Increased circulating levels of MIP-1a and CD14 are associated with the presence of severe stenosis and hypoechoic plaques in patients with carotid atherosclerosis

Background and aims: carotid atherosclerosis, a major cause of ischemic cerebrovascular events, is characterized by a pro-inflammatory and pro-oxidant vascular microenvironment that promotes endothelial dysfunction and the release of inflammatory mediators. Cardiovascular risk assessment is based on traditional risk factors, but the current risk score models have important limitations. The identification of novel blood biomarkers could be useful to improve patient management. The aim of the study was to evaluate the association of selected inflammation- and oxidative stress-related markers with the presence of severe stenosis and/or instability plaque occurrence. Methods: circulating levels of soluble CD40 Ligand, interleukin-10, macrophage inflammatory protein-1, endoglin, CD163, CD14, E-selectin, tumor necrosis factor (MIP)-, monocyte chemoattractant protein-1, C-Reactive Protein and CD40L+ T lymphocytes, total antioxidant capacity, glutathione reductase activity and protein carbonyl content, were determined in patients with carotid atherosclerosis. Results: multiparametric analysis showed significantly lower levels of total antioxidant capacity in patients than in healthy subjects, significantly higher levels of MIP-1 in patients with severe stenosis than in patients with moderate stenosis, and significantly higher levels of CD14 in patients with hypoechoic (vulnerable) lesions compared to those with hyperechoic (stable) ones. ROC curve analysis showed that total antioxidant capacity was able to discriminate between patients and healthy subjects, and that MIP-1 and CD14 were able to discriminate between patients with severe and moderate stenosis and between patients with hypoechoic and hyperechoic lesions respectively. Conclusions: our data indicate circulating MIP-1 and CD14 as markers associated to the occurrence of progressive carotid plaques.