59 Aging and the Cardiovascular System

Senescence is a fundamental life process that results from a complex combination of age-related physiologic changes including changes in aerobic respiration, increased oxidative metabolism and stress, genetic and cellular damage due to the accumulation of mutations, and lifelong exposure to various environmental stresses. Together these events outpace endogenous surveillance and repair mechanisms and/or provoke compensatory responses that become maladaptive and cause cellular and organ dysfunction. And while disease should not be misconstrued as an inevitable consequence of aging, distinctions are often arbitrarily defined, and the difference between diminished biologic reserve and overt dysfunction can be thought of as quantitative instead of qualitative. Although the role of genetics in aging in the broadest spectrum remains poorly understood, examples of hereditary syndromes of premature aging, such as Hutchinson-Gilford syndrome (progeria) and Werner’s syndrome (wherein affected individuals typically die between the second and fourth decades of life), support the notion that aging is at least partly genetically programmed (see Chapter 72).

Although its histologic features vary little across the age spectrum, the presence and severity of atherosclerosis markedly increase with aging. This atherosclerotic burden, along with maladaptive changes associated with aging, accounts for the high mortality and morbidity rates of myocardial infarction (MI) and heart failure in elderly cohorts. Chronic deconditioning, depression, and other confounding comorbidities in elderly persons add yet another layer of complexity in discerning which changes are attributable to age and which to environment (Table 59-1). This chapter focuses on age-related changes in the cardiovascular system and considers strategies that may decrease the risk of death and disability from cardiovascular diseases in elderly individuals.

Table 59-1 Cardiovascular Changes in Elderly Individuals without Overt Disease

Cardiovascular Changes with Age

Myocardial Chambers and Valves

The effects of aging on the myocardium and cardiac valves are dramatic. Deposition of lipids and their peroxidation products occurs throughout the myocardium and the vasculature at the cellular level and in subcellular components such as the mitochondria. DNA denaturization and decreased RNA and protein synthesis accompany these age-related changes, resulting in a diminished capacity for regeneration and repair with age.

Cardiac mass increases for several reasons, including the increased size of individual myocytes and an increased abundance of amyloid, collagen, fat, fibrotic foci, and advanced glycation products, even in the absence of myocardial damage from ischemia or infarction. It is thought that myocyte hypertrophy is a compensatory mechanism in response to the myocyte loss (due to apoptosis, necrosis, or both). Myocyte hypertrophy may also be a physiologic response to the increased hemodynamic stress on the myocardium that results from the chronic increase in peripheral vascular resistance that also occurs with aging. The left atrium tends to enlarge with advancing age, increasing the likelihood that atrial fibrillation (AF) will develop. Fibrosis and calcification of the aortic valve and the mitral annulus may lead to valvular dysfunction.

Investigations have demonstrated that intrinsic myocardial contractility is diminished with age, in large part as a result of higher vascular afterload and the compensatory effects to sympathetic overactivity. Although at rest the normal sitting and submaximal end-systolic volume index is similar in adults between the ages of 20 and 85 years, the response to maximal exercise (seated cycle exercise to >100-watt workload) is significantly attenuated in elderly individuals. A young person can increase left ventricular (LV) ejection fraction by almost 50% to accommodate the demands of intense exercise, from a baseline LV ejection fraction of approximately 62% to 87%. In the elderly heart, only one fifth of this contractile reserve is seen (increasing LV ejection fraction from ~63% to only ~70%), despite the Frank-Starling mechanism and increased LV diastolic pressures. In the elderly, the isovolumic relaxation time may also be prolonged (i.e., the interval increases between the closure of the aortic valve and the opening of the mitral valve) because of slowed ventricular contraction. The peak rate of LV diastolic filling is also reduced approximately 50% with aging. Together these changes lead to the increased propensity toward diastolic dysfunction in elderly individuals and the increased dependence on atrial contraction (“kick”) for augmentation and completion of diastolic LV filling. This diminished diastolic capacity makes elderly individuals more vulnerable to the hemodynamic and symptomatic consequences of AF. Because overall function in the elderly is no better than in younger individuals, with aging, overall cardiac output is unable to meet demand when it is increased due to exertion or other causes.

Impulse Formation and Conduction

As with cardiac contractility, multiple factors contribute to the progressive dysfunction of the cardiac conduction system in aging. Minor quantities of amyloid deposits exist in nearly half of otherwise healthy individuals over 70 years of age. The sinoatrial node may also separate physically from the atrial tissue as fat accumulates around it. In addition, the absolute number of pacemaker cells in the sinus node declines substantially after 60 years of age. The number of pacemaker cells in a 75-year-old may be only 10% of that number in young adulthood. These changes are major contributors to the increased prevalence of sick sinus syndrome with aging. Other age-related abnormalities in the conduction system include an increase in fibrous tissue in the internodal tracts and a diminished density of left-bundle fascicles and distal conducting fibers. These conduction abnormalities are exacerbated by the increase in polyunsaturated fatty acids in cardiac cellular membranes that occurs with aging, resulting in changes in ion thresholds and exchange, as well as in myocardial changes that are proarrhythmic.

Large studies support this increase in arrhythmias in elderly individuals. In a study comparing adults older than 60 years of age to young adults, the presence of atrial ectopic beats was demonstrated in 6% by resting electrocardiography, in 39% with maximal treadmill exercise, and in 88% of those who underwent 24-hour ambulatory monitoring in the group over 60 years old. Though not known to be associated with any adverse outcome, short runs of paroxysmal supraventricular tachycardia are nearly twice as prevalent in octogenarians as in septuagenarians, and are observed in about half of those 65 years of age or older. The prevalence of ventricular ectopic beats rises from 0.5% in those under 40 years of age to 11.5% in those 80 years of age and older, and increases further in those with associated cardiac disease. One study demonstrated that in individuals older than 85 years of age with normal cardiac function the prevalence of ventricular ectopic beats was 5%, as compared to 13% and 28% in those with coronary artery disease and heart failure, respectively. The prognostic significance of isolated ventricular ectopic beats for elderly individuals specifically has not been studied, whether experienced at rest, during continuous 24-hour monitoring, or after treadmill exercise. However, subjects with ventricular ectopic beats on a 2-minute rhythm strip were found to have a 14-fold increase in relative risk of sudden cardiac death in a recent study. Sinoatrial function slows with age, but healthy octogenarians and nonagenarians with resting heart rates lower than 40 to 45 bpm or sinus pauses longer than 2 seconds should be followed carefully, since several studies have shown this group to be at increased risk of syncope and other heart rate–related problems. The PR interval is slightly prolonged with age, primarily from delayed conduction proximal to the His bundle, and the prevalence of first-degree atrioventricular block is 6% to 8% in octogenarians. There is an increased incidence of progression from first-degree atrioventricular block to second- and third-degree block in the elderly as well.

Vasculature

Vessel wall stiffness increases with age (Fig. 59-1

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