Systolic arterial pressure increases with aging. This increase encompasses both the clinically normal and hypertensive ranges of pressure and is due in part to arterial stiffening. To what extent it may be modulated by life style changes that accompany aging is unknown. The stiffer arterial tree transmits the pulse wave with a higher velocity such that reflected waves return to the aortic root during the ejection period. This causes the aortic impedance to increase at this time, leading to a late peak in systolic pressure. Cardiac adaptation to these vascular changes include left ventricular hypertrophy and prolonged Ca2+ activation of contractile proteins leading to prolonged contraction. The resultant delayed contractile relaxation, in part, leads to a slower velocity of early left ventricular filling; however, this is offset by an enhanced atrial contribution to filling. These myocardial adaptations with aging, which in animal models appear, in part at least, to be controlled from within the genome permit a relatively normal heart volume and ejection fraction in the presence of chronically elevated afterload. These changes that occur with aging in otherwise healthy individuals can occur at a younger age in clinical hypertensives and can be produced in young experimental animals by hypertension. Thus, aging has sometimes been referred to as blunted hypertension, or hypertension as accelerated aging.
- Arterial pressure
- Cardiac hypertrophy
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine