Possible involvement of pericytes in intraplaque hemorrhage of carotid artery stenosis.

OBJECTIVE Intraplaque hemorrhage (IPH) is most often caused by the rupture of neovessels; however, the factors of intraplaque neovessel vulnerability remain unclear. In this study, the authors focused on pericytes and aimed to investigate the relationship between IPH and pericytes. METHODS The authors retrospectively analyzed the medical records of all patients with carotid artery stenoses who had undergone carotid endarterectomy at their hospitals between August 2008 and March 2016. Patients with carotid plaques that could be evaluated histopathologically were eligible for study inclusion. Intraplaque hemorrhage was analyzed using glycophorin A staining, and patients were divided into the following 2 groups based on the extent of granular staining: high IPH (positive staining area > 10%) and low IPH (positive staining area ≤ 10%). In addition, intraplaque neovessels were immunohistochemically evaluated using antibodies to CD34 as an endothelial cell marker or antibodies to NG2 and CD146 as pericyte markers. The relationship between IPH and pathology for intraplaque neovessels was investigated. RESULTS Seventy of 126 consecutive carotid stenoses were excluded due to the lack of a specimen for histopathological evaluation; therefore, 53 patients with 56 carotid artery stenoses were eligible for study inclusion. Among the 56 stenoses, 37 lesions had high IPH and 19 had low IPH. The number of CD34-positive neovessels was equivalent between the two groups. However, the densities of NG2- and CD146-positive neovessels were significantly lower in the high IPH group than in the low IPH group (5.7 ± 0.5 vs. 17.1 ± 2.4, p < 0.0001; 6.6 ± 0.8 vs. 18.4 ± 2.5, p < 0.0001, respectively). CONCLUSIONS Plaques with high IPH are associated with fewer pericytes in the intraplaque neovessels. This finding may help in the development of novel therapeutic strategies targeting pericytes.