Auer Johann, Berent Robert, Lassnig Elisabeth, Weber Thomas, Maurer Edwin, Eber Bernd
II. Interne Abteilung mit Kardiologie, Allgemeines Offentliches Krankenhaus der Barmherzigen Schwestern vom Heiligen Kreuz, Wels, Austria.
Herz. 2003 Aug;28(5):393-403. doi: 10.1007/s00059-002-2316-4.
Inhibition of platelet activity at the injured coronary plaque is a target for novel therapeutic strategies. One of these mechanisms is the blockade of the platelet surface membrane glycoprotein (GP) IIb/IIIa receptor, which binds circulating fibrinogen or von Willebrand factor and crosslinks platelets as the final common pathway to platelet aggregation. Intravenous agents directed against this receptor include the chimeric monoclonal antibody fragment abciximab, the peptide inhibitor eptifibatide and nonpeptide mimetics tirofiban and lamifiban.
During percutaneous coronary intervention, an absolute reduction of 1.5-6.5% in the 30-day risk of death, myocardial infarction or repeat urgent revascularization has been observed, with some variability in treatment effect among the agents tested. Treatment effect is achieved early with every modality of revascularization and maintained over the long-term up to 3 years. Increased bleeding risk may be minimized by reduction and weight adjustment of concomitant heparin dosing. In the acute coronary syndromes without ST segment elevation, absolute 1.5-3.2% reductions in 30-day rates of death or myocardial infarction have been achieved with 2- to 4-day courses of eptifibatide or tirofiban. Clinical benefit accrues during the period of drug infusion and is durable. Treatment effect may be enhanced among patients undergoing early coronary revascularization, with evidence of stabilization before intervention and suppression of postprocedural ischemic events.
Thus, blockade of the platelet GP IIb/IIIa receptor reduces ischemic complications when used as an adjunct to percutaneous coronary intervention or the management of acute ischemic syndromes.
抑制受损冠状动脉斑块处的血小板活性是新型治疗策略的一个目标。其中一种机制是阻断血小板表面膜糖蛋白（GP）IIb/IIIa受体，该受体可结合循环中的纤维蛋白原或血管性血友病因子，并使血小板交联，这是血小板聚集的最终共同途径。针对该受体的静脉用药包括嵌合单克隆抗体片段阿昔单抗、肽抑制剂依替巴肽以及非肽模拟物替罗非班和拉米非班。
在经皮冠状动脉介入治疗期间，观察到30天死亡、心肌梗死或再次紧急血运重建风险绝对降低了1.5% - 6.5%，在所测试的药物中，治疗效果存在一定差异。每种血运重建方式都能早期实现治疗效果，并长期维持长达3年。通过减少和调整肝素的伴随给药剂量，可将出血风险增加降至最低。在无ST段抬高的急性冠状动脉综合征中，使用依替巴肽或替罗非班进行2至4天的疗程，可使30天死亡或心肌梗死发生率绝对降低1.5% - 3.2%。临床益处出现在药物输注期间，且持久。在早期进行冠状动脉血运重建的患者中，治疗效果可能会增强，有证据表明在干预前病情稳定且能抑制术后缺血事件。
因此，血小板GP IIb/IIIa受体阻断剂作为经皮冠状动脉介入治疗或急性缺血综合征管理的辅助手段使用时，可减少缺血并发症。
