Uric Acid Expression in Carotid Atherosclerotic Plaque and Serum Uric Acid Are Associated With Cerebrovascular Events

四分位间距 医学 颈动脉内膜切除术 无症状的 黑蒙 胃肠病学 发病机制 内科学 冲程(发动机) 动脉内膜切除术 病理 尿酸 心脏病学 狭窄 机械工程 工程类
作者
Valentina Nardi,Federico Franchi,Megha Prasad,Erica M. Fatica,Mariam P. Alexander,Melanie C. Bois,Josephine Lam,Ravinder J. Singh,Fredric B. Meyer,Giuseppe Lanzino,Yuning Xiong,Esther Lutgens,Lilach O. Lerman,Amir Lerman
出处
期刊:Hypertension [Lippincott Williams & Wilkins]
卷期号:79 (8): 1814-1823 被引量:30
标识
DOI:10.1161/hypertensionaha.122.19247
摘要

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).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.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).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.

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