Biochemical and structural changes occurring in the myocardium with ag
ing are mainly resulting from the association of a general tissue atro
phy with the hypertrophy of the remaining myocytes. Whilst hypertrophy
seems to be a compensatory process to the loss of cardiomyocytes and
to a mild systolic hypertensive condition that accompanies elderly peo
ple, atrophy should be the modification more closely related to aging
'per se.' In support to the free radical theory of aging, several sign
s of oxidative damage have been shown in the aged heart, such as lipof
uscin accumulation, decreased phospholipid unsaturation index, greater
formation of both hydrogen peroxide and 8-hydroxy-2'deoxyguanosine. A
s a compensatory reaction, the activities of the main oxygen-radical s
cavenger enzymes are stimulated in the mitochondria of aged rat heart.
Endothelium-mediated vasoregulation is more susceptible to oxidative
stress in aged with respect to young rats, suggesting that also the va
sculature can be negatively influenced by the oxygen free radicals gen
erated during aging. The possible primary role of oxygen free radicals
in the development of myocardial atrophy is also discussed.