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PubMed1986

Fibrinolytic therapy with streptokinase for established experimental glomerulonephritis.

The efficacy of fibrinolytic therapy with streptokinase was assessed in rabbits developing anti-glomerular basement membrane antibody induced glomerulonephritis. Untreated animals developed renal failure (mean creatinine 615 +/- 120 microM/l) and a severe glomerulonephritis with prominent fibrin deposition. Streptokinase treatment of animals with established disease (creatinine 204 +/- 35 microM/l) reduced renal impairment (creatinine 256 +/- 68 microM/l, p less than 0.025) and fibrin deposition. Treatment of more advanced disease (creatinine 416 +/- 68 microM/l) did not preserve renal function (creatinine, 518 +/- 106 microM/l), although glomerular fibrin deposition was reduced. These studies indicate that fibrinolytic therapy with streptokinase reduces glomerular fibrin deposition and, if used early, protects from loss of renal function.

Animals↗
PubMed1988

Intermittent plasminogen-streptokinase treatment of deep vein thrombosis.

Thrombolytic therapy has been used for treating patients suffering from a variety of clinical disorders including patients suffering from extensive venous and arterial thrombosis. This paper describes a combined approach to lytic therapy consisting of administration of small doses of streptokinase in combination with the infusion of plasminogen. The rationale for this approach is based on recent observations that additional plasminogen will be absorbed into preformed thrombi, rendering them more susceptible to lysis in the presence of activators. Forty-four patients who presented with symptoms and signs of acute or sub-acute deep vein thrombosis (DVT) confirmed by phlebography, were included in this study. Group I: 15 consecutive patients received an infusion of 600,000 units of SK dissolved in 50 ml of physiological saline over a period of half and hour. On the subsequent 4 days, a dose of 300,000 units was given twice daily. Group II: 29 consecutive patients received 60 to 90 mg of pretreated plasminogen dissolved in 50 ml of saline given intravenously over 30 min. and followed by same dosage regimen of SK. Blood samples were taken at varying intervals to assess changes in the haemostatic parameters. These were analysed for levels of alpha 2-antiplasmin, antithrombin III, fibrinogen, plasminogen, fibrinogen and degradation products, fibrinolytic activity and levels of activator complex. Findings observed will be presented. Phlebograms were performed before starting treatment and were repeated at the end of 5 days when the treatment had finished. In Group I--(15 patients)--thrombi remained virtually unchanged in 12 out of 15 patients receiving streptokinase infusion; in 3 (20%) there was partial but extensive lysis. In contrast, in Group II--(29 patients)--in 16 (55%) of 29 patients receiving plasminogen and streptokinase infusion, complete lysis of thrombi was obtained. Seven (24%) showed extensive clearance of venous tree while in remaining 6, thrombi virtually remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Coagulation Tests↗
PubMed1988

Streptokinase--biochemistry and clinical application.

Plasminogen activation to plasmin is due to enzymatic cleavage of a single peptide bond in the zymogen molecule. Streptokinase is not an enzyme and its activation of plasminogen is indirect. Streptokinase forms stoichiometric complexes with plasmin and plasminogen and these complexes activate plasminogen to plasmin. Streptokinase is species selective in its action.

Amino Acid Sequence↗
PubMed1982

Acute coronary artery occlusion during percutaneous transluminal coronary angioplasty: reopening by intracoronary streptokinase before emergency coronary artery surgery to prevent myocardial infarction.

Percutaneous transluminal coronary angioplasty (PTCA) was complicated by acute coronary artery occlusion associated with ST elevation and severe chest pain in three patients. Within 10 minutes, the occluded artery was reopened by an intracoronary (i.c.) infusion of streptokinase, resulting in the disappearance of chest pain and normalization of ST segments. To keep the artery patent, i.c. streptokinase had to be continued until emergency bypass surgery was performed. In two patients, no myocardial infarction occurred, as shown by a normal postoperative left ventricular angiogram. ECG and thallium-201 scintigram. In the other patient, who was admitted with an inferior infarction and underwent PTCA after i.c. lysis, no infarct extension was observed. These results show that i.c. streptokinase rapidly opens an acute coronary artery occlusion complicating PTCA, preventing myocardial infarction.

Adult↗
PubMed1984

Hemorrhage and the products of fibrinogen digestion after intracoronary administration of streptokinase.

