Abstract 64: Mechanism Of Carotid Plaque Vulnerability: Associations Of Pro-and Anti-inflammatory Molecules
Background: Inflammation plays an important role in the development, progression, and rupture of carotid plaques. We examined the relationship between plaque vulnerability and inflammatory molecules using blood samples and histological specimens.
Methods: We examined 58 patients with symptomatic or asymptomatic carotid stenosis, among which 41 underwent carotid artery stenting (CAS) and 17 underwent carotid endarterectomy (CEA). All of these patients were recruited in Mie University Hospital from Sept. 2009 to Mar. 2012 and underwent carotid plaque imaging with MRI. In the 41 patients with CAS, blood samples were obtained in the femoral artery as controls and in the carotid artery just before and after the operation. Emboli attached to the distal protection devices in CAS, or resected tissues after CEA were embedded in paraffin. The serum concentrations of IL-6, IL-10, E-selectin, adiponectin, hs-CRP and pentraxin 3 (PTX3) levels were measured by ELISA. Paraffin-embedded tissues were subjected to histopathologic and immunohistochemical analysis on IL-6, IL-10, E-selectin, PTX3.
Results: The patients with CAS were classified to 22 with stable plaque (stable group) and 19 with vulnerable plaque (vulnerable group). The values of IL-6, E-selectin, hs-CRP and PTX3 in the vulnerable group were higher than those in the stable group, whereas adiponectin and IL-10 were decreased in the vulnerable group as compared to the stable group. The values of PTX3 in the control and intracarotid samples before and after CAS were higher from the vulnerable group than those from the stable group. Pathologically, IL-6 was immunostained in the vulnerable plaques with infiltration of inflammatory cells, and PTX3 was expressed in the endothelial and perivascular cells in the unstable plaques.
Conclusions: The vulnerability of carotid plaques was modulated by upregulation of pro-inflammatory factors and downregulation of anti-inflammatory ones. In addition, PTX3 may be a novel determinant for plaque vulnerability.
- © 2012 by American Heart Association, Inc.