Wagstaff A J, Gillis J C, Goa K L
Adis International Limited, Auckland, New Zealand.
Drugs. 1995 Aug;50(2):289-316. doi: 10.2165/00003495-199550020-00007.
Alteplase is the product of recombinant DNA technology and is chemically identical to endogenous tissue-type plasminogen activator: Plasminogen is converted to plasmin by alteplase, and fibrinolysis of blood thrombi is subsequently stimulated. Alteplase is now firmly established as a treatment of choice in the management of acute myocardial infarction. The efficacy of intravenous alteplase in the treatment of pulmonary thromboembolism has also been established and appears to be similar to that of streptokinase and urokinase in this indication and in arterial thrombotic occlusion. However, its use in this latter indication and in other vascular disorders has not been as extensively documented. Although trials demonstrating the efficacy of intravenous alteplase in patients with deep vein thrombosis and intra-arterial alteplase in patients with arterial thrombotic occlusion exist, reliable data on the efficacy of the fibrinolytic in ischaemic stroke and intracranial haemorrhage are scarce. Little clinical benefit is apparent in patients with unstable angina, although careful use may be warranted in those with definite pretreatment coronary thrombi. Of concern, there is a suggestion that general use of alteplase in patients with unstable angina may be associated with increased incidence of myocardial infarction. The incidence of major haemorrhage associated with alteplase therapy increases with increasing dose and appears to be similar to that seen with other fibrinolytic agents. Thus, further well-designed studies of the use of alteplase in ischaemic stroke and cerebral haemorrhage are required. However, a small subset of patients with unstable angina and definite pretreatment coronary thrombi may benefit from alteplase therapy. Further, preliminary data suggest efficacy in the therapy of deep vein thrombosis and arterial thrombotic occlusion, and alteplase has a proven place in the fibrinolytic treatment of pulmonary thromboembolism.
阿替普酶是重组DNA技术的产物,在化学结构上与内源性组织型纤溶酶原激活剂相同:阿替普酶可将纤溶酶原转化为纤溶酶,随后刺激血栓的纤维蛋白溶解。阿替普酶现已被确认为急性心肌梗死治疗的首选药物。静脉注射阿替普酶治疗肺血栓栓塞的疗效也已得到证实,在这一适应症以及动脉血栓闭塞方面,其疗效似乎与链激酶和尿激酶相似。然而,其在后者适应症及其他血管疾病中的应用尚未有广泛的文献记载。尽管有试验证明静脉注射阿替普酶对深静脉血栓形成患者有效,动脉内注射阿替普酶对动脉血栓闭塞患者有效,但关于纤溶药物在缺血性卒中和颅内出血方面疗效的可靠数据却很少。不稳定型心绞痛患者几乎没有明显的临床益处,不过对于那些有明确预处理冠状动脉血栓的患者,谨慎使用可能是必要的。令人担忧的是,有迹象表明在不稳定型心绞痛患者中普遍使用阿替普酶可能会增加心肌梗死的发生率。与阿替普酶治疗相关的大出血发生率随剂量增加而上升,且似乎与其他纤溶药物相似。因此,需要进一步设计完善的研究来探讨阿替普酶在缺血性卒中和脑出血中的应用。然而,一小部分有明确预处理冠状动脉血栓的不稳定型心绞痛患者可能会从阿替普酶治疗中获益。此外,初步数据表明其在深静脉血栓形成和动脉血栓闭塞治疗中有效,并且阿替普酶在肺血栓栓塞的纤溶治疗中已被证明有一席之地。