Huber K
Abteilung für Kardiologie, Universität Wien.
Z Gesamte Inn Med. 1993 Jun-Jul;48(6-7):316-23.
The main problem after originally successful thrombolytic reperfusion is early thrombotic reocclusion which occurs in up to 20% despite adequate anticoagulant therapy. Early rethrombosis can be attributed to a permanent procoagulatory state caused by residual stenosis, residual thrombosis, by a "paradoxical" procoagulatory effect of the thrombolytic agents used, and by the existence of systemic thrombogenic risk factors. Thereby, most important mechanisms of rethrombosis are generation, exposition and activation of thrombin and a thrombin-induced increase in platelet aggregability. Up to now, therapeutic measures have not proved useful (early balloon angioplasty, prolonged t-PA infusion), have not been effective enough (platelet inhibition with aspirin, anticoagulation with heparin), or are not entirely investigated (combination therapy of fibrin-specific with non-specific thrombolytic agents, use of t-PA mutants with prolonged biological efficacy). As far as thrombin plays the key role in the process of rethrombosis, it is believed that the use of specific and highly active thrombin inhibitors, e.g. hirudin, might mostly be appropriate in solving the problem of "reocclusion".
最初成功进行溶栓再灌注后的主要问题是早期血栓再闭塞，尽管进行了充分的抗凝治疗，其发生率仍高达20%。早期再血栓形成可归因于由残余狭窄、残余血栓形成、所用溶栓剂的“矛盾”促凝作用以及全身血栓形成危险因素的存在所导致的永久性促凝状态。因此，再血栓形成的最重要机制是凝血酶的生成、暴露和激活以及凝血酶诱导的血小板聚集性增加。到目前为止，治疗措施尚未被证明有用（早期球囊血管成形术、延长t-PA输注），不够有效（用阿司匹林抑制血小板、用肝素抗凝），或者尚未得到充分研究（纤维蛋白特异性与非特异性溶栓剂联合治疗、使用具有延长生物效应的t-PA突变体）。鉴于凝血酶在再血栓形成过程中起关键作用，人们认为使用特异性且高活性的凝血酶抑制剂，如水蛭素，可能最适合解决“再闭塞”问题。
