligibility of patients was established by the general practitioner or the ambulance nurse using a standardized questionnaire with (contra-) indications for thrombolytic therapy. Computerized ECG was recorded by ambulance nurses. In the presence of extensive ST segment elevation (sum ST deviation of at least 1.0 mV), eligible patients received either 100 mg alteplase (n = 246) or 50 mg alteplase in the ambulance followed by 0.75 x 10(6) IE streptokinase in hospital (n = 90), or 1.5 x 10(6) IE streptokinase intravenously (n = 193). MAIN OUTCOME MEASUREMENTS: Death and life-threatening complications (ventricular fibrillation, cardiac arrest) and side effects (hypotension, allergic reactions) during transportation to hospital and in the first 24 h following hospitalization, and survival up to 5 years follow-up. RESULTS: From 1988-1993, 529 patients received thrombolytic treatment initiated pre-hospital. The time gained by pre-hospital administration of thrombolysis amounted to 50 min. The rate of complications during transportation and during the first 24 h after hospitalization was low. Hospital mortality was 2% and 1-year mortality 3%. Cumulative survival at 5 years was 92%. This was superior to the 84% 5-year survival observed in a matched group of 239 patients with similar baseline characteristics treated with alteplase in hospital. CONCLUSIONS: Pre-hospital administration of either alteplase or streptokinase is feasible and safe and results in significant time gain. The long-term prognosis is excellent in spite of extensive evolving myocardial infarction upon admission.

Adult↗

PubMed1983

Streptokinase treatment of acute arterial occlusion.

In selected cases, streptokinase, a thrombolytic agent, is an effective alternative to surgical intervention for the treatment of acute arterial occlusions. Successful thrombolysis was achieved in 12 of 16 arterial occlusions (75%) following the intra-arterial infusion of streptokinase at a dosage of 5,000 U per hour. Neither the etiology nor the duration of the occlusions influenced the ability to achieve effective thrombolysis. The major limitation of the technique was the time required to ensure complete thrombolysis (37.5 +/- 17.5 hours). Despite the localized infusion of streptokinase proximal to the arterial obstruction at low dosages, hypofibrinogenemia (100 mg/dl) occurred in five patients and four patients developed a bleeding complication. The use of concomitant heparin (300-500 U per hour) increased the risk of bleeding without increasing thrombolytic potential. Streptokinase treatment of acute arterial occlusions should be used selectively depending on the degree of ischemia, the etiology of the obstruction, and the clinical status of the patient.

Aged↗

PubMed2003

Improvement of microvascular graft equilibration and preservation in non-heart-beating donors by warm preflush with streptokinase.

Using in situ fluorescence microscopy with Sprague Dawley rats, we studied the hypothesis of compromised microvascular kidney perfusion on organ harvest in non-heart-beating donors (NHBDs), and we evaluated the potential benefit of an additional preflush with saline solution containing streptokinase. Aortal flush of NHBD kidneys solely with University of Wisconsin solution resulted in a significantly (P <0.05) reduced functional capillary density (FCD) with increased perfusion heterogeneity compared with kidneys of heart-beating controls. This was associated with an increased lactate dehydrogenase (LDH) release on 24 hr postpreservation rinse of the grafts (76.7+/-18.9 U/L). Warm preflush with low-viscosity Ringer's lactate (RL) solution alone did not influence the decreased renal FCD and the postpreservation LDH release (76.2+/-29.1 U/L). In contrast, the addition of streptokinase to the RL preflush solution resulted in a significant (P <0.05) improvement of FCD with values not statistically different from those of heart-beating controls. This was associated with an attenuation of perfusion heterogeneity and a significantly lowered postpreservation LDH release (17.0+/-2.5 U/L). Furthermore, in transplanted and reperfused NHBD kidney grafts, the use of streptokinase-supplemented RL for preflush during organ harvest significantly (P <0.05) reduced early manifestation of tubular necrosis (29%+/-8%) when compared with kidneys preflushed exclusively with University of Wisconsin solution (56%+/-4%). Thus, we conclude that kidney harvest from NHBDs is prone to severe microvascular perfusion deficits, which are likely to preclude successful preservation of organ integrity during cold storage. Temporary fibrinolytic preflush with streptokinase may represent a feasible tool to improve microvascular graft equilibration, which effectively protects the renal integrity during both cold storage and posttransplant reperfusion.

