The manifestations of certain cardiovascular diseases that lead to heart failure and stroke, such as atherosclerosis and hypertension, likely become altered in advanced age because of interactions that occur between age-associated cardiovascular changes in health and the specific pathophysiologic mechanisms underlying these diseases. These age–disease interactions result in a lower threshold for clinical symptoms, and greater severity and poorer prognosis of these diseases in older versus younger persons. In this regard, the cardiovascular changes that occur during healthy aging should not be considered to reflect a “normal process”; rather, these age-associated changes must be construed as specific risk factors for the aforementioned cardiovascular diseases, and should thus become the targets of interventions designed to prevent the epidemic of cardiovascular disease in the elderly. Such a strategy thus advocates preventive treatment for what is generally considered to be “normal cardiovascular aging.” Effective and efficient prevention of the “risks” associated with cardiovascular aging in apparently healthy individuals and with age–disease interactions in older patients requires a fundamental understanding of these age-associated changes. The present state of our understanding of age-associated changes in cardiovascular structure and function, from the molecular to the human scale, is the focus of this issue of Dialogues in Cardiovascular Medicine...