Cardiovascular aging in health

Although age-associated changes in cardiovascular structure and function do not per se cause clinical cardiovascular disease in older individuals, major age-associated alterations in the cardiovascular response to exercise are evident: there is a striking age-associated decrease in the maximum heart-rate; the maximum stroke volume, however, is not reduced in older individuals. The main mechanism used to maintain stroke volume in older individuals is the Frank-Starling mechanism, although the effectiveness of this mechanism is reduced because of failure to decrease end-systolic volume and increase ejection fraction relative to younger persons. These deficits likely result from deficient intrinsic myocardial performance, and an augmented afterload, both caused in part by a deficiency in β-adrenergic stimulation to enhance myocardial contractility and to reduce the pulsatile components of vascular afterload during exercise. A decrease in the maximum capacity for physical work with aging is caused by both diminished cardiac (heart rate) and peripheral factors. Alterations in cardiac function that exceed the identified limits for healthy aging are most likely manifestations of the interaction between excessive physical deconditioning and cardiovascular disease, both of which are, unfortunately, so prevalent within economically developed populations. Clinical manifestations of specific cardiovascular diseases (e.g., atherosclerosis and hypertension) that lead to heart failure and stroke likely become altered in older persons because interactions occur between age-associated changes in health and specific pathophysiologic mechanisms that underlie a cardiovascular disease (Table 3). This results in a lower threshold for clinical symptoms, greater symptom severity, and poorer prognosis of these diseases in older versus younger persons. In this regard, cardiovascular changes that occur during aging ought not to be considered to reflect a normal process, rather, these specific age-associated changes must be construed as specific risk factors for disease and ought to become targets of interventions designed to prevent the epidemic of cardiovascular disease in later life. Such a strategy advocates preventive treatment for what is now considered to be normal cardiovascular aging. In this regard, lifestyle changes (e.g., exercise and diet) have already been shown to be effective.