阿司匹林抵抗即阿司匹林不能减少血小板血栓素A2的生成并因此引起血小板活化和聚集。阿司匹林抵抗的可能原因包括用量不当、药物相互作用、环氧合酶-1的遗传多态性和涉及血栓素生物合成的其他基因、血栓素生物合成的非血小板源性因素的上调和血小板更新增强。阿司匹林抵抗程度的增强可能与心血管事件风险的增加独立相关。目前还没有一种精确定性和定量分析的方法来检测阿司匹林的抗血小板功能异常,从而解释生物化学的阿司匹林抵抗。今后的研究旨在准确定义阿司匹林抵抗、开发可靠的检测方法并确定相关心血管事件的发生风险。 Aspirin resistance, ie, aspirin, does not reduce platelet thromboxane A2 production and therefore platelet activation and aggregation. Possible causes of aspirin resistance include inappropriate dosage, drug interactions, genetic polymorphisms of cyclooxygenase-1 and other genes involved in thromboxane biosynthesis, upregulation of non-platelet-derived factors of thromboxane biosynthesis and enhancement of platelet turnover . The increased level of aspirin resistance may be independently associated with an increased risk of cardiovascular events. There is currently no accurate qualitative and quantitative analysis of aspirin to detect anti-platelet dysfunction, thereby explaining biochemical Aspirin resistance. Future research aims to accurately define aspirin resistance, develop reliable detection methods and identify the risks associated with cardiovascular events.