Ageing and its Effects on the Cardiovascular System

Summary

The study of the effect of ageing per se on cardiovascular structure and function is hindered by the occurrence of disease processes and lifestyle changes which are inextricably linked to the ageing process.

Both autopsy data and non-invasive techniques such as echocardiography have revealed a progressive hypertrophic increase in left ventricular wall thickness from the third decade of life onwards, although ageing does not lead to wall thicknesses exceeding the upper limit of normal. However, ventricular cavity dimensions are relatively unaffected by age. Left ventricular hypertrophy is an adaptive response to the increase in cardiac afterload caused by age-related arterial dilatation and loss of vascular compliance. In the large arteries, clinically significant intimal thickening and loss of distensibility occur by the age of 60 years, resulting in increased pulse pressure through elevation of systolic pressure. By comparison, the contribution of increased peripheral resistance to the development of hypertension in the elderly is relatively small. With increasing age, prolongation of isovolumic cardiac relaxation and loss of ventricular compliance combine to reduce the efficacy of early ventricular diastolic filling, but an increased atrial contribution to late ventricular filling offsets this, and no loss of left ventricular end-diastolic volume results. Resting cardiac output declines with ageing in healthy subjects. With increasing age, α-adrenoceptor-mediated effects on the vasculature appear to predominate, resulting in net vasoconstriction.

An age-related decline in cardiovascular performance under stress can be demonstrated by the measurement of maximal oxygen consumption during exercise. However, cardiac output is maintained in the disease-free elderly, since an increase in stroke volume compensates for the decline in maximal heart rate which accompanies ageing. It has been postulated that a diminished responsiveness to catecholamines underlies the age-dependent reduction in aerobic capacity.