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首页> 外文期刊>P & T: a peer-reviewed journal for formulary management >Yorapaxar: Targeting a Novel Antiplatelet Pathway
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Yorapaxar: Targeting a Novel Antiplatelet Pathway

机译:Yorapaxar:靶向新型抗血小板途径

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摘要

In the setting of non-ST-segment elevation acute coronary syndromes (NSTE ACS), optimal management includes multitiered antithrombotic therapy. Acute and postcardiac-event antithrombotic management is focused on the central role platelets play in thrombosis. Platelets can be activated by a number of different agonists, including thromboxane A_2 (TXA_2), adenosine diphosphate (ADP), epinephrine, collagen, and thrombin.Aspirin irreversibly inhibits cyclo-oxygenase-1 (COX-1) and impedes the formation of TXA_2, leading to a decrease in platelet activation and aggregation. Clopidogrel irreversibly inhibits the P2Y_12 ADP receptor, also leading to decreased platelet activation and aggregation. The concurrent blockade of multiple platelet-aggregating pathways has been shown to reduce ischemic cardiovascular events compared with aspirin alone in various cardiovascular conditions, and yet there is an increase in bleeding with dual antiplatelet therapy.
机译:在非ST段抬高的急性冠状动脉综合征(NSTE ACS)的情况下,最佳管理包括多层抗血栓治疗。急性和明信片事件性抗栓治疗的重点是血小板在血栓形成中的核心作用。血小板可以被多种不同的激动剂激活,包括血栓烷A_2(TXA_2),二磷酸腺苷(ADP),肾上腺素,胶原蛋白和凝血酶。阿司匹林不可逆地抑制环加氧酶-1(COX-1)并阻止TXA_2的形成。 ,导致血小板活化和聚集减少。氯吡格雷不可逆地抑制P2Y_12 ADP受体,也导致血小板活化和聚集减少。与多种阿司匹林相比,在多种心血管疾病中同时阻断多种血小板聚集途径已显示出可减少缺血性心血管事件,但双重抗血小板治疗的出血量却有所增加。

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