Yildiz Bekir S, Ozkan Emel, Esin Fatma, Alihanoglu Yusuf I, Ozkan Hayrettin, Bilgin Murat, Kilic Ismail D, Ergin Ahmet, Kaftan Havane A, Evrengul Harun
aDepartment of Cardiology, Pamukkale University, DenizlibIzmir Ataturk Training and Research HospitalcIzmir Bozyaka Training and Research Hospital, IzmirdDepartment of Cardiology, Diskapi Training and Research Hospital, AnkaraeDepartment of Public Health, Pamukkale University, Denizli, Turkey.
Blood Coagul Fibrinolysis. 2016 Jun;27(4):412-8. doi: 10.1097/MBC.0000000000000466.
In patients with coronary artery disease (CAD), though aspirin inhibits platelet activation and reduces atherothrombotic complications, it does not always sufficiently inhibit platelet function, thereby causing a clinical situation known as aspirin resistance. As hyperuricemia activates platelet turnover, aspirin resistance may be specifically induced by increased serum uric acid (SUA) levels. In this study, we thus investigated the association between SUA level and aspirin resistance in patients with CAD. We analyzed 245 consecutive patients with stable angina pectoris (SAP) who in coronary angiography showed more than 50% occlusion in a major coronary artery. According to aspirin resistance, two groups were formed: the aspirin resistance group (Group 1) and the aspirin-sensitive group (Group 2). Compared with those of Group 2, patients with aspirin resistance exhibited significantly higher white blood cell counts, neutrophil counts, neutrophil-to-lymphocyte ratios, SUA levels, high-sensitivity C-reactive protein levels, and fasting blood glucose levels. After multivariate analysis, a high level of SUA emerged as an independent predictor of aspirin resistance. The receiver-operating characteristic analysis provided a cutoff value of 6.45 mg/dl for SUA to predict aspirin resistance with 79% sensitivity and 65% specificity. Hyperuricemia may cause aspirin resistance in patients with CAD and high SUA levels may indicate aspirin-resistant patients. Such levels should thus recommend avoiding heart attack and stroke by adjusting aspirin dosage.
在冠状动脉疾病（CAD）患者中，尽管阿司匹林可抑制血小板活化并减少动脉粥样硬化血栓形成并发症，但它并不总是能充分抑制血小板功能，从而导致一种被称为阿司匹林抵抗的临床情况。由于高尿酸血症会激活血小板更新，阿司匹林抵抗可能是由血清尿酸（SUA）水平升高特异性诱导的。因此，在本研究中，我们调查了CAD患者中SUA水平与阿司匹林抵抗之间的关联。我们分析了245例连续的稳定型心绞痛（SAP）患者，这些患者在冠状动脉造影中显示主要冠状动脉闭塞超过50%。根据阿司匹林抵抗情况，分为两组：阿司匹林抵抗组（第1组）和阿司匹林敏感组（第2组）。与第2组相比，阿司匹林抵抗患者的白细胞计数、中性粒细胞计数、中性粒细胞与淋巴细胞比值、SUA水平、高敏C反应蛋白水平和空腹血糖水平显著更高。多变量分析后，高SUA水平成为阿司匹林抵抗的独立预测因素。受试者工作特征分析得出SUA预测阿司匹林抵抗的截断值为6.45mg/dl，敏感性为79%，特异性为65%。高尿酸血症可能导致CAD患者出现阿司匹林抵抗，高SUA水平可能提示阿司匹林抵抗患者。因此，应根据这些水平建议通过调整阿司匹林剂量来预防心脏病发作和中风。
