Circulating visfatin as a marker of carotid stenosis and symptomatic disease in patients undergoing endarterectomy
A Tirandi, M Moriero, F Carbone, S Kraler, M Bertolotto, S Minetti, T F Luescher, G G Camici, F Montecucco, L LiberaleAbstract
Introduction
Atherosclerotic carotid disease is a major cause of stroke and transient ischemic attacks. Visfatin, a pro-inflammatory adipokine, is overexpressed in unstable plaques. This study assessed whether circulating visfatin serves as a biomarker of plaque intraplaque high-risk features and ultrasound-assessed carotid stenosis in patients with severe carotid disease undergoing carotid endarterectomy (CEA).
Methods
In patients undergoing carotid endarterectomy, preoperative blood samples and carotid plaques were collected for histological characterization of intraplaque features. Plasma visfatin was quantified using ELISA. Participants were classified as either symptomatic (recent ipsilateral ischemic stroke within the prior 30 days) and as asymptomatic (no recent cerebrovascular event). Outliers were excluded using predefined boxplot-based criteria. Group differences were assessed using the Mann-Whitney test, correlations with Spearman’s R, and associations with individual outcomes were examined using linear and logistic regression models adjusted for clinical, biochemical, and histological covariates.
Results
The final cohort included 37 symptomatic and 169 asymptomatic patients, with no significant differences in age or sex. Symptomatic patients had greater ultrasound-assessed stenosis (80% vs. 75%, p = 0.035). Circulating visfatin correlated with ultrasound-assessed stenosis (ρ = 0.232, p = 0.001) and with features of plaque instability (Figure 1). In adjusted linear regression, visfatin independently associated with ultrasound-assessed stenosis (β = 1.30, 95% CI: 0.28–2.32, p = 0.013; Figure 2A), although this was not confirmed when adjusting for intraplaque features (Figure 2B). Logistic regression showed that visfatin independently predicted symptomatic disease after adjustment for clinical variables (OR = 1.27, 95% CI: 1.04–1.56, p = 0.021; Figure 2C) and after further adjustment for intraplaque features (OR = 1.82, 95% CI: 1.79–2.99, p = 0.010; Figure 2D).
Conclusions
Circulating visfatin predicts both ultrasound-assessed carotid stenosis and symptomatic disease in patients with severe carotid stenosis undergoing CEA. Visfatin may represent a promising biomarker for future studies evaluating plaque progression and symptom risk, including those involving patients with earlier stages of carotid atherosclerosis.For image description, please refer to the figure legend and surrounding text.For image description, please refer to the figure legend and surrounding text.