Heat Shock Protein Expression in the Aging Cardiovascular System

Mammalian aging is accompanied by a progressive decline in most physiologic functions and in particular by a decreased ability to maintain homeostasis when faced with conditions of stress (Shock et al., 1984; Martin et al., 1993). The cardiovascular system is no exception as aging constitutes a major risk factor for the development of cardiovascular disease, with the incidence of hypertension, atherosclerosis, stroke and myocardial infarction all increasing markedly with advancing age (Wei and Gersh, 1987; Stout, 1987; Wei, 1992). The mechanisms responsible for these age-related changes are not clear, but significant histological, biochemical and functional alterations occur in both the myocardium (e.g. left ventricular hypertrophy, diminished sensitivity to β-adrenergic hormones, and interstitial fibrosis) and vasculature (e.g. thickening of vessel walls, smooth muscle cell relocation and reduced compliance) with aging (reviewed in Lakatta, 1993; Isoyama et al., 1994; Crow et al., 1996). In addition, and perhaps of greatest significance, elderly patients are much more vulnerable to acute cardiovascular stress. Aged hearts are more susceptible to post ischemic injury than are young hearts, and older individuals display an increased tendency to develop cardiac failure following hemodynamic stress (Isoyama et al., 1994).