Although epidemiologic studies have revealed that high plasma cholesterol or high homocysteine levels, as well as diabetes, hypertension and smoking are important risk factors for atherosclerotic vascular disease, the deleterious effects of these conditions can be delayed or significantly attenuated by therapeutic interventions. Since the population in the Western world is aging, advancing age itself became one of the most significant risk factors for the development of atherosclerosis. Atherosclerosis is a chronic inflammatory disease, however, the mechanisms by which advanced age per se promotes vascular inflammation are not well understood. In the present review the authors propose a model for age-related alterations in cytokine expression, increased oxidative stress and decreased bioavailability of NO that underlie a pro-inflammatory phenotype of aged vessels promoting the development of atherosclerosis in the elderly.