Hemorrhage was prospectively identified in 26 of 116 consecutive patients (23%) who were receiving intracoronary streptokinase for occlusive coronary thrombi producing infarction. Bleeding was not influenced by the dose of streptokinase or the method of cardiac catheterization. Before treatment, prothrombin time and partial thromboplastin time were normal in both bleeders and nonbleeders. Fibrinogen levels measured by bioassay after streptokinase (mean +/- SEM) were 62 +/- 29 mg/dl in patients with major bleeding, 111 +/- 26 mg/dl in patients with minor bleeding, and 109 +/- 13 mg/dl in nonbleeders (p = NS). The regression slope b calculated from poststreptokinase fibrinogen time-concentration data in 71 patients was 4.7 mg/dl/hr. However, mean fibrinogen concentrations calculated at sequential 5 hr intervals revealed no net regeneration for the first 20 hr after thrombolysis. The apparent fibrinogen regeneration rate was less than normal (31 mg/kg/day) for more than 10 hr but subsequently increased to 94 +/- 10 mg/kg/day by the second day. The initial apparent latency of fibrinogen regeneration paralleled the sharp rise in fibrinogen degradation products, which began to decline after 20 hr of treatment but remained elevated well into the second day. Because of their anticoagulant effects, these products may interfere with the fibrinogen assay, causing spuriously low results. Thus, whether the early delay in fibrinogen regeneration is real or simply a reflection of the effects of fibrinogen degradation products on the bioassay, it signals the time for caution in initiating systemic heparin therapy.

Blood Coagulation Factors↗
PubMed1985

The effects of the rate of intravenous infusion of streptokinase and the duration of symptoms on the time interval to reperfusion in patients with acute myocardial infarction.

We studied the influence of the following variables on the time interval from initiation of an intravenous infusion of 750,000 U of streptokinase until reperfusion (reperfusion time) in 140 consecutive patients with an evolving acute myocardial infarction: (1) the rate of infusion of streptokinase, (2) the duration of chest pain before initiation of treatment, (3) patient age, (4) patient sex, (5) location of infarction, (6) history of previous myocardial infarction, and (7) pretreatment pathologic Q waves. The time of reperfusion was recognized by clinical criteria that were completely concordant with the anatomic findings in all 119 patients in whom patency or occlusion of the artery of infarction was established at delayed angiography (n = 116) or at postmortem examination (n = 3). The mean reperfusion time for the 129 patients for whom data were available was 49 +/- 36 min. The reperfusion time was inversely related to the rate of infusion of streptokinase (r = .41, p less than .001), but this effect of infusion rate appeared to plateau at rates of greater than 500 U/kg/min. In the 64 patients receiving infusions at rates of 500 U/kg/min or less, the mean reperfusion time was 60 +/- 40 min, whereas in the 58 patients receiving the drug at rates greater than 500 U/kg/min it was 35 +/- 22 min (p less than .001). The duration of chest pain before treatment was the only other studied variable found to influence the reperfusion time, but only at infusion rates of less than 250 U/kg/min (r = .6, p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1985

The hypotensive effect of intravenous streptokinase in patients with acute myocardial infarction.

We studied the hypotensive effect of a rapid intravenous infusion of high-dose streptokinase in 98 patients with an acute myocardial infarction. The systolic blood pressure fell from 132 +/- 20 (range 90 to 174) to 97 +/- 21 mm Hg (range 58 to 152) at 15 +/- 8 min (range 4 to 40) after the commencement of the streptokinase infusion (p less than .001). A fall in diastolic blood pressure from 80 +/- 16 (range 51 to 105) to 61 +/- 15 mm Hg (range 32 to 92) accompanied the fall in systolic pressure (p less than .001). The fall in blood pressure was associated with an increase in heart rate (73 +/- 14 to 78 +/- 17 beats/min, p less than .001), preceded the appearance of clinical signs of reperfusion by 37 +/- 38 min and was similar in magnitude and timing in patients with anterior and inferior infarction. There were direct relationships between the rate of infusion of streptokinase and both the magnitude (r = .49, p less than .001) and the rate of fall of systolic blood pressure (r = .67, p less than .001) as well as both the magnitude and rate of fall of diastolic blood pressure. In most patients, the fall in blood pressure was transient (9 +/- 6 min, range = 2 to 30) and easily managed by slowing or stopping the infusion, placing the patient in the Trendelenburg position, or by administering an infusion of low-dose norepinephrine or dopamine. However, in four patients with severe left ventricular dysfunction, severe hypotension persisted for more than 60 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Incomplete lysis of thrombus in the moderate underlying atherosclerotic lesion during intracoronary infusion of streptokinase for acute myocardial infarction: quantitative angiographic observations.

