Abstract 511: Total Circulating Adiponectin Levels and its Receptors are Associated with Histological and Immunohistochemical Features of Carotid Plaque Instability
Introduction. Evidence shows that low plasma levels of adiponectin, a vasculoprotective adipokine, are associated with coronary artery disease and carotid-intima media thickness. The current study investigated for the first time the association between adiponectin and carotid plaque instability, namely the association between circulating adiponectin, expression of its receptors (AR1/AR2), and plaque instability as assessed by histology/immunohistochemistry.
Methods. 100 patients scheduled for carotid endarterectomy were recruited from the Royal Victoria Hospital, Montreal. Blood samples were collected to determine total adiponectin levels. Carotid plaque specimens were stained with hematoxylin and eosin and immunostained for CD3 (lymphocytes), CD68 (macrophages/foam cells), von Willebrand Factor (vWF, neovascularization), and AR1/AR2. A vascular pathologist categorized the plaques according to AHA classification and with a semi-quantitative scale of plaque instability. The intensity and percentage of macrophages/foam cells stained with AR1/AR2 were assessed using an optical microscope scoring method.
Results. Patients with less infiltration of CD68+ inflammatory cells in their plaques had higher levels of total circulating adiponectin (12.26 + 6.74 μg/ml) when compared to patients with greater infiltration (8.99 + 6.97 μg/ml; p=0.010). The intensity of AR1 expression on macrophages was directly associated with overall grade of inflammation and neovascularization (p=0.025 and p=0.05 respectively). A trending inverse association was noted between the percentage of macrophages expressing AR1 and overall stability (p=0.084). Expression of vWF was inversely associated with the percentage of macrophages and foam cells expressing AR2 (p=0.033 and p=0.002, respectively), while increase cap infiltration was detected in plaques with a lower intensity of AR2 expression (p=0.013).
Conclusion. Patients whose plaques were characterized as unstable were found to have lower plasma levels of total adiponectin, a higher expression of AR1 and a lower expression of AR2 in their plaques. These results suggest a potential role for adiponectin in the development of plaque instability, as well as differential roles for its two receptors.
- © 2013 by American Heart Association, Inc.