阿司匹林抵抗及对策

阿司匹林广泛应用于心血管事件的预防，减少了心血管事件的发生。阿司匹林通过不可逆地和脂肪酸环氧化酶结合，抑制血小板聚集的激动剂血栓素A2的合成，发挥抗血小板聚集作用。但也有一些患者服用阿司匹林过程中有的血小板聚集能力和临床缺血事件不能被抑制。阿司匹林抵抗通常是指阿司匹林治疗未能引起预期的生物学效应抑制血栓素的生物合成或未能预防血栓事件的现象。导致这种现象的确切原因较复杂，包括不适当应用药物的相互作用，剂量不足，环氧化酶-1基因的多态性，及非血小板依赖血栓形成途径等有关。临床医生应该了解这些导致阿司匹林抵抗的因素，规范阿司匹林的应用剂量，适当地联合应用其他药物治疗。

Aspirin Resistance and Its Clinical Strategies

Aspirin is commonly used to reduce the risk of ischaemic events in patients with cardiovascular disease. Aspirin inhibits platelets by irreversibly binding to cyclooxygenase and blocking the synthesis of thromboxane A2. However, patients were treated with aspirin still suffer ischaemic events, and laboratory assessment of platelet function reveals persistent platelet aggregation despite regular aspirin therapy in a significant proportion of patients at high risk of ischaemic events. Aspirin resistance refers to less than expected suppression of thromboxane A2 production by aspirin and has been reported to be independently associated with an increased risk of adverse cardiovascular events. Possible causes of aspirin resistance include poor compliance, drug interaction, inadequate aspirin dose, increase turnover of platelets, genetic polymorphisms of cyclo--oxygenase-- 1, and upregulation of alternate （ non-- platelet） pathways of thromboxane production. Laboratory methods used to detect aspirin resistance include those that measure thromboxane A2 production and thromboxane A2- dependent platelet function. Instead physicians should be aware of the factors that may impair aspirin function, ensure that they use an appropriate dose of aspirin and optimise compliance with aspirin therapy.