Thrombolytic recanalization of the obstructed coronary lumen was studied in 32 patients receiving intracoronary streptokinase for 60 to 90 min during acute myocardial infarction. The process was viewed at high arteriographic magnification and was quantified with computer-assisted measurements from repeated single-plane views. The variability of the method for this application was 0.15 to 0.18 mm on minimum diameter estimates. Structural details were seen that are not commonly appreciated at conventional magnification. The recanalized lumen appears to form along an interface between the thrombus and the vessel wall, progressively enlarging its minimum arteriographic diameter to 0.65 +/- 0.24 mm (+/- 1 SD) at the end of the short-term infusion of streptokinase reflecting a final percent stenosis of 77 +/- 10%. In nine infarct lesions found patent 5 +/- 3 weeks later, the recanalized lumen further improved an average of 0.34 mm in minimum diameter (p less than .005) and 13% stenosis (p less than .01). A thin film of contrast medium surrounding the obstructing thrombus faintly defined the boundaries of the original atherosclerotic lumen in all but two cases. The "original stenosis" measured 1.25 +/- 0.32 mm in minimum diameter and 56 +/- 14% stenosis when first visualized; it was unchanged throughout the course of infusion of streptokinase. In five patients catheterized 10 +/- 12 weeks before their infarction, the original stenosis averaged 1.15 +/- 0.22 mm in the preinfarct angiogram, as compared with 1.17 +/- 0.23 mm in its faintly defined form during thrombolytic therapy (p = NS). In 10 cases, this original lesion was less than a 50% stenosis, and in 21 cases less than 60%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Risk stratification for 1 year survival based on characteristics identified in the early hours of acute myocardial infarction. The Western Washington Intracoronary Streptokinase Trial.

We evaluated the relationship between baseline factors defined at 4.6 +/- 2.1 hr after onset of acute myocardial infarction and 1 year survival in 245 patients entered in the Western Washington Intracoronary Streptokinase Trial. Univariate statistics identified a significant relationship between 10 of these factors and survival. Multivariate analysis identified three factors as being most closely related to survival: (1) left ventricular ejection fraction (LVEF) (p less than .0001), (2) treatment with streptokinase (p = .03), and (3) location of infarction (p = .04). Mathematic models based on this analysis and applied to our patients identified high- and low-risk subgroups for 1 year mortality. Patients receiving standard, not interventional, therapy with anterior infarction and an LVEF of 50% or less and those with inferior infarction and an LVEF of 39% or less comprised the high-risk group. For patients receiving standard therapy, 1 year mortality was 41% in the high-risk group and 4% in the low-risk group. The models illustrated the magnitude of benefit of streptokinase treatment and achievement of complete reperfusion for those at low and high risk. We conclude that LVEF determined in the first hours of acute myocardial infarction is the most important of all baseline factors for prediction of 1 year survival. Mathematic models based on left ventricular function measured as ejection fraction are useful for risk stratification in this setting.

Adult↗
PubMed1991

Relative importance of thrombin compared with plasmin-mediated platelet activation in response to plasminogen activation with streptokinase.

BACKGROUND: Platelet activation occurs in vivo during pharmacologic thrombolysis and may contribute to recurrent thrombosis. Plasmin does not directly activate platelets except at high concentrations; thus, the mechanisms for platelet activation during thrombolysis remain undefined. Increases in thrombin activity also occur in patients treated with fibrinolytic agents and may contribute to activation of platelets. We have shown that one mechanism for increased thrombin activity is activation of the coagulation system by plasmin. METHODS AND RESULTS: In the present study we sought to determine whether activation of platelets in response to pharmacologic activation of plasminogen in plasma is due primarily to plasmin or mediated by increased thrombin activity. Platelet-rich citrated plasma (PRP) was recalcified and incubated with 1,000 IU/ml of streptokinase or 1.0 caseinolytic units/ml of plasmin. Concentrations of fibrinopeptide A, a marker of thrombin activity, increased markedly over 10 minutes in plasma incubated with streptokinase or plasmin, but not in PRP incubated without plasminogen activator. Platelet activation characterized by the secretion of 14C-serotonin occurred within 2-4 minutes after thrombin activity increased. In stirred recalcified PRP, platelet aggregation was accelerated from 3.6 +/- 0.5 to 2.5 +/- 0.3 minutes (p less than 0.01) when incubated with 1,000 IU/ml of streptokinase. Leupeptin and aprotinin, inhibitors of plasmin activity, markedly attenuated platelet activation in response to pharmacologic activation of plasminogen. However, inhibition of thrombin with heparin, hirudin, or D-Phe-D-Pro-L-Arg-chloromethylketone was more effective in inhibiting the acceleration of platelet activation induced by plasminogen activation, despite the elaboration of plasmin activity. CONCLUSIONS: Activation of platelets during coronary thrombolysis may be due in part to increased procoagulant activity induced by plasminogen activation as well as other factors that promote platelet activation in vivo.

