Background:Uric acid (UA) concentration within carotid plaque and its association with cerebrovascular events have not been detected or quantified. Systemically, serum UA is a marker of inflammation and risk factor for atherosclerosis. However, its association with carotid plaque instability and stroke pathogenesis remains unclear. In patients undergoing carotid endarterectomy, we aimed to determine whether UA is present differentially in symptomatic versus asymptomatic carotid plaques and whether serum UA is associated with cerebrovascular symptoms (stroke, transient ischemic attack, or amaurosis fugax).Methods:Carotid atherosclerotic plaques were collected during carotid endarterectomy. The presence of UA was assessed using Gomori methenamine silver staining as well as anti-UA immunohistochemical staining and its quantity measured using an enzymatic colorimetric assay. Clinical information was obtained through a retrospective review of data.Results:UA was more commonly detected in symptomatic (n=23) compared with asymptomatic (n=9) carotid plaques by Gomori methenamine silver (20 [86.9%] versus 2 [22.2%]; P=0.001) and anti-UA immunohistochemistry (16 [69.5%] versus 1 [11.1%]; P=0.004). UA concentration was higher in symptomatic rather than asymptomatic plaques (25.1 [9.5] versus 17.9 [3.8] µg/g; P=0.021). Before carotid endarterectomy, serum UA levels were higher in symptomatic (n=341) compared with asymptomatic (n=146) patients (5.9 [interquartile range, 4.6–6.9] mg/dL versus 5.2 [interquartile range, 4.6–6.2] mg/dL; P=0.009).Conclusions:The current study supports a potential role of UA as a potential tissue participant and a systemic biomarker in the pathogenesis of carotid atherosclerosis. UA may provide a mechanistic explanation for plaque instability and subsequent ischemic cerebrovascular events.

中文翻译：

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颈动脉粥样硬化斑块中的尿酸表达和血清尿酸与脑血管事件相关

背景：尚未检测或量化颈动脉斑块内的尿酸 (UA) 浓度及其与脑血管事件的关系。全身性地，血清 UA 是炎症的标志物和动脉粥样硬化的危险因素。然而，其与颈动脉斑块不稳定性和中风发病机制的关系仍不清楚。在接受颈动脉内膜切除术的患者中，我们旨在确定 UA 在有症状和无症状的颈动脉斑块中是否存在差异，以及血清 UA 是否与脑血管症状（中风、短暂性脑缺血发作或一过性黑蒙）相关。方法：收集颈动脉粥样硬化斑块颈动脉内膜切除术。使用 Gomori 甲胺银染色以及抗 UA 免疫组织化学染色评估 UA 的存在，并使用酶比色测定法测量其数量。临床信息是通过对数据的回顾性审查获得的。结果：与无症状（n=9）颈动脉斑块相比，使用 Gomori 甲胺银（20 [86.9%] 对 2 [22.2%] ];P = 0.001）和抗 UA 免疫组织化学（16 [69.5%] 对 1 [11.1%]；P = 0.004）。UA 浓度在有症状而非无症状斑块中更高（25.1 [9.5] 对 17.9 [3.8] µg/g；P = 0.021）。颈动脉内膜切除术前，有症状患者（n=341）的血清 UA 水平高于无症状患者（n=146）（5.9 [四分位距，4.6-6.9] mg/dL 对 5.2 [四分位距，4.6-6.2] mg/ dL; P = 0.009). 结论：目前的研究支持 UA 作为潜在的组织参与者和系统性生物标志物在颈动脉粥样硬化发病机制中的潜在作用。UA 可能为斑块不稳定和随后的缺血性脑血管事件提供机制解释。