Department of Clinical Sciences, Karolinska Institutet Danderyd Hospital, SE-182 88 Stockholm, Sweden.
J Intern Med. 2010 Feb;267(2):191-208. doi: 10.1111/j.1365-2796.2009.02205.x.
The rationale for thrombolysis, the most promising pharmacological approach in acute ischaemic stroke, is centred on the principal cause of most ischaemic strokes: the thrombus that occludes the cerebral artery, and renders part of the brain ischaemic. The occluding thrombus is bound together within fibrin. Fibrinolysis acts by activation of plasminogen to plasmin; plasmin splits fibrinogen and fibrin and lyses the clot, which then allows reperfusion of the ischaemic brain. Thrombolytic agents include streptokinase (SK) and recombinant tissue-type plasminogen activator (rt-PA) amongst others under test or development. SK is nonfibrin-specific, has a longer half-life than tissue-type plasminogen activator (t-PA), prevents re-occlusion and is degraded enzymatically in the circulation. rt-PA is more fibrin-specific and clot-dissolving, and is metabolized during the first passage in the liver. In animal models of ischaemic stroke, the effects of rt-PA are remarkably consistent with the effects seen in human clinical trials. For clinical application, some outcome data from the Cochrane Database of Systematic Reviews which includes all randomized evidence available on thrombolysis in man were used. Trials included tested urokinase, SK, rt-PA, pro-urokinase, or desmoteplase. The chief immediate hazard of thrombolytic therapy is fatal intracranial bleeding. However, despite the risk, the human trial data suggest the immediate hazards and the apparent substantial scope for net benefit of thrombolytic therapy given up to 6 h of acute ischaemic stroke. So far the fibrin-specific rt-PA is the only agent to be approved for use in stroke. This may be due to its short half-life and its absence of any specific amount of circulating fibrinogen degradation products, thereby leaving platelet function intact. The short half-life does not leave rt-PA without danger for haemorrhage after the infusion. Due to its fibrin-specificity, it can persist within a fibrin-rich clot for one or more days. The molecular mechanisms with regards to fibrin-specificity in thrombolytic agents should, if further studied, be addressed in within-trial comparisons. rt-PA has antigenic properties and although their long-term clinical relevance is unclear there should be surveillance for allergic reactions in relation to treatment. Although rt-PA is approved for use in selected patients, there is scope for benefit in a much wider variety of patients. A number of trials are underway to assess which additional patients - beyond the age and time limits of the current approval - might benefit, and how best to identify them.
溶栓治疗是急性缺血性脑卒中最有前途的药物治疗方法,其基本原理是针对大多数缺血性脑卒中的主要病因:阻塞大脑动脉的血栓,导致部分大脑缺血。阻塞的血栓与纤维蛋白结合在一起。纤维蛋白溶解通过激活纤溶酶原转化为纤溶酶;纤溶酶分解纤维蛋白原和纤维蛋白,溶解血栓,从而使缺血的大脑再灌注。溶栓药物包括链激酶(SK)和重组组织型纤溶酶原激活剂(rt-PA)等,目前正在进行测试或开发。SK 是非纤维蛋白特异性的,半衰期长于组织型纤溶酶原激活剂(t-PA),可防止再闭塞,并在循环中被酶降解。rt-PA 更具纤维蛋白特异性和血栓溶解作用,在肝脏的首次通过中被代谢。在缺血性脑卒中的动物模型中,rt-PA 的作用与人类临床试验中的作用非常一致。为了临床应用,使用了 Cochrane 系统评价数据库中的一些来自临床试验的结果数据,这些数据包括了人类溶栓治疗的所有随机证据。试验包括测试尿激酶、SK、rt-PA、前尿激酶或地西溶栓酶。溶栓治疗的主要即时危险是致命性颅内出血。然而,尽管存在风险,人类试验数据表明,在急性缺血性脑卒中 6 小时内,溶栓治疗的即时危害和明显的明显获益范围。到目前为止,只有纤维蛋白特异性 rt-PA 被批准用于中风治疗。这可能是由于其半衰期短,没有任何特定数量的循环纤维蛋白原降解产物,从而使血小板功能保持完整。rt-PA 的半衰期短,在输注后仍有出血的危险。由于其纤维蛋白特异性,它可以在富含纤维蛋白的血栓中持续存在 1 天或更长时间。在纤维蛋白特异性溶栓药物的分子机制方面,如果进一步研究,应该在试验内比较中加以解决。rt-PA 具有抗原性,尽管其长期的临床相关性尚不清楚,但应监测与治疗相关的过敏反应。尽管 rt-PA 已被批准用于某些患者,但在更广泛的患者中仍有获益的可能。目前正在进行多项试验,以评估哪些额外的患者(超出当前批准的年龄和时间限制)可能受益,以及如何最好地识别他们。