Ultrastructural and immunohistochemical study of advanced atherosclerotic lesions in human carotid wall.

Atherosclerosis is a degenerative-inflammatory process that develops in the artery wall,1 involving a progressive accumulation of lipids. Mechanisms underlying atherosclerosis development and progression are still unclear whereas, studies on humans that evaluate and correlate circulating and tissue markers of inflammation, vascular calcification and plaque instability are still lacking.Therefore, our work will focus on the ultrastructural characterization of plaque phenotype in patients with early chronic kidney disease, suffering from cardiovascular disease. Carotid endoartherectomy samples were collected from 10 diabetic and 5 nondiabetic patients presenting carotid stenosis, with or without history of cardiovascular events. Samples were fixed in glutaraldehyde and prepared for transmission and scanning electron microscopic-correlated analyses. A histopathologic control was performed on semithin sections. Immunohistochemistry for galectin-3 was also performed. The endothelial layer was generally absent, being usually replaced by a fibrous thin cap, in which macrophages and inflammatory cells were often found. Smooth muscle cells (SMC) switched into fibroblast-like actively-secreting cells or apoptotic cells, were observed in the degenerated tunica media. Micro-calcium deposits were seen among SMC cellular debris. Atherosclerotic lesions were defined as stable if the surface was smooth and plane, and unstable when the surface was rough, with fractures or ulceration and/or thrombosis. Galectin-3 was expressed predominantly in unstable lesions and staining was positive mostly in macrophages but also in SMC. In conclusion, inflammation is strictly associated with microcalcification in unstable atherosclerotic lesions.