Key result
Antecedent streptokinase therapy for myocardial infarction was associated with greatly enhanced platelet reactivity (p<0.0001) and reduced in vitro streptokinase efficacy compared to controls.
Why the study?
Does prior streptokinase therapy for myocardial infarction cause resistance to subsequent streptokinase-induced thrombolysis?
Case-Control (n=43)
Does prior streptokinase therapy for myocardial infarction cause resistance to subsequent streptokinase-induced thrombolysis?
Prior administration of streptokinase for myocardial infarction significantly reduces the efficacy of subsequent streptokinase therapy due to enhanced platelet reactivity and resistance.
Answers are grounded in this paper and cite their sources.
May warrant caution with repeat streptokinase; leaves open whether resistance affects clinical re-infarction outcomes.
AIMS: To assess the efficacy of second-time administration of streptokinase (SK). First-time thrombolysis with SK in myocardial infarction (MI) is established but the efficacy of subsequent SK is unknown. METHODS AND RESULTS: Platelet reactivity to shear stress, spontaneous and SK-induced thrombolysis were measured in vitro in 28 patients who had received SK for MI and compared to 15 controls. SK antibody (Ab) titres were inversely related to time from MI. Platelet reactivity was greatly enhanced in patients (p < 0.0001). Spontaneous thrombolysis in patients was poor and in 17 failed to occur. In contrast, thrombolysis occurred in all but 1 control. In patients platelet reactivity was strongly related to thrombolytic activity (r = -0.516; p = 0.0029). SK in vitro was at least 4 times more effective in controls than in patients. CONCLUSION: The chances of achieving patency with second administration of SK are poor. Ab titre is not a reliable predictor of resistance.
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Gorog et al. (1999) conducted a case-control in Myocardial Infarction (n=43). Antecedent streptokinase therapy vs. Controls was evaluated on Platelet reactivity (p=<0.0001). Antecedent streptokinase therapy for myocardial infarction was associated with greatly enhanced platelet reactivity (p<0.0001) and reduced in vitro streptokinase efficacy compared to controls.
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