Responses to hemodynamic stress in the aged heart.
In aged individuals the incidence of heart failure is higher than in younger subjects. Ischemic events are also common in the aged heart because of changes in the coronary vasculature and myocytes caused by aging. Adaptational responses to increased hemodynamic overload and to ischemia in the aged heart are discussed at the molecular, cellular and organ levels. One characteristic of the aged heart is a limited capacity 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 and 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 induction of immediate early genes in the aged heart was not observed after more severe stress. With regard to the coronary vasculature, the age at which pressure-overload begins seems to be one of the important factors which determine the vascularity of hypertrophied hearts. Late-onset pressure-overload decreased dilator reserve in spite of the absence of myocardial hypertrophy. Thus, the responses to stress in the aged heart are quite different from those in the young heart. The limited capacity for adaptation to hemodynamic overload and poor protective mechanisms against stress may be causes of the higher incidence of heart failure in the aged.
First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
S
S
Isoyama
N
N
Ito
M
M
Komatsu
Y
Y
Nitta
K
K
Abe
M
M
Aoki
T
T
Takishima
D000368:Aged; D000375:Aging / Q000502:physiology*; D006332:Cardiomegaly / Q000503:physiopathology; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000502:physiology; D006321:Heart / Q000502:physiology*; D006339:Heart Rate; D006360:Heat-Shock Proteins / Q000235:genetics; D006439:Hemodynamics / Q000502:physiology*; D006706:Homeostasis; D006801:Humans; D009206:Myocardium / Q000473:pathology; D014655:Vascular Resistance
D006360:Heat-Shock Proteins