Effect Of Intravenous Streptokinase Research Articles

Streptokinase inhibits pulmonary tumor seeding in an animal experimental model

One aspect of the metastatic process involves entrapment of tumor cells within the microcirculation of organs in a "fibrin-platelet mesh." We postulate that destruction of this mesh by fibrinolysis might discourage tumor seeding, thereby inhibiting metastasis. To study this hypothesis, the effect of intravenous streptokinase on pulmonary tumor seeding was examined in a rodent model. In vitro experiments demonstrated that streptokinase had no cytotoxic or cytostatic effect on the Mtln3 cell line. Pharmacokinetic studies showed that at 30,000 U/kg, streptokinase caused systemic fibrinolysis in the Fischer rat, as demonstrated by the thrombin time and fibrin plate lysis assay. Streptokinase administered at this dose, 30 min after tumor cell injection, caused a significant decrease in pulmonary tumor seeding (median 23.0 in the streptokinase-treated group vs. 67.5 in untreated controls, P < 0.0001, Mann-Whitney U-test). Analysis of fibrin degradation products in the streptokinase-treated group suggested that this effect might be secondary to fibrinolysis. The implications of these findings are discussed.

Streptokinase for Inferior Myocardial Infarction

To the editors: I am concerned that the Midgette and colleagues' meta-analysis (1) of the effect of intravenous streptokinase on mortality due to acute inferior myocardial infarction may be misinte...

Meta-analysis: Streptokinase reduces mortality in suspected myocardial infarction

Source Citation Midgette AS, O'Connor GT, Baron JA, Bell J. Effect of intravenous streptokinase on early mortality in patients with suspected acute myocardial infarction. A meta-analysis by anatomic location of infarction. Ann Intern Med. 1990;113:961-8.

Effect of intravenous streptokinase on the relation between initial ST-predicted size and final QRS-estimated size of acute myocardial infarcts: Clemmensen P, Grande P, Saunamaki K, et al J Am Coll Cardiol 16: 1252–1257 Nov 1990

Effect of intravenous streptokinase on the relation between initial ST-predicted size and final QRS-estimated size of acute myocardial infarcts: Clemmensen P, Grande P, Saunamaki K, et al J Am Coll Cardiol 16: 1252–1257 Nov 1990

Effect of intravenous streptokinase on the relation between initial ST-predicted size and final QRS-estimated size of acute myocardial infarcts

Thrombolytic therapy has been documented to reduce acute myocardial infarct size. The previously established relation between initial ST segment elevation and final electrocardiographic (ECG) myocardial infarct size in patients without coronary reperfusion might therefore be altered by thrombolytic therapy. The effect of intravenous Streptokinase on this relation was therefore studied in 73 patients with initial acute myocardial infarction who had participated in the Second International Study of Infarct survival (ISIS-2). Patients who received Streptokinase were considered as one group and patients who did not receive streptokinase as a control group. Final myocardial infarct size, which was estimated from the QRS score, was predicted from the admission standard ECG by previously developed formulas based on ST segment elevation.In the 40 control patients there was no change from ST-predicted to final QRS-estimated infarct size (median 17.7% versus 18.3%; p = NS). In the 33 patients in the streptokinase group, there was a highly significant decrease from predicted to final myocardial infarct size (median 21.9% versus 16.2%; p < 0.0002). This decrease was found for both anterior (median 23.7% versus 19.5%; p < 0.03) and inferior (median 21.9% versus 12.0%; p = 0.001) infarct locations. Multiple regression analysis adjusting for differences in predicted infarct size confirmed the significance of Streptokinase on the difference in infarct size (p = 0.006). Based on the variability of the percent change from predicted to final infarct size in the control group, a threshold decrease ≥20% is required for identification of salvage. Application of this threshold identified 10 (25%) of 40 control patients and 20 (61%) of 33 patients in the Streptokinase group (p < 0.005).Thus, intravenous Streptokinase significantly changes the relation between predicted and final acute myocardial infarction size, demonstrating the potential of the standard ECG for noninvasive evaluation of myocardial salvage after thrombolytic therapy.

