RESPONSES TO HEMODYNAMIC STRESS IN THE AGED HEART

In aged individuals the incidence of heart failure is higher than in y ounger subjects. Ischemic events are also common in the aged heart bec ause of changes in the coronary vasculature and myocytes caused by agi ng. Adaptational responses to increased hemodynamic overload and to is chemia in the aged heart are discussed at the molecular, cellular and organ levels. One characteristic of the aged heart is a limited capaci ty for adaptation with hypertrophy to increased mechanical load. This age-related attenuation of the hypertrophic response may be attributed to the diminished induction of proto-oncogenes such as c-fos, c-myc a nd c-jun by hemodynamic stress. This diminution results from the aging of the heart per se and may be modulated by extracardiac factors. An age-related diminution was also observed in the mRNA induction of heat shock proteins by transient ischemia. However, this diminished induct ion of immediate early genes in the aged heart was not observed after more severe stress. With regard to the coronary vasculature, the age a t which pressure-overload begins seems to be one of the important fact ors which determine the vascularity of hypertrophied hearts. Late-onse t pressure-overload decreased dilator reserve in spite of the absence of myocardial hypertrophy. Thus, the responses to stress in the aged h eart are quite different from those in the young heart. The limited ca pacity for adaptation to hemodynamic overload and poor protective mech anisms against stress may be causes of the higher incidence of heart f ailure in the aged.