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PubMed1984

The effect of streptokinase on intramyocardial hemorrhage, infarct size, and the no-reflow phenomenon during coronary reperfusion.

The purpose of this study was to determine whether streptokinase exacerbates intramyocardial hemorrhage during coronary reperfusion, has any intrinsic effect on myocardial infarct size other than its ability to lyse proximal thrombi in coronary arteries, and can abolish the no-reflow phenomenon. Anesthetized open-chest dogs underwent coronary occlusion for 3 hr followed by 3 hr of reperfusion. Area of infarct was assessed by tetrazolium staining, anatomic zone of no-reflow by injection of the fluorescent dye thioflavin S at the end of the reperfusion period, regional blood flow during occlusion and reperfusion by the radioactive microsphere technique, and extent of gross hemorrhage by assessment of photographic enlargements of the heart slices. Area of infarction of the left ventricle was similar in control (13.4 +/- 3.6%) and streptokinase-treated dogs (13.0 +/- 2.9%; p = NS). Seven of eight dogs in the untreated group had anatomic perfusion defects as assessed by thioflavin S at the end of the reperfusion phase; seven of eight dogs in the streptokinase group had anatomic perfusion defects. There was no difference in the extent of gross hemorrhage between the two groups (6.5 +/- 2.1% of left ventricle in controls and 5.7 +/- 2.3% in streptokinase-treated dogs). Severe depression of regional blood flow during reperfusion was present within the infarcted tissue and was associated with an anatomic perfusion defect as defined by thioflavin S; there was moderate depression of flow within the noninfarcted, salvaged subepicardium. In a separate series of experiments, infarcts were assessed for hemoglobin content. Intramyocardial hemoglobin levels were not higher after fibrinolytic therapy plus reperfusion compared with reperfusion alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1984

A randomized trial of intravenous and intracoronary streptokinase in patients with acute myocardial infarction.

The clinical effects of intravenous streptokinase in patients with acute myocardial infarction were compared with those of intracoronary streptokinase in a randomized, prospective study. Comparisons were also made with a historical control group. Fifty patients were entered into the study at 2.4 +/- 1.2 hr after onset of pain, and 27 were assigned to intravenous and 23 to intracoronary therapy. The doses of streptokinase averaged 212,000 U ic and 845,000 U iv (0.75 X 10(6) U/5 hr, n = 14 or 10(6) U/1 hr, n = 13). Results of studies of the two intravenous dosage schedules were similar and so were combined. Streptokinase was administered at 2.8 +/- 1.0 hr after onset of pain in the intravenous and at 4.3 +/- 1.4 hr in the intracoronary drug group (p less than .001). Convalescent (day 10) radionuclide ejection fractions were 54 +/- 14% for the intravenous and 50 +/- 16% for the intracoronary drug group. Change in ejection fraction from day 1 to 10 tended to be greater after intravenous drug: 5.1% (p less than .08) vs 1.2% (NS). Semiquantitative regional wall motion indexes in the infarct zone showed significant and similar modest improvement from admission to day 10 in both groups (p less than .02). Accelerated enzyme-release kinetics were noted after both therapies. Times of peak enzyme levels for patients on intravenous and intracoronary drug were, respectively, 12.5 +/- 5.0 and 11.5 +/- 4.3 hr for creatine kinase MB isoenzyme and 31.7 +/- 11.8 and 28.1 +/- 12.7 hr for lactic dehydrogenase (LDH). Peak LDH-1 level was lower in patients receiving intravenous drug than in the historical control group (p less than .05). Electrocardiographically summed ST segments diminished rapidly after therapy in both groups; Q wave development was similar and overall R wave loss was equivalent and less extensive compared with in historical control subjects. Infarct pain requiring morphine was diminished similarly in both treatment groups. Incidence of early arrhythmias and heart failure also did not differ. Posttherapy ischemic events and early surgery tended to be more common in the intracoronary group and bleeding was more common in the intravenous group. Intravenous drug did not decrease early hospital mortality (intravenous drug = 5, historical control = 4, intracoronary drug = 1); the differences in this parameter among groups were not significant. At convalescent angiographic evaluation, anterograde perfusion was present in 73% of those receiving intravenous and 76% of those receiving intracoronary drug.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1986

Which patients benefit most from early thrombolytic therapy with intracoronary streptokinase?

