Abstract：
The glycoprotein (GP) IIb/IIIa receptor is found integrin present in platelet aggregations. GP IIb/IIIa antagonists interfere with platelet cross-linking and platelet-derived thrombus formation through the competition with fibrinogen and von Willebrand factor. Currently, three parenteral GP IIb/IIIa competitors (tirofiban, eptifibatide, and abciximab) are approved for clinical use in patients affected by percutaneous coronary interventions (PCI) in the location of acute coronary syndrome (ACS). GP IIb/IIIa antagonists have their mechanism of action in platelet aggregation prevention, distal thromboembolism, and thrombus formation, whereas the initial platelet binding to damage vascular areas is preserved. This work is aimed to provide a comprehensive review of the significance of GP IIb/IIIa inhibitors as a sort of antiplatelet agent. Their mechanism of action is based on factors that affect their efficacy. On the other hand, drugs that inhibit GP IIb/IIIa already approved by the FDA were reviewed in detail. Results from major clinical trials and regulatory practices and guidelines to deal with GP IIb/IIIa inhibitors were deeply investigated. The cardiovascular pathology and neuro-interventional surgical application of GP IIb/IIIa inhibitors as a class of antiplatelet agents were developed in detail. The therapeutic risk/benefit balance of currently available GP IIb/IIa receptor antagonists is not yet well elucidated in patients with ACS who are not clinically evaluated regularly for early cardiovascular revascularization. On the other hand, in patients who have benefited from PCI, the antiplatelet therapy intensification by the addition of a GP IIb/IIIa receptor antagonist (intravenously) may be an appropriate therapeutic strategy in reducing the occurrence of risks of thrombotic complications related to the intervention. Development of GP IIb/IIIa inhibitors with oral administration has the potential to include short-term antiplatelet benefits compared with intravenous GP IIb/IIIa inhibitors for long-term secondary preventive therapy in cardiovascular disease. But studies showed that long-term oral administration of GP IIb/IIIa receptor inhibitors has been ineffective in preventing ischemic events. Paradoxically, they have been linked to a high risk of side effects by producing prothrombotic and pro-inflammatory events.
摘要：
发现糖蛋白(GP)IIb/IIIa受体是存在于血小板聚集中的整合素。GPIIb/IIIa拮抗剂通过与纤维蛋白原和血管性血友病因子的竞争来干扰血小板交联和血小板衍生的血栓形成。目前,三个肠胃外GPIIb/IIIa竞争者(替罗非班，依替巴肽,和abciximab）被批准在急性冠状动脉综合征（ACS）位置接受经皮冠状动脉介入治疗（PCI）的患者中临床使用。GPIIb/IIIa拮抗剂在预防血小板聚集方面有其作用机制，远端血栓栓塞,和血栓形成，而最初的血小板与损伤血管区域的结合被保留。这项工作旨在对GPIIb/IIIa抑制剂作为一种抗血小板药物的意义进行全面综述。它们的作用机制基于影响其功效的因素。另一方面,我们对FDA已经批准的抑制GPIIb/IIIa的药物进行了详细审查.深入研究了来自主要临床试验以及处理GPIIb/IIIa抑制剂的监管实践和指南的结果。详细开发了GPIIb/IIIa抑制剂作为一类抗血小板药物的心血管病理学和神经介入手术应用。目前可用的GPIIb/IIa受体拮抗剂的治疗风险/益处平衡尚未在ACS患者中得到很好的阐明，这些患者没有定期进行早期心血管血运重建的临床评估。另一方面,在从PCI获益的患者中,通过添加GPIIb/IIIa受体拮抗剂(静脉注射)强化抗血小板治疗可能是降低与干预相关的血栓性并发症风险发生的适当治疗策略.与静脉内GPIIb/IIIa抑制剂相比，口服GPIIb/IIIa抑制剂的开发有可能包括短期抗血小板益处，用于心血管疾病的长期二级预防治疗。但是研究表明，长期口服GPIIb/IIIa受体抑制剂对预防缺血事件无效。矛盾的是,它们通过产生血栓前和促炎事件与副作用的高风险有关.
