Intracoronary streptokinase in clinical practice

Timmis, Gerald C.; Gangadharan, V.; Hauser, Andrew M.; Ramos, Renato G.; Westveer, Douglas C.; Gordon, Seymour

doi:10.1016/0002-8703(82)90266-6

Cited by 75 publications

(26 citation statements)

References 30 publications

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“…If systemic fibrinogen levels less than 100 mg/dl are accepted as a measure of systemic fibrinolysis, then the incidence of systemic fibrinolysis is also significantly greater with streptokinase than with urokinase. While initial reports of intracoronary thrombolysis suggested little systemic effect on the coagulation system,8 several reports confirm significant reduction in systemic fibrinogen levels after infusion of intracoronary streptokinase.10 11 It is possible that the rate and duration of infusion of streptokinase we used is excessive for intracoronary infusion, thereby leading to a systemic effect on fibrinogen levels. The total duration of the streptokinase infusion was longer than the urokinase infusion in our study, but duration of infusion seems to have little relationship to fall in fibrinogen levels for streptokinase ( figure 1).…”

Section: Discussionmentioning

confidence: 97%

Intracoronary thrombolysis in patients with acute myocardial infarction: comparison of the efficacy of urokinase with streptokinase.

Tennant¹,

Dixon²,

Venable³

et al. 1984

Circulation

125

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The efficacy of intracoronary urokinase and streptokinase were compared in 80 patients with acute myocardial infarction in a prospective, randomized, double-blind study. Urokinase was infused into the occluded coronary artery at 6000 U/min, and streptokinase was infused at 2000 U/min. 756 MethodsThis was a randomized, double-blind, parallel study of the efficacy of intracoronary urokinase (Abbokinase; Abbott Pharmaceuticals) and streptokinase (Streptase; Hoechst-Roussel Pharmaceuticals, Inc.) in treating patients with acute myocardial infarction.Patients were eligible for inclusion in the study under the following conditions: (1) typical symptoms of myocardial infarction occurred less than 12 hr before infusion, (2) electrocardiogram showed short-term changes of myocardial infarction, (3) no specific contraindication to thrombolytic therapy existed, and (4) angiographic demonstration of a completely occluded vessel related to the infarct. After informed consent was obtained, the hospital pharmacy randomized the patient to receive either urokinase or streptokinase. Unlabeled thrombolytic solution, containing either streptokinase at a concentration of 500 IU/ml or urokinase at a concentration of 1500 U/ml, was supplied by the pharmacy. All medical personnel and the clinical investigators outside the pharmacy were blinded as to the thrombolytic drug used. Baseline coagulation studies before catheterization included measurements of serum fibrinogen, fibrin split products, thrombin time, prothrombin time, partial thromboplastin time, and plasminogen levels. In the catheterization laboratory, left ventricular and coronary angiography were performed. Heparin was given without knowledge of the treatment group in bolus doses ranging from 2500 U to 10,000 U. The thrombolytic solution was then infused into the occluded infarct-related vessel at a rate of 4 ml/min (

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Section: Discussionmentioning

confidence: 97%

Intracoronary thrombolysis in patients with acute myocardial infarction: comparison of the efficacy of urokinase with streptokinase.

Tennant¹,

Dixon²,

Venable³

et al. 1984

Circulation

125

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“…The incidence of such events, particulary in the setting of thromboembolic fragmentation is unknown; however, such events have been observed," 9 and probably account for the lower incidence of angiographically demonstrated occlusions when patients are examined more than 12 hours after the signal stroke. 71 Dalai and colleagues reported spontaneous recanalization of carotid territory thromboembolic arterial occlusions within 10 minutes to 18 days of the control angiogram in a prospective serial angiographic study of 9 acute stroke patients.'…”

Section: Spontaneous Thrombolysis In Acute Strokementioning

confidence: 99%

Thrombolytic therapy in stroke: possibilities and hazards.

Zoppo¹,

Zeumer²,

Harker³

1986

Stroke

202

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patients with various thrombolytic agents, and to weigh the relative risk of intracerebral hemorrhage in patients treated with fibrinolytic agents for stroke and for other thrombotic disorders. Mechanism of ThrombolysisArterial thrombosis and thrombus extension involve to varying degrees the processes of endothelial injury, platelet aggregation and release, and thrombin generation. Thrombin-mediated fibrinogen cleavage results in fibrin formation which is required for thrombus stabilization.80 Thrombin-mediated fibrin formation occurs in direct relation to platelet activation by several mechanisms. Platelets promote activation of the early stages of intrinsic coagulation by a process that involves a factor XI receptor and high molecular weight kininogen.81 Also, factors V and VHI interact with platelet membrane phospholipids to facilitate the activation of factor X to Xa and the conversion of prothrombin to thrombin.82 Platelet-bound thrombinmodified factor V (factor Va) serves as a high affinity platelet receptor for factor Xa. 83 Consequently, the rate of thrombin generation is accelerated 10 3 fold, providing a potent positive feedback mechanism for initiation of thrombin formation on the platelet surface, fibrin network formation in the thrombus, and indirectly, fibrinolysis.Thrombus dissolution is, in large part, mediated by fibrinolysis localized within the thrombus.84 " 86 Fibrin (and fibrinogen) degradation is catalyzed by plasmin, the product of plasminogen activation. 87 In the consolidating thrombus plasminogen binds to fibrin and to platelets, allowing local release of plasmin within the thrombus. The circulating plasminogen activators, tissue plasminogen activator (tPA) and single chain urokinase plasminogen activator (scuPA), catalyze plasby guest on

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“…'6 On the other hand, we have found that the risk of hemorrhage is not a function of the success of thrombolysis or of its degree. 17 This is probably true because the degree of clot dissolution does not always parallel the extent of the lytic state resulting from the systemic effects of streptokinase. 18 19 Duckert et al 20 stated that the lytic state, if severe, can contribute to hemorrhage; others have suggested that this may be caused by lysis of hemostatic plugs.…”

mentioning

confidence: 99%

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

Timmis¹,

Gangadharan²,

Ramos³

et al. 1984

Circulation

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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, 1 11 ±+ 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.

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Intracoronary streptokinase in clinical practice

Cited by 75 publications

References 30 publications

Intracoronary thrombolysis in patients with acute myocardial infarction: comparison of the efficacy of urokinase with streptokinase.

Intracoronary thrombolysis in patients with acute myocardial infarction: comparison of the efficacy of urokinase with streptokinase.

Thrombolytic therapy in stroke: possibilities and hazards.

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

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