ECG and enzymatic indicators of therapeutic success after intravenous streptokinase for acute myocardial infarction

Thrombolytic therapy has been documented to result in reperfusion of jeopardized myocardium and reduction in the size of the acute myocardial infarction (AMI). The effect of intravenous streptokinase on a creatine kinase-MB (CK-MB) reperfusion index and an ECG estimate of myocardial salvage was therefore studied in 65 patients with a first AMI, randomized to treatment with streptokinase (n = 33) or placebo (control group, n = 32). Reperfusion was defined as a CK-MB appearance rate constant (k 1) > 0.185. The final AMI size was first predicted from the admission standard ECG by previously developed formulas based on ST segment elevation. The final AMI size was estimated from the QRS score on the predischarge ECG. Myocardial salvage was defined as a ≥20% decrease from predicted to final AMI size. The k 1 value in the control group was significantly lower than that in the streptokinase group (median 0.157 versus 0.328; p = 0.0001). Accordingly the reperfusion rate was higher in the streptokinase group than in the control group (88% versus 34%; p = 0.0002). The difference in AMI size (final-predicted) was significantly greater in the streptokinase group than in the control group (median −7% versus +1%; p = 0.0001). Myocardial salvage occurred in 60% and 19%, respectively ( p = 0.004). A significant correlation was found between CK-MB reperfusion and ECG salvage: 19 of 20 streptokinase-treated patients with salvage also had reperfusion. Despite similar reperfusion rates among patients randomized to treatment with streptokinase early (≤4 hours) and late (5 to 12 hours) after the onset of symptoms, the patients treated earller had a significantly greater difference in AMI size (median −11% versus −3%; p = 0.02). The 19 patients identified in the streptokinase group as having both myocardial reperfusion and salvage showed a trend toward a lower two-dimensional echocardiographic wall motion score than the 14 patients having either or none (median 11 versus 22; p = 0.17), indicating more preserved left ventricular function. Thus, serial CK-MB and ECG analysis in patients with AMI undergoing thrombolytic therapy provides a noninvasive means for assessing therapeutic success.

Effect of Intravenous Streptokinase as Compared with That of Tissue Plasminogen Activator on Left Ventricular Function after First Myocardial Infarction

In a double-blind trial comparing two thrombolytic agents as treatment for acute myocardial infarction, we randomized 270 consecutive patients an average (+/- SD) of 2.5 +/- 0.6 hours after the onset of chest pain from a first myocardial infarction--135 to receive intravenous streptokinase (1.5 million units over 30 minutes) and 135 to receive intravenous recombinant tissue plasminogen activator (rt-PA) (100 mg over three hours). The primary end point was left ventricular function as assessed by cineangiography performed three weeks after infarction. The effects of the two agents on left ventricular function were similar. The ejection fraction was identical (58 +/- 12 percent) in both groups. The end-systolic volume was 61 +/- 29 ml in the streptokinase group and 66 +/- 31 ml in the rt-PA group (P not significant). Patency rates at three weeks for the infarct-related artery were also similar (75 percent in the streptokinase group and 76 percent in the rt-PA group). Reinfarction rates at 30 days were the same (5 percent) in both groups. One patient had a fatal intracerebral hemorrhage 13 hours after receiving rt-PA, and another had a fatal cerebellar hemorrhage 21 hours after receiving rt-PA for reinfarction nine days after treatment with streptokinase. An intention-to-treat analysis revealed that mortality at 30 days was 3.7 percent in the rt-PA group as compared with 7.4 percent in the streptokinase group (P greater than 0.2). Follow-up for a mean of 9.0 months revealed no significant difference in survival; we observed 12 deaths (8.9 percent) in the streptokinase group and 8 deaths (5.9 percent) in the rt-PA group (P = 0.34). We conclude that rt-PA and streptokinase, in the doses given, have similar effects on left ventricular function after a first myocardial infarction. Because of the small number of deaths, it is not possible to determine whether their effects on mortality are similar.