Background: Neoangiogenesis inside the atherosclerotic plaques has been linked to progression of the disease. Egfl7, a key player in adult angiogenesis, was found to be upregulated in response to vascular injury in rats. Egfl7 encodes for miR-126-3p and miR-126-5p. Specific information about miRNA-126-5p and its expression in cardiovascular disease is scarce in comparison to that of miR-126-3p. Objectives: A gene expression study was conducted to investigate the levels of Egfl7 and miRNA126-5p in human carotid artery atherosclerotic plaques aiming to gain a better understanding of the role of neoangiogenesis within plaques and the mechanisms causing atherosclerosis progression. Methods:Egfl7 and miR-126-5p levels were studied in 14 plaque samples and 14 control samples using real-time PCR. The fold change between the carotid artery plaque tissue and control tissue was calculated using the 2(-CT) method. Results:Egfl7 was upregulated in the 11 plaque samples compared to controls, while expression levels of miR-126-5p was higher in eight of the plaque samples and lower in six as compared to control samples. Upregulation of miR-126-5p expression was correlated with high low-density lipoprotein (LDL) cholesterol (p=0.023). Conclusions: Our findings suggest that the upregulation of Egfl7 promotes neoangiogenesis within the plaques, contributing to disease progression.