The effect of thrombolysis in acute myocardial infarction on enzymatic infarct size, left ventricular function, and early mortality was studied in subsets of patients in a randomized trial. Early thrombolytic therapy with intracoronary streptokinase (152 patients) or with intracoronary streptokinase preceded by intravenous streptokinase (117 patients) was compared with conventional treatment (264 patients). All 533 patients were admitted to the coronary care unit within 4 hr after onset of symptoms indicative of acute myocardial infarction. Four hundred eighty-eight patients were eligible for this detailed analysis, and 245 of these were allocated to thrombolytic therapy and 243 to conventional treatment. Early angiographic examinations were performed in 212 patients allocated to thrombolytic therapy. Patency of the infarct-related artery was achieved in 181 patients (85%). Enzymatic infarct size, as measured from cumulative alpha-hydroxybutyrate dehydrogenase release, was smaller in patients allocated to thrombolytic therapy (median 760 vs 1170 U/liter in control patients, p = .0001). Left ventricular ejection fraction measured by radionuclide angiography before discharge from the hospital was higher after thrombolytic therapy (median 50% vs 43% in control patients, p = .0001). Three month mortality was lower in patients allocated to thrombolytic therapy (6% vs 14% in the control group, p = .006). With the use of multivariate regression analysis, infarct size limitation, improvement in left ventricular ejection fraction, and three month mortality were predicted by sum of the ST segment elevation, time from onset of symptoms to admission, and Killip class at admission. Thrombolysis was most effective in patients admitted within 2 hr after onset of symptoms and in patients with a sum of ST segment elevation of 1.2 mV or more. On the other hand, no beneficial effects of streptokinase on enzymatic infarct size, left ventricular function, or mortality were observed in the subset of patients with a sum of ST segment elevation of less than 1.2 mV who were admitted between 2 and 4 hr after onset of symptoms.

Cardiac Catheterization↗

PubMed1991

Thrombolytic therapy with streptokinase stimulates collagen breakdown.

BACKGROUND: Plasmin is capable of degrading extracellular matrix components such as collagen in vitro. To evaluate the significance of this for in vivo conditions, we set out to study the effect of streptokinase, which acts by converting plasminogen to plasmin, on the serum concentrations of the amino-terminal propeptide of type III procollagen (PIIINP) and the carboxy-terminal propeptide of type I procollagen (PICP). METHODS AND RESULTS: Twenty-three patients with suspected acute myocardial infarction were included in the study; 17 of them received thrombolytic therapy, and six were treated conservatively. PIIINP and PICP were assayed with radioimmunoassays. Kinetics of creatine kinase-MB release were determined to differentiate reperfusers from nonreperfusers. Composite curves of creatine kinase-MB release were constructed for different patient subgroups. During streptokinase infusion the serum concentrations of PIIINP increased rapidly, with a maximum mean increase of 50% (from 2.2 +/- 0.2 to 3.3 +/- 0.3 micrograms/l) in 45 minutes. A similar increase was also observed in two patients who received thrombolytic therapy but did not subsequently develop any myocardial infarction determined on the basis of enzyme release. The relative increase in PIIINP during streptokinase treatment was higher in those acute myocardial infarction patients with probable reperfusion than those with nonprobable reperfusion. Corresponding changes in PIIINP were not seen in the control group. Two days later there was a second increase in serum PIIINP for both patient groups. This change coincided with a similar increase in PICP. CONCLUSIONS: We conclude that streptokinase, probably by activation of plasminogen to plasmin, stimulates the breakdown of type III collagen during thrombolytic therapy. This phenomenon may decrease the risk of rethrombosis of the affected artery if the exposed collagen is responsible for thrombosis formation, but it could also be involved in the development of hemorrhagic complications during thrombolytic therapy. The second increase in PIIINP levels probably indicates type III collagen synthesis of the infarcted area. This investigation represents a pilot study, and more studies on the effects of various thrombolytic agents on interstitial collagen metabolism are obviously needed.

