Endothelial adhesion molecule expression is enhanced in the aorta and internal mammary artery of diabetic patients.

BACKGROUND: Diabetes mellitus is a major risk factor for the development of atherosclerosis but the mechanisms involved remain unclear. The expression of leukocyte adhesion molecules at the endothelial surface is a primary step in the recruitment of leukocytes into the intima and the subsequent development of lipid-containing foam cell lesions. Increased levels of circulating adhesion molecules have been identified in diabetic patients, but the distribution in the arterial wall has not been described.

MATERIALS AND METHODS: Frozen sections were prepared from aorta and internal mammary artery obtained during bypass surgery from 12 diabetic and 16 nondiabetic patients. Adhesion molecules (intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-Selectin), macrophages, and lymphocytes were identified and quantified using immunohistochemistry; intimal hyperplasia was quantified.

RESULTS: Endothelial expression of VCAM-1 and intimal smooth muscle cell expression of both VCAM-1 and ICAM-1 was increased in the aortas from diabetic patients. Intimal hyperplasia in aorta and internal mammary artery sections was significantly greater in diabetic tissue. Macrophages, T-lymphocytes, oil-red-O-stained lipid, glycated albumin, and glycated LDL were observed in the aorta of both diabetic and nondiabetic samples.

CONCLUSIONS: The increased incidence of VCAM-1 and ICAM-1 in the aorta may partly explain the enhanced atherosclerosis associated with diabetes mellitus, and their presence in established lesions may emphasize their long-term importance. The intimal hyperplasia observed in the bypass vessel may be a contributing factor to the increased incidence of restenosis in diabetic patients.