The Role of FGF23 in Carotid Endarterectomy: A Systematic Review of Mechanisms and Outcomes

Abstract

Background/Objectives: Carotid artery disease is a condition affecting 3% of the general population, which significantly contributes to the development of cerebrovascular events. Fibroblast Growth Factor-23 (FGF-23) is a hormone that has been linked to atherosclerosis and increased cardiovascular risk, including stroke and myocardial infarction. This review explores the association of FGF-23 with carotid artery disease progression in an endarterectomy clinical context. Methods: Leaning on Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA), a search was performed relying on MEDLINE, Scopus and Web of Science, identifying publications focused on the correlation between serum FGF-23 and carotid artery disease. Assessment of studies' quality was made using National Heart, Lung and Blood Institute Study Quality Assessment Tool (NHLBI). Results: Three observational studies, comprising 1039 participants, were included. Elevated FGF-23 levels were consistently associated with unstable plaque features, including intraplaque neovascularization, as identified through Superb Microvascular Imaging (SMI). Plasma levels of inflammatory mediators, such as Interleukin-6 (Il-6), Monocyte Chemoattractant Protein-1 (MCP-1), and Osteoprotegerin (OPG), positively correlated with carotid artery disease, but their link to unstable plaques was conflicting. None of the studies investigated clinical complications following carotid endarterectomy. Conclusions: FGF-23 is a potential biomarker for plaque vulnerability in carotid artery disease. Despite promising findings, limitations such as small sample sizes and lack of longitudinal data suggest the need for larger and more diverse studies to improve risk stratification and inform personalized treatment strategies for carotid atherosclerosis.