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Mediators of Inflammation
Volume 2016 (2016), Article ID 9153673, 10 pages
Research Article

Intraplaque Expression of C-Reactive Protein Predicts Cardiovascular Events in Patients with Severe Atherosclerotic Carotid Artery Stenosis

1First Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa, 6 Viale Benedetto XV, 16132 Genoa, Italy
2Division of Cardiology, Foundation for Medical Researches, Department of Medical Specialties, University of Geneva, 64 Avenue de la Roseraie, 1211 Geneva, Switzerland
3Unit of Toxicology, University Centre of Legal Medicine, Geneva-Lausanne, Rue Michel-Servet 1, 1211 Geneva, Switzerland
4IRCCS AOU San Martino-IST, 10 Largo Benzi, 16132 Genoa, Italy
5Vascular and Endovascular Surgery Unit, Department of Surgery, IRCCS AOU San Martino-IST, 10 Largo Benzi, 16132 Genoa, Italy
6Clinic of Hematology, Department of Internal Medicine, University of Genoa, IRCCS AOU San Martino-IST, 10 Largo Benzi, 16132 Genoa, Italy
7Division of Laboratory Medicine, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, 4 Rue Gabrielle-Perret-Gentil, 1205 Geneva, Switzerland
8Centre of Excellence for Biomedical Research (CEBR), University of Genoa, 9 Viale Benedetto XV, 16132 Genoa, Italy

Received 15 July 2016; Accepted 22 August 2016

Academic Editor: Francesca R. Spinelli

Copyright © 2016 Aldo Bonaventura et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Serum c-reactive protein (CRP) was suggested for the assessment of intermediate cardiovascular (CV) risk. Here, systemic or intraplaque CRP levels were investigated as predictors of major adverse cardiovascular events (MACEs) in patients with severe carotid stenosis. CRP levels were assessed in the serum and within different portions (upstream and downstream) of carotid plaques of 217 patients undergoing endarterectomy. The association between CRP and intraplaque lipids, collagen, neutrophils, smooth muscle cells (SMC), and macrophage subsets was determined. No correlation between serum CRP and intraplaque biomarkers was observed. In upstream portions, CRP content was directly correlated with intraplaque neutrophils, total macrophages, and M1 macrophages and inversely correlated with SMC content. In downstream portions, intraplaque CRP correlated with M1 and M2 macrophages. According to the cut-off point (CRP > 2.9%) identified by ROC analysis in upstream portions, Kaplan-Meier analysis showed that patients with high CRP levels had a greater rate of MACEs. This risk of MACEs increased independently of age, male gender, serum CRP, and statin use. In conclusion, in patients with severe carotid artery stenosis, high CRP levels within upstream portions of carotid plaques directly and positively correlate with intraplaque inflammatory cells and predict MACEs at an 18-month follow-up period.