Adenosine↗

PubMed1986

The use of regional, low dose streptokinase in recently thrombosed arterial grafts.

Between August 1983 and January 1985, 20 patients aged 33-77 years, with occluded lower limb bypass grafts, were on 23 occasions treated with streptokinase via intra-arterial infusion. Streptokinase (5000 units/h) was effective in clearing occluded grafts in 15 patients on 16 occasions. The median duration of occlusion in these patients was 5 days and the median duration of streptokinase infusions was 24 h. Completion angiography following streptokinase thrombolysis revealed five graft stenoses and 12 outflow stenoses or occlusions. In two grafts no cause for graft failure could be identified. These results permitted the surgeon to make an accurate pre-operative assessment of the definitive therapy required to ensure graft patency.

Adult↗

PubMed1992

Streptokinase morbidity--more common than previously recognised.

Streptokinase is the thrombolytic agent most commonly used for the treatment of acute myocardial infarction. We report eight patients who developed late uncommon adverse reactions to streptokinase probably due to immune complex disease. The clinical manifestations included vasculitic rashes, abnormal renal and liver function tests and a syndrome resembling adult respiratory distress syndrome. Major adverse events with streptokinase such as stroke, bleeding and other allergic reactions, have been previously documented but the morbidity related to delayed reactions has not been widely recognised. These reactions produced significant morbidity resulting in prolonged hospital stay and may need to be considered in the decision to use streptokinase.

Adult↗

PubMed2004

International collaborative study to establish the 3rd International Standard for Streptokinase.

An international collaborative study was organized to calibrate a replacement for the current (2nd) International Standard (IS) for Streptokinase, stocks of which are almost exhausted. Two candidate preparations were assayed against the 2nd IS in a study involving 16 laboratories in 12 countries: preparation 88/824 (coded B), and preparation 00/464 (C and D, coded duplicates). Laboratories could use two methods provided, either a fibrin clot lysis assay or a solution chromogenic method, or an in-house method. Laboratories were encouraged to perform more than one method if possible. With the exception of one laboratory which gave outlying results for preparation 00/464, there was good agreement within and between laboratories and no significant differences between potencies using the different methods employed. This study demonstrates that a solution chromogenic assay is an acceptable format for potency determination of the streptokinase preparations in this study and fibrin is not necessary. It has now been agreed that a solution chromogenic plasminogen activation assay replace the current euglobulin reference method for streptokinase activity determination in the European Pharmacopoeia. Study participants, SSC of the International Society on Thrombosis and Haemostasis and the Expert Committee on Biological Standardization (ECBS) at the World Health Organization approved preparation 00/464 (C,D in the study) as the 3rd IS for Streptokinase with a potency of 1030 IU per ampoule.

Drug Stability↗

PubMed1993

An overview of the patency and stroke rates following thrombolysis with streptokinase, alteplase, and anistreplase used to treat an acute myocardial infarction.

The results of an overview of early (90-240 min) and late (24 hours or more) patency and of stroke rates for each of the three commercially available thrombolytic agents, streptokinase, alteplase, and anistreplase are presented. Studies included in this analysis are all those published between 1985 and March 1992 and focus on the licensed dosage regimens of each agent. The rates of early and late patency for streptokinase were 64.7% and 80.8%; for alteplase, 66.6% and 73.7%; and for anistreplase, 72.1% and 84.5%. The rates of total and hemorrhagic stroke for streptokinase were 0.69% and 0.17%; for alteplase, 1.27% and 0.50%; and for anistreplase 0.91% and 0.38%. These results provided evidence that the rates of early and late patency appeared to be greatest for anistreplase and that the rates of stroke are within "acceptable" ranges for all three thrombolytic agents with streptokinase affording the lowest rate.

Anistreplase↗