Collagen↗

PubMed1994

A pilot, early angiographic patency study using a direct thrombin inhibitor as adjunctive therapy to streptokinase in acute myocardial infarction.

BACKGROUND: The success of streptokinase in acute myocardial infarction is hampered by the high failure rate to achieve early reperfusion. This study evaluates the possible benefit of Hirulog (Biogen, Cambridge, Mass), a direct thrombin inhibitor, as adjunct therapy to streptokinase to enhance early patency and prevent rethrombosis. Heparin has been shown to be of very limited benefits in this setting. METHODS AND RESULTS: Forty-five patients were randomized to Hirulog or heparin (2:1 ratio). Coronary angiography documented a TIMI 2 or 3 flow after 90 minutes in 77% of the patients treated with Hirulog and streptokinase and in 47% of patients treated with heparin and streptokinase (P < .05) and after 120 minutes in 87% and 47% of patients, respectively (P < .01). TIMI 3 flow was established in 77% of patients with Hirulog compared with 40% with heparin (P < .02). The clinical outcome and the bleeding rate was also favorable to Hirulog; no reocclusion was observed at late angiography performed 4.7 days later. CONCLUSIONS: Hirulog in this pilot study significantly improved the early patency rate of the infarct-related artery with a favorable clinical profile. This new direct thrombin inhibitor exhibits promise as adjunctive therapy to thrombolysis.

Coronary Angiography↗

PubMed1990

Accelerated thrombolysis and reperfusion in a canine model of myocardial infarction by liposomal encapsulation of streptokinase.

The aim of thrombolytic therapy for acute myocardial infarction with plasminogen activators such as streptokinase is to lyse the coronary thrombus and reestablish blood flow as quickly as possible so that heart tissue loss is minimized and mortality rates are improved. Streptokinase has been encapsulated in large unilamellar phospholipid vesicles and tested in an animal model of acute myocardial infarction. The time required to restore vessel patency has been reduced more than 50% when compared with findings for free streptokinase. The total dosage of streptokinase required was lower, and smaller remnant thrombi were observed with the encapsulated agent. Results from this initial unoptimized study may have significant implications for further reduction in mortality from heart attacks by therapy with plasminogen activators.

Animals↗

PubMed1990

Incidence of cerebral hemorrhage after treatment with tissue plasminogen activator or streptokinase following embolic stroke in rabbits [corrected].

We studied thrombolysis in an animal model of embolic stroke to determine the safety of tissue plasminogen activator and streptokinase. We occluded the middle cerebral arteries of 137 rabbits with radiolabeled blood clots and administered tissue plasminogen activator (n = 49), streptokinase (n = 40), or saline (n = 48) at various times after embolization. We assessed the rate of thrombolysis and cerebral hemorrhage 24 hours later. Both drugs were very effective in producing thrombolysis. Compared with saline, streptokinase caused a significant increase in the rate of cerebral hemorrhage (p less than 0.05), but tissue plasminogen activator did not. We conclude that thrombolytic therapy for acute stroke should be safer with tissue plasminogen activator than with streptokinase.

Animals↗

PubMed1976

Deep vein thrombosis treated with streptokinase or heparin. A randomized study.

Randomly assigned streptokinase or heparin therapy was studied in 50 patients with deep vein thrombosis of less than 2 weeks' duration. Venography was performed prior to therapy, after 3 days, and after 10 days. Two radiologists who were unaware of the patient's therapy compiled a single average lytic score for each patient at each time interval. Lysis of venous thrombi was significantly greater with streptokinase than with heparin after 3 days, but not after 10 days of treatment. Lytic scores achieved with streptokinase were significantly better than those achieved with heparin therapy (P less than .01) in male patients who were symptomatic for 3 days or less. In females, regardless of the duration of symptoms, thrombolytic results obtained with streptokinase were not significantly different than results obtained with heparin.

Female↗

PubMed1976

Deep vein thrombosis treated with streptokinase or heparin. Follow-up of a randomized study.

