Carotid stenosis is the narrowing of the carotid arteries due to atherosclerosis. Our goal in this study was to search for copy number variants (CNV) in the human genome which may be related to risk of plaque formation and rupture. We obtained DNA from age matched patients at Hospital das Clínicas, in Campinas. Our cohort is composed by 15 patients with asymptomatic carotid stenosis and 15 with symptomatic carotid stenosis. All samples were genotyped using a SNP microarray and analysed. We identified various CNVs located in genes of the complement system, cytoskeletal remodelling and cell adhesion pathways. In our samples, we observed deletions in genes from both classical and lectin pathways of the complement system. Low levels of lectin binding mannose (MBL), is related to enhanced plaque formation. In addition, we found three patients with duplications in UPAR. The urokinase-type plasminogen activator receptor is part of the cytoskeletal remodelling pathway and has been previously associated to plaque rupture due to its increased expression in macrophages. Furthermore, we found a duplication in the PKC gene in one patient. It is known that Protein Kinase C, present at the cell adhesion pathway, when active stimulates the adhesion of monocytes to endothelial cells, therefore accelerating plaque formation. Overall, our results indicate that genes related to plaque formation and rupture were either duplicated or deleted in patients with asymptomatic carotid stenosis.