Do hypertension and aging have a similar effect on the myocardium?

Vascular stiffening and a modest increase in cardiac mass with advancing age in man resemble similar alterations accompanying chronic arterial hypertension. In both hypertensive and elderly normotensive individuals, systolic pump function at rest is not altered, while early filling rate and volume are decreased. Although this abnormality is often attributed to the cardiac hypertrophy per se, prolonged isometric relaxation, which occurs with aging in man and animals and in some types of experimental hypertension, is an equally plausible mechanism. In the aged rat, prolonged relaxation can be attributed to a prolonged myoplasmic Ca++ transient with excitation. This occurs amidst a constellation of other cellular changes, among which are a markedly prolonged transmembrane action potential, diminished sarcoplasmic reticulum Ca++ pumping rate, and altered myosin isozyme composition. Many of these changes occur in cardiac muscle of younger animals with cardiac hypertrophy due to chronic increased afterload. While the magnitude of these alterations with advanced age is as great as those with chronic hypertension in younger animals, the magnitude of left ventricular hypertrophy with aging is far less than that in experimental hypertension. Furthermore, with aging, these alterations occur not only in the myocardium of the left but also of the right heart (which does not hypertrophy). Thus, myocardial hypertrophy per se does not appear to be the common link between cellular changes due to aging and those due to hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)