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Rescue thrombolysis: alteplase as adjuvant treatment after streptokinase in acute myocardial infarction

机译:抢救溶栓:阿替普酶作为链激酶激酶治疗急性心肌梗死的辅助治疗

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Background—In acute myocardial infarction patients who do not reperfuse their infarct arteries shortly after thrombolytic treatment have a high morbidity and mortality. Management of this high risk group remains problematic, especially in centres without access to interventional cardiology. Additional thrombolytic treatment may result in reperfusion and improved left ventricular function. Methods—Failure of reperfusion was assessed non-invasively as less than 25% reduction of ST elevation in the electro-cardiographic lead with maximum ST shift on a pretreatment electrocardiogram, 37 patients with acute myocardial infarction who showed electrocardio-graphic evidence of failed reperfusion 30 minutes after 1.5 MU streptokinase over 60 minutes were randomly allocated to receive either alteplase (tissue type plas-minogen activator (rt-PA) 100 mg over three hours) (19 patients) or placebo (18 patients). 43 patients with electrocardio-graphic evidence of reperfusion after streptokinase acted as controls. Outcome was assessed from the Selvester Q wave score of a predischarge electrocardiogram and a nuclear gated scan for left ventricular ejection fraction 4-6 weeks after discharge. Results—Among patients in whom ST segment elevation was not reduced after streptokinase, alteplase treatment resulted in a significantly smaller electrocardio-graphic infarct size (14% (8%) v 20% (9%), P = 0.03) and improved left ventricular ejection fraction (44 (10%) v 34% (16%), P = 0.04) compared with placebo. This benefit was confined to patients who failed fibrinogenolysis after streptokinase (fib-rinogen > 1 g/l). In patients in whom ST segment elevation was reduced after streptokinase, infarct size and left ventricular ejection fraction were not significantly different from those in patients treated with additional alteplase. Conclusion—Patients without electrocar-diographic evidence of reperfusion after streptokinase may benefit from further thrombolysis with alteplase.
机译:背景—在急性心肌梗塞中,溶栓治疗后不久未再灌注梗塞动脉的患者有很高的发病率和死亡率。高危人群的管理仍然存在问题,尤其是在没有介入心脏病学治疗的中心。额外的溶栓治疗可能导致再灌注并改善左心室功能。方法—无创性评估再灌注失败,因为预处理前心电图的最大心电图偏移使心电图导线中ST升高降低不到25%,37例急性心肌梗死患者表现出心电图证据显示再灌注失败30 1.5 MU链激酶在60分钟后的60分钟内随机分配接受阿替普酶(组织型血浆纤溶酶原激活剂(rt-PA)100毫克,历时3小时)(19例患者)或安慰剂(18例)。 43例链激酶激酶后有心电图再灌注证据的患者作为对照。根据出院前心电图的Selvester Q波评分和出院后4-6周左心室射血分数的核门控扫描评估结果。结果—在链激酶治疗后ST段抬高未降低的患者中,阿替普酶治疗可显着减小心电图梗死面积(14%(8%)v 20%(9%),P = 0.03)并改善左心室与安慰剂相比,射血分数(44(10%)v 34%(16%),P = 0.04)。这种益处仅限于在链激酶治疗后纤维蛋白原溶解失败的患者(纤维蛋白原> 1 g / l)。在链激酶治疗后ST段抬高降低的患者中,梗死面积和左心室射血分数与接受其他阿替普酶治疗的患者无明显差异。结论—链激酶激酶后无心电图再灌注证据的患者可能会因阿替普酶进一步溶栓而受益。

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