Abstract 540: Plasma Cell Infiltration and Mucoid Degeneration in the Media of Ascending Aorta in Patients with Coronary Artery Disease

Introduction Atherosclerosis results in inflammatory changes in the aortic intima, but little is known regarding medial changes. The inflammatory diseases of the aorta and large artery display characteristic features of inflammatory cell infiltration in the media, and they are usually diagnosed by medial changes. Aims Atherosclerosis of the ascending aorta coexists with coronary artery disease. The aim of this study was to investigate the atherosclerotic changes in 44 biopsy specimens of media of the ascending aorta associated with coronary artery disease. Methods We compared plasma cells, and matrix metalloproteinase (MMP)-2-, -9- and -12-positive cells immunohistochemically, and we also compared mucoid degeneration and fibrosis determined by special staining using a point-counting method, for groups with a variable number of coronary stenotic (≥75 %) lesions. Results and Conclusion To investigate the appearance of plasma cells, smooth muscle cells, and mucoid degeneration in the media of the atherosclerotic aorta, we examined three cadavers with known atherosclerosis. CD38-positive plasma cells are pleomorphous in the aortic media. Desmin-positive smooth muscle cells appeared fibrous or solitary spindle cells. Mucoid degeneration was shown in all three cadaver cases. In patients with one to three coronary stenotic lesions, plasma cells and mucoid degeneration were low in the aortic media. With four to five lesions, both plasma cells and mucoid degeneration increased significantly compared with those in the group with one to three lesions, and MMP-12-positive cells significantly decreased. In patients with six to nine lesions, the number of plasma cells was significantly lower than in patients with four or five lesions, whereas mucoid degeneration significantly increased. There was no change in fibrosis. In conclusion, both the infiltration of short lived plasma cells and the exudation of proteoglycan are known to be regarded as characteristic features in the autoimmune disease. The delayed stage in our study is suggested to be caused by autoimmune reaction. If the cause of the delayed medial atherosclerosis stage is found, then more effective therapies to suppress its development can be introduced.