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Anti-Platelet Drug Resistance

机译:抗血小板耐药性

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Laboratory aspirin unresponsiveness ("resistance") has been reported over the last 30 years, ranging between 5-50%, applying different methods, among individuals with a variety of cardiovascular disorders. From early works it has been realized that different methods give different results, depending on the end point of the tests. Thus results of testing plasma and urinary thrombaxane metabolites suggest a very low rate of laboratory resistance (LR) whereas platelet aggregation in response to arachidonic acid (AA) yields a relatively higher LR rate. Recently similar observation has been made regarding the response to clopidogrel as well. The main questions arising from these studies are:a) what are the mechanisms responsible for the LR phenomenon? b) does LR confer adverse clinical outcome? c) is there a way to overcome LR in an attempt to improve outcome? and d) what are the available methods suitable for testing aspirin and clopidogrel LR.
机译:在过去30年中报告了实验室阿司匹林没有反应(“抵抗”),介于5-50%之间,施用不同的方法,包括各种心血管障碍的个体。从早期作品中,已经意识到不同的方法给出不同的结果,这取决于测试的终点。因此,测试等离子体和尿血栓发球菌的结果表明了实验室抗性(LR)的非常低的速率,而蛋白酸(AA)的血小板聚集产生相对较高的LR速率。最近对氯吡格雷的反应进行了类似的观察。这些研究产生的主要问题是:a)对LR现象负责的机制是什么? b)LR是否有助于临床结果? c)有没有办法克服LR以改善结果?而d)适用于测试阿司匹林和氯吡格雷LR的可用方法是什么。

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