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Alterations in cardiovascular structure and function with advancing age
Insights
Aging affects cardiovascular structure and function, leading to arterial stiffening and left ventricular hypertrophy. While resting systolic function remains unchanged, aerobic capacity and maximal heart rate decline with age.
Area of Science:
- Cardiovascular Physiology
- Gerontology
- Internal Medicine
Background:
- Aging complicates the study of cardiovascular changes due to intertwined diseases and lifestyle factors.
- Age-related arterial stiffening increases systolic blood pressure, imposing a greater load on the heart.
- A modest concentric left ventricular hypertrophy develops with age as an adaptive mechanism.
Purpose of the Study:
- To elucidate the specific effects of aging on cardiovascular structure and function.
- To differentiate age-related changes from disease and lifestyle influences.
- To investigate the impact of aging on cardiac mechanics and exercise capacity.
Main Methods:
- Echocardiography and radionuclide techniques to assess resting systolic left ventricular function.
- Measurement of aerobic exercise capacity, including total work performance and maximal oxygen consumption.
- Analysis of age-related changes in arterial stiffness, blood pressure, and heart rate during exercise.
Main Results:
- Resting systolic left ventricular function is unaffected by aging.
- Aerobic exercise capacity declines with age, with a slower decline in physically active individuals.
- Maximal exercise heart rate universally declines with age.
- Cardiac output at rest and during exercise shows no decline in carefully screened subjects, with the Frank-Starling mechanism compensating for reduced heart rate.
Conclusions:
- Aging leads to arterial stiffening and left ventricular hypertrophy, but resting cardiac function is preserved.
- Aerobic capacity and maximal heart rate decrease with age, though physical activity mitigates this decline.
- The cardiovascular system adapts to aging, with mechanisms like the Frank-Starling response maintaining cardiac output during exercise.
Abstract:
The greatest difficulty in studying the effects of aging on cardiovascular structure and function lies in separating the effects of aging itself from those of the inextricably entwined disease processes and life-style changes that accompany aging. Age-related stiffening of the arterial tree results in an increased systolic blood pressure, which appears to impose a greater load on the heart. Probably as an adaptive mechanism to maintain normal wall stress, a modest age-associated concentric left ventricular hypertrophy develops, which approximates 30% between ages 25 and 80. The decrease in mitral valve E-F slope and increase in the left atrial dimension, which are seen with advancing age, may be construed as the consequences of a thicker-walled, less compliant left ventricle. Systolic left ventricular function, measured at rest either by echocardiography or radionuclide techniques, is unaffected by aging. Aerobic exercise capacity, whether measured as total work performance or maximal oxygen consumption declines with age, although in subjects who maintain a high level of physical activity, the decline appears to be approximately half of the 10% per decade decrease seen in sedentary persons. An age-related decline in maximal exercise heart rate has been a universal finding. Although several studies over the past 4 decades have found cardiac output to decrease with age, both at rest and during exercise, a recent study of subjects carefully screened to exclude latent coronary artery disease found no such decline in cardiac output. In these subjects, the age-related decline in maximal heart rate and systolic emptying at peak exercise was offset by an increased utilization of the Frank-Starling mechanism. An attractive hypothesis for explaining the hemodynamic profile of a decreased maximum heart rate, increased preload and decrease in ejection fraction at maximal effort, despite elevated norepinephrine levels, is an age-associated, diminished end-organ responsiveness similar to beta-adrenergic blockade.