Mounsey J P, Skinner J S, Hawkins T, MacDermott A F, Furniss S S, Adams P C, Kesteven P J, Reid D S
Northern Regional Cardiothoracic Centre, Freeman Hospital, Newcastle upon Tyne.
Br Heart J. 1995 Oct;74(4):348-53. doi: 10.1136/hrt.74.4.348.
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.
Failure of reperfusion was assessed non-invasively as less than 25% reduction of ST elevation in the electrocardiographic lead with maximum ST shift on a pretreatment electrocardiogram. 37 patients with acute myocardial infarction who showed electrocardiographic evidence of failed reperfusion 30 minutes after 1.5 MU streptokinase over 60 minutes were randomly allocated to receive either alteplase (tissue type plasminogen activator (rt-PA) 100 mg over three hours) (19 patients) or placebo (18 patients). 43 patients with electrocardiographic 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.
Among patients in whom ST segment elevation was not reduced after streptokinase, alteplase treatment resulted in a significantly smaller electrocardiographic 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 (fibrinogen > 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.
Patients without electrocardiographic evidence of reperfusion after streptokinase may benefit from further thrombolysis with alteplase.
急性心肌梗死患者在溶栓治疗后未及时使梗死动脉再灌注，其发病率和死亡率较高。对这一高危群体的管理仍然存在问题，尤其是在没有介入心脏病学服务的中心。额外的溶栓治疗可能会实现再灌注并改善左心室功能。
通过在治疗前心电图上ST段移位最大的导联中，ST段抬高降低幅度小于25%来无创评估再灌注失败情况。37例急性心肌梗死患者在60分钟内静脉滴注150万单位链激酶30分钟后心电图显示再灌注失败，将其随机分为两组，分别接受阿替普酶（组织型纤溶酶原激活剂（rt-PA）100mg，静脉滴注3小时）治疗（19例患者）或安慰剂治疗（18例患者）。43例链激酶治疗后心电图显示再灌注的患者作为对照组。出院前通过心电图的塞尔维斯特Q波评分以及出院后4至6周进行的核素门控扫描评估左心室射血分数来评估治疗结果。
在链激酶治疗后ST段抬高未降低的患者中，与安慰剂相比，阿替普酶治疗使心电图梗死面积显著减小（14%（8%）对20%（9%），P = 0.03），左心室射血分数得到改善（44%（10%）对34%（16%），P = 0.04）。这一益处仅限于链激酶治疗后纤维蛋白溶解失败（纤维蛋白原>1g/l）的患者。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额外阿替普酶治疗的患者相比无显著差异。
链激酶治疗后无心电图再灌注证据的患者可能从阿替普酶进一步溶栓治疗中获益。