Fibrinolysin↗
PubMed1994

Activation of complement and kinin systems after thrombolytic therapy in patients with acute myocardial infarction. A comparison between streptokinase and recombinant tissue-type plasminogen activator.

BACKGROUND: We have previously shown that treatment with streptokinase induces abrupt complement activation and transient neutropenia in patients with acute myocardial infarction (AMI). The purpose of this study was to compare the effects of two different thrombolytic agents--streptokinase (SK) and recombinant tissue-type plasminogen activator (rTPA)--on activation of the complement and kinin systems in plasma of patients with AMI. METHODS AND RESULTS: Forty-one patients with AMI who were eligible for thrombolytic therapy were studied. Twenty-three patients were treated with streptokinase (1.5 million IU IV over 60 minutes) and 18 were treated with rTPA (8 with bolus of 10 mg IV, followed by 50 mg infused over 60 minutes and then 40 mg infused over 120 minutes; 10 patients were administered rTPA and heparin according to the accelerated infusion protocol indicated by the GUSTO study). C4a and C3a were measured by radioimmunoassay, soluble terminal complement components (SC5b-9) and anti-SK IgG antibodies were measured by ELISA. Cleaved high molecular weight kininogen (HK) was quantitated in plasma by SDS-PAGE and immunoblotting analysis. C4a levels were significantly and similarly increased in both groups, whereas the levels of C3a and SC5b-9 after rTPA infusion were only slightly elevated and were significantly lower than after SK. No differences were observed between patients treated with slow or accelerated rTPA regimens. The titer of antibodies to SK was highly correlated with the levels of C3a and SC5b-9, whereas a lesser correlation was observed with C4a. Treatment with rTPA did not induce the transient neutropenia observed after SK infusion. The cleavage products of HK were significantly greater after SK than after rTPA infusion. CONCLUSIONS: Our results show that both thrombolytic agents activate the classic complement pathway and that plasmin could be the common trigger for this phenomenon. A significant activation of the complement common pathway (from C3 to terminal components) was observed only with SK infusion and is attributable to the rapid formation of immunocomplexes between SK and anti-SK antibodies present in plasma as a consequence of previous streptococcal infections. The minimal activation of C5 component of the common pathway explains the absence of leukopenia in patients treated with rTPA. Cleavage of HK, larger after SK than after rTPA infusion, represents a condition enhancing the generation of bradykinin by kallikrein. The recent experimental data that indicate a damaging effect of complement activation on the infarcted zone and the contrasting favorable effect consequent to bradykinin formation raise some questions about the clinical importance of the different biological consequences of SK versus rTPA.

Adult↗
PubMed1995

Randomized double-blind comparison of two doses of Hirulog with heparin as adjunctive therapy to streptokinase to promote early patency of the infarct-related artery in acute myocardial infarction.

BACKGROUND: An improved survival rate is a consequence of successful reperfusion of the infarct-related artery. This double-blind, randomized trial investigated the potential of Hirulog, a direct thrombin inhibitor, to improve the early patency rates obtained with streptokinase and aspirin. METHODS AND RESULTS: Angiographic patency of the culprit coronary artery lesion was assessed 90 and 120 minutes after the initiation of streptokinase and aspirin and again after 4 +/- 2 days in 68 patients with acute myocardial infarction. Patients were randomized to Hirulog 0.5 mg/kg per hour for 12 hours followed by 0.1 mg/kg per hour (low dose), Hirulog 1.0 mg/kg per hour for 12 hours followed by placebo (high dose), or to heparin 5000 U bolus followed by 1000 U/h titrated to an activated partial thromboplastin time (aPTT) 2 to 2.5 times control after 12 hours. At 90 minutes, TIMI flow grade 2 or 3 was observed in 96% of patients treated with the low dose of Hirulog, in 79% with the high dose, and in 46% with heparin (P = .006) and TIMI flow grade 3 was observed in 85%, 61%, and 31% of patients, respectively (P = .008). At 120 minutes, these figures were 100%, 82%, and 62% for TIMI flow grades 2 and 3 (P = .046) and 92%, 68%, and 46% for TIMI flow grade 3 (P = .014). At 90 minutes, the relative risk for restoring TIMI flow grade 3 was 2.77 with Hirulog 0.5 mg/kg per hour compared with heparin (95% confidence limits, 1.21 to 6.35; P < .001) and 1.4 compared with Hirulog 1.0 mg/kg per minute (95% confidence limits, 1.00 to 1.51; P = .04). Patients who received a placebo infusion after 12 hours experienced more clinical events and reocclusion during the following 4 days than patients in the other two groups. CONCLUSION: Hirulog yields higher early patency rates in the culprit coronary artery than heparin when used as adjunctive therapy to streptokinase and aspirin in the early phase of acute myocardial infarction. High doses are not required and may be less effective than lower doses, which suggests that too much thrombin inhibition may be harmful.

