Background: Advanced glycation endproducts (AGEs) have been postulated to play a major role that governs aging and diabetes-associated vascular damage through receptor and non-receptor mediated process. In this study, we investigated whether AGEs participate in the development of coronary artery disease(CAD) and arterial stiffness in diabetic and nondiabetic subjects. Subjects and Methods: Serum concentration of AGEs were measured using non-competitive enzyme linked immunosorbent assay in 142 consecutive patients (mean age: 63짹9 years, male 56%) who received coronary angiography for the study of chest pain or suspected CAD (the number of significantly stenosed vessels: 0, n=60; 1, n=36; 2, n=28; 3, n=22). Arterial stiffness was estimated by central pressure during cardiac catheterization and peripheral pressure using an automatic wave form analyzer. Results: Patient were classified into 3 group based on fasting blood glucose, defined as normal, impaired fasting glucose(IFG) and diabetes, which were under appropriate treatments of risk factors for CAD, respectively. Serum concentration of AGEs were significantly higher in diabetes than in normal and IFG (3.01짹0.76, 2.51짹0.78 and 2.64짹0.85 mU/ml, p=0.003). Serum AGEs, not fasting glucose and HbA1c, were positively correlated with the severity of CAD in diabetes (r=0.59, p<0.001). Serum AGEs did not show relation with parameters of arterial stiffness in any subgroup. In multiple regression analysis, only the serum concentration of AGEs were independently associated with the severity of CAD in diabetes (棺=-0.66, p=0.25). Conclusions: The measurement of serum AGEs concentration are useful predictor of vascular damage in diabetic milieu. AGEs might participate in the pathogenesis of CAD with a less or un-modifiable manner and should be considered as a potential target for treatment of CAD.