Twenty-seven patients with deep vein thrombosis whose primary therapy was randomized between streptokinase and heparin were reevaluated clinically and by ascending venography after a mean period of 7 months. Normal venograms were found in 6 (40%) of the streptokinase-treated patients and in 1 patient (8%) who had heparin therapy. Segmental valve preservation was found in 1 patient from each group. All patients with complete or partial valve preservation became asymptomatic. Vein recanalization without preservation of valves occurred in 18 patients: 8 (54%) of those on streptokinase, and 10 (83%) of those on heparin. At the time of follow-up, 11 of these 18 patients, including 8 who had had prior thrombosis, reported peripheral edema; the postphlebitic syndrome developed in 1. Factors favoring a good outcome of acute venous thrombosis were (1) no prior thrombotic disease, (2) localized thrombosis, and (3) prompt streptokinase therapy.

Adult↗

PubMed1990

Thrombolytic versus fibrinogenolytic activity of rt-PA and streptokinase in patients with acute myocardial infarction.

In this study the concentration of plasma breakdown products of cross-linked fibrin (XDP), serum fibrinogen-fibrin degradation products (FDP), and plasma fibrinogen were measured before and at the end of the administration of single-chain recombinant tissue-type plasminogen activator (rt-PA, 100 mg IV over three hours) or streptokinase (1.5 million units over one hour), respectively, in two groups, each composed of 22 patients with acute myocardial infarction. The XDP concentration was not statistically different between the two groups at the end of thrombolytic treatment, whereas FDP and fibrinogen concentrations were significantly different (FDP: streptokinase 396 +/- 287 vs rt-PA 177 +/- 222 micrograms/mL, p less than 0.01; fibrinogen: streptokinase 71 +/- 43 vs rt-PA 181 +/- 49 mg/dL, p less than 0.001). These results indicate that the two drugs have equipotent thrombolytic activity at this administration regimen but that rt-PA causes a markedly more selective lysis of fibrin in comparison with streptokinase.

Adult↗

PubMed1993

Clinical and angiographic features of patients with an occluded versus a patent infarct vessel after intravenous streptokinase for acute myocardial infarction.

Despite early treatment with thrombolytic agents for acute myocardial infarction, a significant portion of patients fail to achieve a patent infarct artery. To study the various factors related to achieving patency in the infarct vessel, 201 patients who received streptokinase within six hours of symptoms were studied. All patients underwent cardiac catheterization during the same hospitalization at 5.40 +/- 3.26 days after admission. Forty-five (22.4%) patients were found to have an occluded infarct artery (group 1) and 156 (77.6%) had a patent infarct vessel (group 2). There was no difference in the time from onset of symptoms to receiving streptokinase between the two groups. The two groups were similar to each other with regard to age, gender, history of myocardial infarction or angina, and major risk factors for coronary disease. Coagulation parameters before and after streptokinase therapy, reflecting the lytic state, were similar in both groups. The left ventricular end diastolic pressure was significantly higher and the left ventricular ejection fraction was significantly lower in group 1 than in group 2. These observations suggest that despite early initiation of thrombolytic therapy in patients with acute myocardial infarction, a significant portion of patients fail to achieve a patent infarct artery. This failure cannot be explained by the observed clinical parameters or the lytic state after streptokinase.

Adult↗

PubMed1999

Concomitant use of intraaortic balloon counterpulsation and streptokinase in acute anterior myocardial infarction.

Using a prospective, nonrandomized design, the authors sought to determine whether concomitant use of intraaortic balloon counterpulsation (IABP) and streptokinase in acute anterior myocardial infarction (MI) would improve the in-hospital mortality rate and angiographic findings. The study included 45 patients with an acute anterior MI. All patients received intravenous streptokinase. Among these, 25 patients had concomitant IABP while the remaining 20 patients had streptokinase alone. All patients underwent cardiac catheterization. Patients treated with concomitant IABP had a significantly higher frequency of thrombolysis in myocardial infarction (TIMI) grade 3 flow (n: 11; 44% vs n: 1; 5%, p<0.05), and there was a trend toward a lower in-hospital mortality rate in the IABP group (n: 0; 0% vs n: 3; 15%, p=0.08). The angiographic presence of thrombus image and grade > or =2 coronary collateral circulation to the infarct-related coronary artery for the IABP and non-IABP groups did not differ significantly. The preliminary results of this study suggest that concomitant use of IABP and streptokinase in acute anterior MI increases the incidence of TIMI grade 3 flow and may have decreased the in-hospital mortality rate without unacceptable rates of vascular or hemorrhagic complications.

