Cardiac aging, like aging in general, is a complex process involving numerous cellular and molecular changes, which along the way contribute to the expression of the multiple phenotypes of aging, "the different faces" of cardiac aging. Several plausible theories have been considered to explain aging, e.g., evolution, free radical, somatic mutation, etc; and at this time it is most likely that these different theories are intertwined with each other without a definitive "winner", reflecting a mixture of genetic and epigenetic elements found in most aged individuals with cardiovascular defects. The demonstration in numerous animal models of the dramatic alterations in life-span achieved by gene engineering or dietary modifications, such as caloric restriction, further underscores the interplay of both genetic and environmental factors involved in aging, as well as acting through molecular and signaling pathways operative in the heart and the vasculature.


Aging and decreasing heart function occurring together has been amply documented, and our knowledge of age associated cardiac pathologies has outpaced our understanding of the basic mechanisms underlying these processes. At present, genomics, proteomics and recombinant DNA techniques are increasingly applied to the study of cardiac cell structure and function. Their role in aging, in general, and in the aging heart, in particular, will finally be unveiled. With the availability of the Human Genome Project, and an ever increasing number of animal models and new and exciting molecular technologies, the unraveling of the underlying basic mechanisms of cardiac aging have already begun. In this book, the genetic and molecular basis of cardiovascular aging will be discussed and a comprehensive assessment of the bioenergetics changes occurring in human and animal models of cardiac aging, current diagnostic and future therapeutic modalities will be presented.

Other: M.J. Goldenthal, G.W. Moe