ABSTRACT
Advancing age is accompanied by multiple cardiovascular changes, even in apparently healthy adults. Thickening and stiffening of the large arteries 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 occursdue 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. However, an age-associated increase in late diastolic filling preserves end-diastolic volume. Aerobic exercise capacity declines approximately 10% per decade in cross-sectional studies; in longitudinal studies, this decline is accelerated in the elderly. Reductions in peak heart rate and peripheral oxygen utilization but not stroke volume 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. Conduction disorders, including sinus node and atrioventricular node dysfunction and bundle branch blocks, and both supraventricular and ventricular arrhythmias become more common with age. The prognostic significance of any arrhythmia or conduction disturbance depends primarily on the presence and severity of associated heart disease. Although many of these cardiovascular aging changes are considered “normative,” they may lower the threshold for development of cardiovascular disease.
