Department of Cardiovascular Surgery, Tianjin Medical University General Hospital, Tianjin 300052, China.
Chin Med J (Engl). 2011 Jun;124(11):1731-4.
Aspirin is widely used in the secondary prevention of coronary artery diseases, including myocardial infarction, stroke, and vascular related deaths. However, the antiplatelet effect of aspirin appears to be variable and aspirin resistance (AR) is currently still controversial for Chinese patients. The aim of this study was to describe the prevalence of AR, and identify possible risk factors associated with a lack of response to aspirin treatments in patients with unstable coronary artery disease.
Platelet function tests with arachidonic acid (ARA) and urinary 11-dehydro-thromboxane B2 (11-DH-TXB2) concentrations were performed in 262 patients with unstable coronary artery disease who had not been taking aspirin before admission. ARA induced platelet aggregation and 11-DH-TXB2 were detected to evaluate the functional and biochemical responses to aspirin before and on days 1, 4, and 10 after aspirin administration. Six-month follow-up was completed in patients who developed AR to evaluate the effect of aspirin in a long-term treatment. GP1Bα (C1018T), Pl (A1/A2), P2Y1 (A1622G), TBXA2R (T924C) were also detected to evaluate the influence of genetic variant on aspirin responsiveness.
A total of 8.8% of patients were indentified as AR at the first day after aspirin treatment. The level of urine 11-DH-TXB2 in the AR group was higher compared to non-AR group (P < 0.05). There was no relationship between ARA induced platelet aggregation and urinary 11-DH-TXB2 levels (r = 0.038, P = 0.412). The results of DNA sequencing showed that TBXA2R-924TT homozygotes had a significantly high rate of AR. Logistic regression demonstrated that diabetes was an independent risk factor of AR.
In the beginning period of administration, aspirin was not a sufficient factor that inhibits platelet aggregation. TBXA2R-924T allele was involved in AR. Diabetes was an independent risk factor of AR.
阿司匹林广泛用于冠心病（包括心肌梗死、中风和血管相关死亡）的二级预防。然而，阿司匹林的抗血小板作用似乎存在差异，目前阿司匹林抵抗（AR）在中国患者中仍存在争议。本研究旨在描述 AR 的流行率，并确定不稳定型冠状动脉疾病患者对阿司匹林治疗无反应的可能相关危险因素。
对 262 例入院前未服用阿司匹林的不稳定型冠状动脉疾病患者进行花生四烯酸（ARA）和尿 11-脱氢血栓素 B2（11-DH-TXB2）浓度的血小板功能检测。在服用阿司匹林之前、之后的第 1、4 和 10 天检测 ARA 诱导的血小板聚集和 11-DH-TXB2，以评估阿司匹林治疗前和治疗后的功能和生化反应。对发生 AR 的患者进行 6 个月的随访，以评估长期治疗中阿司匹林的效果。还检测了 GP1Bα（C1018T）、Pl（A1/A2）、P2Y1（A1622G）、TBXA2R（T924C），以评估遗传变异对阿司匹林反应性的影响。
在服用阿司匹林后的第一天，共有 8.8%的患者被确认为 AR。AR 组的尿 11-DH-TXB2 水平高于非 AR 组（P<0.05）。ARA 诱导的血小板聚集与尿 11-DH-TXB2 水平之间没有关系（r=0.038，P=0.412）。DNA 测序结果显示，TBXA2R-924TT 纯合子的 AR 发生率明显较高。Logistic 回归表明，糖尿病是 AR 的独立危险因素。
在开始用药的初期，阿司匹林并不是抑制血小板聚集的充分因素。TBXA2R-924T 等位基因与 AR 有关。糖尿病是 AR 的独立危险因素。