Cardiac Catheterization↗

PubMed1989

Anaphylactic reaction to streptokinase with first exposure: case report and review of the literature.

Thrombolytic therapy has become an accepted part of the management of acute myocardial infarction. One agent with widespread use in this setting is streptokinase. We report the case of a 62-year-old man who experienced an anaphylactic reaction with cardiopulmonary arrest immediately after receiving streptokinase 1.5 million units iv administered for an acute anterior wall myocardial infarction. The patient had no history of prior exposure to streptokinase, chronic allergic reactions, or reactive airway disease. Five other cases of anaphylaxis to streptokinase are also reviewed.

Anaphylaxis↗

PubMed1993

Intrapleural streptokinase as adjunctive treatment for persistent empyema in pediatric patients.

Successful treatment of persistent empyema by intrapleural streptokinase is described in five pediatric patients. Their ages ranged from 18 months to 7 years. All experienced dramatic improvement in the resolution of their empyemas following intrapleural streptokinase. Improved chest tube drainage occurred concurrently with clinical improvement. Intrapleural instillation of streptokinase appears to be a safe adjunctive therapeutic tool to facilitate drainage of persistent empyema in the small number of pediatric patients in whom it has been employed. Additional study will be required to further assess the long-term therapeutic efficacy and consequences of intrapleural streptokinase therapy.

Chest Tubes↗

PubMed1988

Treatment of massive acute pulmonary embolism. The use of low doses of intrapulmonary arterial streptokinase combined with full doses of systemic heparin.

The efficacy of low-dose, locally administered streptokinase (SK) combined with full therapeutic systemic doses of heparin was investigated. Seven patients with angiographically proven massive acute pulmonary embolism were treated. Streptokinase, 10,000-20,000 units/hour, was administered directly into the left or right pulmonary artery for 9 to 24 hours. Heparin was administered concurrently. The number of unperfused segments of the infused lung shown on the lung scan decreased from 5 +/- 2 to 2 +/- 1 after 12-24 hours (p less than .01). No change was shown in the contralateral lung. The angiographic index of severity score in the infused lung decreased from 16 +/- 1 to 9 +/- 4 (p less than .01). The partial pressure of oxygen in arterial blood improved within four hours. In spite of the low doses of streptokinase, however, two major bleeding episodes occurred that required blood transfusion. In conclusion, low dose intrapulmonary streptokinase, combined with intravenous heparin, may provide a therapeutic option in patients with life-threatening massive acute pulmonary embolism in whom full dose lytic therapy may be hazardous, although even low dose lytic therapy was associated with risk.

Aged↗

PubMed1987

Preclinical pharmacological evaluation of anisoylated plasminogen streptokinase activator complex.

