Cardiovascular disease is a main cause of morbidity and a leading cause of death of elderly Americans. Studies identifying the pathophysiological mechanisms underlying cardiovascular aging hold promise to develop treatments to delay/prevent coronary artery disease and stroke in the elderly. Evidence supporting the roles of oxidative stress and inflammation in the cardiovascular aging process is presented in detail in this review. Mammalian lifespan ranges hundred-fold and we propose that long-living species may be useful models for successful cardiovascular aging in humans. Comparative studies exploiting the large differences in maximum lifespan potential and cardiovascular aging patterns may be particularly relevant. Comparisons of mechanisms related to oxidative stress, oxidative stress resistance and redox signaling between long-living species and shorter-living ones may elucidate key mechanisms for delaying cardiovascular aging. We discuss the potential use of three long-lived but mouse-sized mammalian species, the naked mole-rat (Heterocephalus glaber), the white-footed mouse (Peromyscus leucopus) and the little brown bat (Myotis lucifugus) to test predictions of the oxidative stress theory of aging and elucidate mechanisms by which cardiovascular aging can be delayed.