Aspirin↗
PubMed1989

Streptokinase treatment versus calcium overload blockade in experimental thromboembolic stroke.

Thromboembolic brain ischemia was produced in dogs using an autologous blood clot model. The effect of postembolic treatment with flunarizine and streptokinase on hemispheric cerebral metabolic rate for oxygen (CMRO2), oxygen extraction ratio (OER), and cerebral blood flow (CBF) was studied by positron emission tomography (oxygen-15 technique) 24 hours after the insult. We studied five groups of experimental dogs and compared them with a control group of nonembolized dogs. Group I received no treatment, Group II was treated locally with 500,000 IU streptokinase starting 30 minutes after the insult, Group III received streptokinase locally 30 minutes after the insult and 0.1 mg/kg i.v. flunarizine immediately after the insult and 2 hours later, Group IV received flunarizine as Group III, and Group V was orally pretreated with 0.5 mg/kg/day flunarizine during 2 weeks preceding embolization. Compared with the contralateral hemisphere, in the embolized hemisphere a significant reduction of CMRO2 (-25% to -40%) and CBF in normocapnia (-35%) and hypercapnia (-50%) was observed in Groups I, II, and V. In Groups III and IV, CMRO2, OER, and CBF of the embolized hemisphere were within the normal range during normocapnia and hypercapnia; the extent of the ischemic lesions was markedly less than in the other groups of experimental dogs. We conclude that flunarizine treatment after experimental thromboembolic stroke had a favorable influence on brain tissue. Chronic preventive flunarizine treatment failed to have a beneficial effect.

Animals↗
PubMed1990

Delayed treatment with a t-PA analogue and streptokinase in a rabbit embolic stroke model.

Fibrinolytic therapy may be effective in the treatment of ischemic stroke, and clinical trials are under way. We evaluated two fibrinolytic agents, an analogue of tissue plasminogen activator (Fb-Fb-CF, the catalytic fragment of the tissue plasminogen activator molecule with a prolonged serum half-life, n = 10) and streptokinase (n = 7), in a rabbit model of embolic stroke. Both agents were given 3 hours after stroke onset, a time relevant to the clinical setting. Fb-Fb-CF was significantly better (p less than 0.04) than saline (n = 7) in restoring blood flow to previously occluded intracranial arteries, but streptokinase was ineffective. Neither fibrinolytic agent was associated with a substantial risk for intracerebral hemorrhagic side effects. Our study demonstrates that Fb-Fb-CF can safely and effectively reperfuse rabbit intracranial arteries 3 hours after occlusion, while streptokinase does not.

Animals↗
PubMed2001

Early reinfarction after fibrinolysis: experience from the global utilization of streptokinase and tissue plasminogen activator (alteplase) for occluded coronary arteries (GUSTO I) and global use of strategies to open occluded coronary arteries (GUSTO III) trials.

