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目的:比较行急诊经皮冠状动脉介入治疗（PCI）的ST段抬高型心肌梗死（STEMI）患者在服用替格瑞洛和氯吡格雷期间血清尿酸水平的变化，并初步探讨血清尿酸水平的变化对血小板反应性的影响。方法:选取2017年4月至2020年1月于阜外医院行急诊PCI存活出院且接受阿司匹林和替格瑞洛或氯吡格雷治疗的STEMI患者，分为替格瑞洛组和氯吡格雷组。收集患者的基线临床资料，检测基线和术后30 d血清尿酸和肌酐水平，术后30 d采用光学透射比浊法测量二磷酸腺苷诱导和花生四烯酸诱导的最大聚集率。采用多因素logistic回归分析30 d时血清尿酸升高的独立相关因素，并分析血清尿酸水平对血小板反应性的影响。结果:共纳入患者967例，年龄（59.4±12.1）岁，女性163例（16.9%）。替格瑞洛组550例（56.9%），氯吡格雷组417例（43.1%）。2组基线血清尿酸和肌酐水平差异无统计学意义。替格瑞洛组30 d血清尿酸水平［（347.2±96.5）mmol/L比（341.2±105.3）mmol/L，n P=0.009］、血清尿酸变化量［46.4（-2.4，88.1）mmol/L比25.0（-21.9，73.0）mmol/L，n P=0.001］以及血清尿酸变化百分比［13.2%（-0.01%，29.0%）比7.9%（-5.7%，25.0%），n P=0.007］均高于氯吡格雷组。替格瑞洛组30 d血清肌酐水平低于氯吡格雷组［（89.7±21.3）μmol/L比（94.4±43.9）μmol/L，n P0.05）。logistic回归分析显示，校正混杂因素后，服用替格瑞洛是30 d血清尿酸升高的独立相关因素（n OR=1.582，95% n CI：1.023～2.447，n P=0.039）。2组血清尿酸水平的变化对血小板聚集率和血小板高反应性均无影响。n 结论:STEMI患者服用替格瑞洛30 d后血清尿酸水平升高，且增幅超过氯吡格雷服用者。初步研究显示，服用替格瑞洛和氯吡格雷期间，血清尿酸水平的升高没有增加血小板高反应性的比例。“,”Objectives:To compare the impact of ticagrelor or clopidogrel on serum uric acid levels among patients with ST-segment elevation myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention (PCI) and further evaluate the effects of variation of serum uric acid levels on platelet reactivity.Methods:STEMI patients who admitted to Fuwai Hospital from April 2017 to January 2020, and underwent primary PCI and discharged alive with aspirin and ticagrelor or clopidogrel were included in this study. Patients were divided into ticagrelor group and clopidogrel group. The baseline clinical data were collected. Serum uric acid and creatinine levels at baseline and 30 days post-PCI were measured. Light transmittance aggregometry was used to assess maximum aggregation rate induced by adenosine diphosphate and arachidonic acid. The changes of serum uric acid and creatinine were compared between the two groups. Multivariate logistic regression was performed to evaluate independent related factors for rise in the uric acid levels, and the effect of variation of serum uric acid level on platelet reactivity was analyzed.Results:A total of 967 patients were included, the age was (59.4±12.1) years, and 163 case were female. There were 550 cases in ticagrelor group (56.9%) and 417 cases in clopidogrel group (43.1%). Baseline serum uric acid and creatinine levels were similar between the 2 groups. At 30 days, the serum uric acid level [(347.2±96.5) mmol/L vs. (341.2±105.3) mmol/L, n P=0.009] and absolute [46.4 (-2.4, 88.1) mmol/L vsn . 25.0 (-21.9, 73.0) mmol/L, n P=0.001] and percentage [13.2 (-0.01, 29.0) % vs. 7.9 (-5.7, 25.0) %, n P=0.007] increase in the serum uric acid levels were significantly higher in ticagrelor group than in clopidogrel group. The level of serum creatinine at 30 days was significantly lower in ticagrelor group than in clopidogrel group [(89.7±21.3) μmol/L vs. (94.4±43.9) μmol/L,n P0.05). Logistic regression analysis showed that, after adjusting for confounding factors, ticagrelor therapy was an independent related factor of serum uric acid elevation (n OR=1.582, 95% n CI:1.023-2.447, n P=0.039). The variation of the serum uric acid levels did not affect platelet aggregation and the percentage of high platelet reactivity in both groups.n Conclusions:Ticagrelor use is related to a significant increase in the serum uric acid levels at 30 days post-PCI in this patient cohort. The variations in the uric acid levels do not increase the percentage of high platelet reactivity in STEMI patients treated with ticagrelor or clopidogrel.