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

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.

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.

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.

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.