An ideal thrombolytic (or fibrinolytic) agent is one which would generate the formation of plasmin only where it is required, i.e. bound to fibrin within the thrombus. However, the capacity of even the newer thrombolytic agents to achieve localised plasmin generation within the thrombus is relative and depends on the concentration of the agent administered. For all available activators, the concentration required for effective clinical thrombolysis is also capable of converting plasminogen to plasmin within the circulation (plasminaemia). Since the action of plasmin is not specific to fibrin, plasminaemia results in dissolution not only of fibrin but also of several other clotting factors. For example, plasmin can degrade fibrinogen and cause impaired haemostasis. The plasminogen activators which are available, or have been developed to date, include streptokinase, urokinase, pro-urokinase, anisoylated plasminogen-streptokinase activator complex (APSAC) and tissue plasminogen activator (t-PA). All of these agents have the same biochemical mechanism of action, cleaving an arginine-valine bond in the plasminogen molecule to form plasmin, but they differ with regard to other important properties. The first property to be considered is clot specificity; the ability to dissolve fibrin as opposed to fibrinogen, and also to dissolve the clot as opposed to a haemostatic plug. Unfortunately, fibrin specificity does not equate entirely with thrombus specificity, and all currently developed plasminogen activators, by dissolving fibrin, will induce the destruction of haemostatic extravascular plugs as well as intravascular thrombi. Thus, no agent is thrombus-specific in this respect. The degree of fibrinogenolysis does vary between plasminogen activators. Those which have the least effect on haemostasis or clotting capability would seem, at first, to be preferable. However, a short term reduction in fibrinogen could also be beneficial, since it may reduce the incidence of early reocclusion and, by reducing blood viscosity, improve microcirculation to the infarct zone. The intrinsic efficiency of the plasminogen activators is a second important property. In vitro, under conditions pertaining to the circulation, urokinase is about 10 times more efficient than t-PA at converting glu-plasminogen to plasmin (on the basis of the Vmax to Km ratio), while streptokinase-plasmin is 20 times more efficient. The efficiency of these activators is increased in the presence of fibrin and lys-plasminogen, 1800-fold for t-PA, 8-fold for urokinase and 180-fold for streptokinase-plasmin.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1987

Analysis of coagulation and fibrinolysis after intravenous anisoylated plasminogen streptokinase activator complex or heparin in patients with acute myocardial infarction. A Belgian multicentre study.

A multicentre randomised trial including 87 patients admitted for acute myocardial infarction compared the effects of a single intravenous bolus of an anisoylated plasminogen streptokinase activator complex (APSAC) 30 units with those of heparin treatment on haemostasis during the first 4 days after treatment. In the APSAC group, a rapid and significant reduction in fibrinogen, plasminogen and alpha 2-antiplasmin was observed, associated with an increase of fibrin(ogen) degradation products, reflecting a strong systemic lytic activity. None of these parameters were significantly modified by heparin, but the anticoagulant effect was apparent as assessed by the activated partial thromboplastin time. The systemic fibrinolysis induced after different regimens of streptokinase infusion demonstrated that an intravenous bolus of APSAC 30U was as potent as streptokinase 500,000 or 1,500,000IU administered intravenously over 45 minutes and definitely more fibrinolytic than intracoronary infusion of streptokinase 250,000IU. Despite the demonstrated fibrin specificity of the drug at a low dose, a high dose of APSAC (30U intravenously) induced an important systemic lytic state for at least 12 hours.

Anistreplase↗

PubMed1987

Anisoylated plasminogen streptokinase activator complex (APSAC). A review of its mechanism of action, clinical pharmacology and therapeutic use in acute myocardial infarction.

APSAC is a new thrombolytic agent with advantages over conventional therapy such as streptokinase. In particular, it is suitable for intravenous administration over 4 to 5 minutes, in contrast with the prolonged infusion required with intravenous streptokinase, thus facilitating treatment of acute myocardial infarction outside a coronary care unit. Additionally, its fibrinolytic action is theoretically selective for fibrin associated with thrombi, which should minimise systemic fibrinolysis. However, in practice, systemic fibrinolysis does occur to some extent in most patients, but clinically significant haemorrhagic complications are rare. At the recommended dose of 30U injected intravenously over a period of 4 to 5 minutes in patients with acute myocardial infarction of less than 6 hours' duration, reperfusion of occluded coronary arteries occurs in about 72% of patients (range 53 to 91% in individual studies). Subsequent reocclusion has been reported in 0 to 20% of patients in most studies, with an average reocclusion rate of around 10%. The reperfusion rate compares favourably with that reported for intracoronary streptokinase and has tended to be superior to that with intravenous streptokinase. Thus, APSAC is an important advance in thrombolytic therapy for patients with acute myocardial infarction. Of particular importance is its relative ease of administration, reducing the dependence on coronary care units with catheterisation facilities, and the associated costs and delays in implementing treatment. APSAC should result in effective thrombolytic therapy being rapidly introduced after acute myocardial infarction in a wider proportion of patients than was previously feasible.

Anistreplase↗