Heart disease in older individuals can be characterised as the result
of 2 processes, hypertension and atherosclerosis, which are the major
causes of heart failure in the elderly population. The aging heart und
ergoes changes at the molecular, cellular and organ levels. These age-
related changes may then be modulated by pathological conditions, such
as hypertension, and by the reduction of blood pressure. One characte
ristic of the aged heart is a limited capacity for adaptation, by hype
rtrophy, to increased mechanical load. This age-related attenuation of
the hypertrophic response may be attributed to the diminished inducti
on of proto-oncogenes such as c-fos, c-myc and c-jun. This diminution
results from aging of the heart per se and may be modulated by extraca
rdiac factors. With regard to the coronary vasculature, the age at whi
ch hypertension develops seems to be an important factor for determini
ng the vascularity of hypertrophied hearts. Late-onset hypertension is
not accompanied by coronary angiogenesis, and it decreases dilator re
serve in spite of the absence of myocardial hypertrophy. In contrast,
mechanical overload in infant hearts is accompanied by angiogenesis an
d normal dilator reserve. In principle, the normalisation of hypertens
ion results in the regression of myocardial hypertrophy and decreased
coronary dilator reserve. In aged hearts, it is not clear how hyperten
sion-induced myocardial hypertrophy or coronary vascular changes regre
ss. Although antihypertensive treatment is clearly associated with an
improvement of cardiovascular mortality and morbidity in hypertensive
elderly individuals, it remains unclear how treatments ameliorate the
hypertension-induced alterations.