Faraday Nauder, Becker Diane M, Yanek Lisa R, Herrera-Galeano Jesus Enrique, Segal Jodi B, Moy Taryn F, Bray Paul F, Becker Lewis C
Division of Cardiac Surgical Intensive Care, Department of Anesthesiology/Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA.
Am J Cardiol. 2006 Sep 15;98(6):774-9. doi: 10.1016/j.amjcard.2006.04.015. Epub 2006 Jul 28.
Resistance to inhibition of platelet function by aspirin may contribute to future myocardial infarction and stroke. Adverse cardiovascular outcomes have been associated with aspirin resistance on several different platelet function assays, including the level of urinary 11-dehydro thromboxane B2 (Tx-M), platelet aggregation to arachidonic acid and adenosine diphosphate, and closure time on the platelet function analyzer-100. We examined the concordance of these aspirin-resistance assays and their relation to cardiovascular risk factors in a primary prevention population. Asymptomatic patients (n = 1,311) at increased risk for coronary heart disease were evaluated before and after 2 weeks of aspirin (81 mg/day). Aspirin resistance was defined according to published criteria for these 3 assays of platelet function. Subjects were characterized for the presence of atherosclerosis risk factors. Agreement among the 3 assays was poor. Only 5 patients met aggregation criteria for aspirin resistance. Attenuated suppression of urinary Tx-M by aspirin was associated with a greater atherosclerotic risk profile and Framingham risk score in multivariable regression analysis. Aspirin resistance by platelet function analyzer-100 was associated only with increased von Willebrand factor levels and not with atherosclerotic risk profile. In conclusion, in a primary prevention population, different published criteria for aspirin resistance classify distinct groups of patients as aspirin resistant with very little overlap. Higher Tx-M, which reflects decreased suppression of thromboxane production in vivo, is the only criterion associated with atherosclerosis risk factors, suggesting that this measurement may represent the most relevant approach for identifying asymptomatic subjects whose aspirin treatment will "fail."
对阿司匹林抑制血小板功能产生抵抗可能会增加未来发生心肌梗死和中风的风险。在几种不同的血小板功能检测中，不良心血管结局都与阿司匹林抵抗有关，这些检测包括尿11-脱氢血栓素B2（Tx-M）水平、血小板对花生四烯酸和二磷酸腺苷的聚集反应，以及血小板功能分析仪-100上的闭合时间。我们在一个一级预防人群中研究了这些阿司匹林抵抗检测方法之间的一致性及其与心血管危险因素的关系。对有冠心病风险增加的无症状患者（n = 1311）在服用阿司匹林（81毫克/天）2周前后进行了评估。根据已发表的这3种血小板功能检测标准来定义阿司匹林抵抗。对受试者的动脉粥样硬化危险因素进行了特征描述。这3种检测方法之间的一致性较差。只有5名患者符合阿司匹林抵抗的聚集标准。在多变量回归分析中，阿司匹林对尿Tx-M抑制作用减弱与更大的动脉粥样硬化风险特征和弗雷明汉姆风险评分相关。血小板功能分析仪-100检测出的阿司匹林抵抗仅与血管性血友病因子水平升高有关，而与动脉粥样硬化风险特征无关。总之，在一级预防人群中，不同的已发表的阿司匹林抵抗标准将不同组的患者归类为阿司匹林抵抗，且重叠很少。较高的Tx-M反映了体内血栓素生成抑制作用的降低，是与动脉粥样硬化危险因素相关的唯一标准，这表明该测量方法可能是识别阿司匹林治疗“无效”的无症状受试者的最相关方法。
