Changes in cardiovascular function with aging

EG Lakatta - European heart journal, 1990 - academic.oup.com
EG Lakatta
European heart journal, 1990academic.oup.com
Overall cardiovascular function at rest in most healthy elderly individuals is adequate to
meet the body's need for pressure and flow. The resting heart rate is unchanged. Heart size
is essentially not different in younger vs older adults, but heart wall thickness increases
modestly, due largely to an increase in myocyte size. While the early diastolic filling rate is
reduced, an enhanced atrial contribution to ventricular filling in elderly individuals maintains
filling volume at a normal level. Although systolic pressure at rest increases with age, the …
Abstract
Overall cardiovascular function at rest in most healthy elderly individuals is adequate to meet the body's need for pressure and flow. The resting heart rate is unchanged. Heart size is essentially not different in younger vs older adults, but heart wall thickness increases modestly, due largely to an increase in myocyte size. While the early diastolic filling rate is reduced, an enhanced atrial contribution to ventricular filling in elderly individuals maintains filling volume at a normal level. Although systolic pressure at rest increases with age, the resting end-systolic volume and election fraction are not altered, due partly to the increase in left ventricular thickness. Physical work capacity declines with advancing age, but the extent to which this can be attributed to a decrement in cardiac reserve is not certain. Part of the age-related decline in maximum oxygen consumption appears to be due to peripheral rather than central circulatory factors, e.g. to a decrease in muscle mass with age during exercise, the ability to direct blood flow to muscles, and the ability of muscle to utilize oxygen. Some elderly individuals exhibit cardiac dilatation which produces an increased stroke volume sufficient to counter the well-known age-related decrease in exercise heart rate, such that high levels of cardiac output can be maintained during exercise. Still, in these individuals, the exercise-induced reduction in end-systolic volume and increase in ejection fraction is less than in younger individuals. A similar haemodynamic profile occurs in individuals of any age who exercise in the presence of β-adrenergic blockade. Alterations in cardiac function which exceed the identified limits for aging changes for healthy elderly individuals are most likely a manifestation of the interaction of physical deconditioning and cardiovascular disease, which are, unfortunately, so prevalent within our society.
Oxford University Press