Age-associated changes in cardiovascular structure and function: a fertile milieu for future disease

Abstract

Important changes occur in the cardiovascular system with advancing age, even in apparently healthy individuals. Thickening and stiffening of the large arteries develop due to collagen and calcium deposition and loss of elastic fibers in the medial layer. These arterial changes cause systolic blood pressure to rise with age, while diastolic blood pressure generally declines after the sixth decade. In the left ventricle, modest concentric wall thickening occurs due to cellular hypertrophy, but cavity size does not change. Although left ventricular systolic function is preserved across the age span, early diastolic filling rate declines 30-50% between the third and ninth decades. Conversely, an age-associated increase in late diastolic filling due to atrial contraction preserves end-diastolic volume. Aerobic exercise capacity declines approximately 10% per decade in cross-sectional studies; in longitudinal studies, however, this decline is accelerated in the elderly. Reductions in peak heart rate and peripheral oxygen utilization but not stroke volume appear to mediate the age-associated decline in aerobic capacity. Deficits in both cardiac β-adrenergic receptor density and in the efficiency of postsynaptic β-adrenergic signaling contribute significantly to the reduced cardiovascular performance during exercise in older adults. Although these cardiovascular aging changes are considered "normative", they lower the threshold for the development of cardiovascular disease, which affects the majority of older adults.

Fig. 1

Age-associated changes in arterial structure and stiffness in healthy normotensive volunteers from the Baltimore Longitudinal Study of Aging (BLSA). Panel A Aortic root echocardiographic diameter, r = 0. 65, P \ 0.001 (from reference 3). Panel B Carotid intimal-medial thickness, r = 0.68, P \ 0.001 (from reference 5). Panel C Aortofemoral pulse wave velocity, men, dashed line and squares, r = 0.50, P \ 0.001; women, solid line and triangles, r = 0.63, P \ 0.001 (from reference 14). Panel D Carotid artery augmentation index, men, solid line and squares, r = 0. 63, P \ 0.001; women, dashed line and diamonds, r = 0.61, P \ 0.001 (from reference 14)

Fig. 2

Conceptual framework for age-associated changes in cardiovascular structure and function (from reference 32)

Fig. 3

Reduction in radionuclide-derived early left ventricular diastolic filling with age at rest and during maximal upright cycle exercise in healthy BLSA volunteers. The decline in peak filling rate with age was significant, both at rest and during exercise, r = − 0.64, P \ 0.05, for each condition. The inset displays a typical transmitral Doppler echocardiographic flow profile of a young and older adult (from reference 34)

Fig. 4

Longitudinal changes in peak oxygen consumption (VO2) and its components, maximal heart rate and oxygen pulse, in healthy BLSA volunteers. Whereas the decline in maximal heart rate across successive decades remains relatively constant at * 5%/decade, there is an accelerated age-associated decline in oxygen pulse that parallels that for peak VO2 (from reference 42)