BACKGROUND: Trials report a 2% to 6% incidence of reinfarction after fibrinolysis for acute myocardial infarction (MI). We combined the Global Utilization of Streptokinase and Tissue plasminogen activator (alteplase) for Occluded coronary arteries (GUSTO I) and Global Use of Strategies To Open occluded coronary arteries (GUSTO III) populations to better define frequency, timing, and clinical predictors of in-hospital reinfarction. METHODS AND RESULTS: In 55 911 patients with ST-segment elevation myocardial infarction (MI) who were receiving fibrinolysis, we compared baseline characteristics and mortality rate by reinfarction incidence and developed multivariable logistic regression models to predict in-hospital reinfarction and composite of death or reinfarction. Reinfarction occurred in 2258 patients (4.3%) a median of 3.8 days after fibrinolysis; rates did not differ between GUSTO I (4.0%) and GUSTO III (4.2%) or by fibrinolytic assignment (streptokinase, 4.1%; alteplase, 4.3%; reteplase, 4.5%; combined streptokinase and alteplase, 4.4%; P=0.55). Advanced age, shorter time to fibrinolysis, non-US enrollment, nonsmoking status, prior MI or angina, female sex, anterior MI, and lower systolic blood pressure were associated significantly with reinfarction. Patients with reinfarction had higher mortality at 30 days (11.3% versus 3.5% without reinfarction; odds ratio, 3.5; P<0.001) and from 30 days to 1 year (4.7% versus 3.2%; hazard ratio, 1.5; P<0.001). Significant multivariate predictors of in-hospital death or reinfarction included age, Killip class, systolic and diastolic blood pressures, heart rate, anterior MI, smoking status, prior MI, sex, and country of enrollment (all P<0.001). CONCLUSIONS: Reinfarction occurs infrequently after fibrinolysis but confers increased risk of 30-day and 1-year mortality. Some predictors of reinfarction differ from known predictors of death after MI. Improved treatment and prevention strategies for reinfarction deserve study.

Aged↗
PubMed1996

Temperature- and pH-sensitive terpolymers for modulated delivery of streptokinase.

Controlled release devices were designed which respond to changes in pH and temperature by reversibly swelling and deswelling to control release of streptokinase. Copolymer hydrogels composed of N-isopropylacrylamide (NIPAAm) and methacrylic acid (MAA) as well as terpolymer hydrogels containing NIPAAm, acrylic acid (AA), and 2-hydroxyethyl methacrylate (HEMA) were synthesized. Hydrogels containing NIPAAm display a change in swelling behavior across the lower critical solubility temperature of PNIPAAm, whereas hydrogels with MAA and AA swelled only at high pH values due to the ionization of carboxylic pendant groups. HEMA was chosen as a third component to add mechanical strength and integrity to the hydrogel. Pulsatile pH- and temperature-dependent swelling studies were performed to determine the extent and rate at which the hydrogels swell in response to changing conditions. Results showed that increasing the NIPAAm concentration in the copolymers or terpolymers resulted in a higher degree of temperature-sensitive swelling. Synthesis of a terpolymer in which segments rich in NIPAAm were distributed within P(AA-co-HEMA) chains led to hydrogels displaying increased temperature sensitivity. Streptokinase was incorporated into the hydrogels, and its release was observed under the combined effects of temperature and pH. The streptokinase release pattern followed the swelling state of the hydrogel, with drug release occurring at a significantly higher rate from the most swollen hydrogels.

Acrylamides↗
PubMed1992

Effects of intravenous streptokinase and CLS 2210 (calcium dobesilate) on the biochemical markers of early acute myocardial infarction: a historic comparison with both studies.

In a previous double-blind, randomized study, CLS 2210 (a new formulation of calcium dobesilate) or placebo was administered by intravenous infusion to 41 patients having their first acute myocardial infarction. In the present study 19 comparable patients were treated intravenously with streptokinase under identical conditions and the results compared with those from the previous study. In all patients administration was begun within three hours of onset of symptoms and continued over seventy-two hours. Blood samples were taken for the measurement of serum activity of creatine kinase and its isoenzyme MB, and the serum and urinary concentrations of myoglobin and glycosaminoglycans were also measured. The purpose of this study was to determine the effects of CLS 2210, placebo, and streptokinase on these biochemical markers of acute myocardial infarction, thereby assessing their actions in limiting myocardial necrosis. In the CLS 2210-treated patients, the levels of serum creatine kinase and serum and urinary myoglobin were significantly lower than in the placebo patients throughout the seventy-two hours (p = 0.01, 0.005, 0.004 respectively). The levels of creatine kinase MB and serum glycosaminoglycan in the CLS 2210 patients were initially higher than in the placebo patients but fell below placebo levels between the fortieth and fifty-fifth hours, respectively (p = 0.89, 0.02). Only the glycosaminoglycan urinary concentrations were higher in the CLS 2210 group than in the placebo group throughout (p = 0.0005). The values for the six variables investigated showed no statistically significant difference between placebo and streptokinase.(ABSTRACT TRUNCATED AT 250 WORDS)

Benzenesulfonates↗
PubMed1995

The effect of streptokinase on return to work 18 months after a first myocardial infarction.

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

Adult↗