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 st ep in the recruitment of leukocytes into the intima and the subsequent deve lopment of lipid-containing foam cell lesions. Increased levels of circulat ing adhesion molecules have been identified in diabetic patients, but the d istribution in the arterial wall has not been described. Materials and methods. Frozen sections were prepared from aorta and interna l mammary artery obtained during bypass surgery from 12 diabetic and 16 non diabetic patients. Adhesion molecules (intercellular adhesion molecule-1 (I CAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-Selectin), macrop hages, and lymphocytes were identified and quantified using immunohistochem istry; intimal hyperplasia was quantified. Results. Endothelial expression of VCAM-1 and intimal smooth muscle cell ex pression of both VCAM-1 and ICAM-1 was increased in the aortas from diabeti c patients. Intimal hyperplasia in aorta and internal mammary artery sectio ns 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 mellit us, 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 p atients. (C) 1999 Academic Press.