I have presented a picture of cardiovascular aging that resembles the situation with vision, where in the absence of actual disease, near vision changes with age and cataracts appear with age but after these are corrected, vision remains markedly unchanged with age. For the undiseased heart, intrinsic cardiac muscle function and the inotropic response to nonsympathetic mediators, along with coronary perfusion, are well maintained with age. There are, however, some changes that do occur with age. Cellular hypertrophy occurs, both because of cell drop out and because of some chamber hypertrophy secondary to increased impedance to left ventricular ejection. As a result of the hypertrophy, there is some prolongation of systole secondary to delayed relaxation. This is typical of what occurs in hypertension induced hypertrophy as well. These age-related changes are of critical importance and are the background for the entire discussion of the interplay between hypertension and disease. The large arteries do in fact stiffen with age. Thus, even without hypertension, there is an age-related increased impedance to ejection, a greater systolic load, a lower coronary perfusion pressure, and an increased pulse wave velocity. Added to this is the failure of the entire β-sympathetic system to respond as well in the elderly as in the younger individuals with a resultant decrease in the vasodilating response. Both the chronotropic and inotropic response to sympathetic mediation is diminished so that states that put sudden loads on the left ventricle, such as accelerated hypertension or myocardial infarction, have more severe results in the elderly. Also acute hypertension may produce less hypertrophy in the elderly and therefore place more hemodynamic stress on the left ventricle than in young adults.
ASJC Scopus subject areas
- Internal Medicine