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

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

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish (US)
Pages (from-to)1814-1823
Number of pages10
Issue number8
StatePublished - Aug 1 2022


  • atherosclerosis
  • carotid artery diseases
  • inflammation
  • plaque, atherosclerotic
  • stroke
  • uric acid

ASJC Scopus subject areas

  • Internal Medicine


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