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Cardiovascular Disease in the Elderly
Aging is a normal physiological process associated with a decline in organ system function. Changes of cardiovascular physiology intertwine with pathophysiology of cardiovascular disease (CVD). Although disease should not be misconstrued as an inevitable consequence of aging, distinctions are often arbitrarily defined, and the difference between diminished biological reserve and overt dysfunction can be thought of as quantitative rather than 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 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 3 ).
Age is a strong independent risk factor for CVD, and a powerful predictor of cardiovascular disability, morbidity, and mortality. Our society is aging, and the healthcare system is therefore facing a challenge to care for the growing older adult population with CVD. Unfortunately, patients older than 75 years of age are underrepresented in clinical studies that assess safety and efficacies of diagnostic and therapeutic approaches. Therefore, the clinical evidence obtained from younger populations may not be readily applicable to older populations. Understanding key aspects of cardiovascular physiology in older adults, their unique clinical characteristics, and responses to therapy can serve a foundation to guide clinical practice. Frailty, depression, and other confounding comorbidities in older adults add yet another layer of complexity in discerning which changes are attributable to aging and which ones to disease or environment ( Table 73.1 ). This chapter summarizes the cardiovascular physiology of older adults, describes clinical features of common CVD, and considers strategies that may decrease the risk of death and disability from these diseases in older adults.
TABLE 73.1
Cardiovascular Changes in Older Adults Without Overt Disease
| Measured Change | Functional Consequence |
|---|---|
| Myocardium | |
| Increased interventricular septal thickness; increased cardiac mass per body mass index in women | Increased propensity for diastolic dysfunction |
| Prolonged action potential, calcium, transient, and contraction velocity (in animal models); desensitization of myocardial β-adrenergic receptors | Decreased intrinsic contractile reserve and function |
| Reduced early and peak left ventricular filling rate and increased pulmonary capillary wedge pressure | Greater dependence on atrial kick, and physiological S 4 heart sound |
| Cardiac Valves | |
| Fibrosis and calcification of the aortic valve and the mitral annulus | Valvular stiffening |
| Vasculature | |
| Thickening of the media and subendothelial layers; increased vessel tortuosity | Decreased vessel compliance; increased hemodynamic shear stress and lipid deposition in the arterial walls |
| Large elastic arteries (e.g., aorta, carotid artery) become thicker, tortuous, and more dilated. | Increased peripheral vascular resistance and earlier reflected pulse waves, and consequent late augmentation of systolic pressure |
| Impulse Formation and Propagation | |
| Substantial decrease in sinoatrial pacemaker cell population, with separation from atrial musculature due to surrounding fatty tissue accumulation Increase in collagenous and elastic tissue in all parts of the conduction system Decreased density of bundle fascicles and distal conduction fibers Reduced threshold for calcium overload and for diastolic after-depolarizations and ventricular fibrillation |
Diminished intrinsic sinus and resting heart rates Slight PR interval prolongation; increased incidence of ventricular ectopy Propensity toward bundle branch blocks and abnormal conduction Lower threshold for atrial and ventricular arrhythmias; increased fibrosis and myocyte death |
| Autonomic System | |
| Diminished autonomic tone, especially parasympathetic; increased sympathetic nerve activity and circulating catecholamine levels | Decreased spontaneous and respiratory-related heart rate variability |
Cardiovascular Physiology in Older Adults
As a result of decades of complex molecular and cellular aging, which are processes that are under the influence of both genetics and environmental factors, cardiovascular physiology in older adults is characterized by (1) increased arterial stiffness; (2) increased ventricular stiffness, and reduced ventricular compliance and cardiac reserve; (3) impaired β-adrenergic, parasympathetic function, and autonomic reflexes; and (4) degenerative changes of the conduction system.
Increased Vascular Stiffness
Age-related changes occur throughout the arterial wall ( Fig. 73.1 ). Decreased distensibility or increased stiffness of the large central arteries is a hallmark of vascular aging. Processes include complex molecular mechanisms such as oxidative stress, endothelial dysfunction (decreased production of nitric oxide), inflammation, matrix production and/or degradation, vascular cell migration and proliferation, and vascular calcification. Senile cardiac transthyretin-related amyloidosis and other β-sheet protein accumulations are also associated with arterial aging. Blood flow in the aging arterial system becomes less laminar as vessels become more tortuous and endothelial cells show greater heterogeneity in size, shape, and axial orientation. These changes together result in large artery stiffening, decreased compliance and recoil, and a diminished capacity to absorb the pulsatile wavefront produced by the ejecting heart. Hemodynamic consequences of these changes include: (1) increased systolic pressure and pulse pressure; (2) increased left ventricular (LV) afterload, contraction, and oxygen requirements; and (3) decreased coronary filling pressure.
The peripheral arterial tree also shows morphological and physiological decline. The average aortic root size is approximately 14 mm/m 2 for both sexes in the early twenties and increases to 17 mm/m 2 in healthy octogenarians. With increases in the aortic diameter, individuals have an increased risk of aneurysm formation and aortic dissection. Large-caliber vessels thicken progressively. The intima-medial wall thickness of carotid arteries is 0.03 mm in the young and doubles by the age of 80 years. After the fourth decade of life, renal blood flow per gram of kidney weight decreases progressively, probably because of increased renal arterial resistance.
Peak oxygen use (VO 2 max ), a measure of work capacity and physical conditioning, declines by approximately 50% by 80 years of age compared with the VO 2 max of a 20-year-old individual (~10% loss per decade of life). Aside from age-associated decline in cardiac function, up to one-half of the VO 2 max impairment is attributable to poor peripheral oxygen extraction and use, largely from inefficient redistribution of blood flow to skeletal muscles.
Reduced Ventricular Compliance and Cardiac Reserve
Primary changes in cardiomyocytes during aging include: an increase in size; a decrease in numbers, with an alteration in the myocyte-to-fibroblast ratio; and an increase in the abundance of lipids and their peroxidation products, including amyloid, collagen, fat, fibrotic foci, and advanced glycation products. These processes result in gross hypertrophy. Aging also diminishes the capacity for regeneration and repair of injured cardiomyocytes. The intrinsic myocardial contractility is diminished with age, in large part as a result of higher vascular afterload and compensatory effects of 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-W workload) is significantly attenuated in older adults. A young person can increase the 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 older adult 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 older adults, 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 relaxation. 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 older adults and the increased dependence on atrial contraction (“kick”) for augmentation and completion of diastolic LV filling. This diminished diastolic capacity makes older adults more vulnerable to the hemodynamic and symptomatic consequences of atrial fibrillation (AF). With aging, cardiac output may no longer be able to meet increased demands of exertion, illness, or severe physical or emotional stresses.
In addition, the left atrium tends to enlarge with advancing age, increasing the likelihood that AF will develop. Fibrosis and calcification of the aortic valve and the mitral annulus may lead to valvular dysfunction.
Impaired Beta-Adrenergic and Parasympathetic Function
Decreased responses to β-adrenergic and parasympathetic stimulation and reflex are other hallmarks of aging. Age-related postsynaptic signaling deficits attenuate β-adrenergic modulation of heart rate variability and vascular tone, muting compensatory increases in heart rate and exercise reserve capacity. The maximum heart rate achieved in 20-year-old individuals is approximately 180 beats/min, but it is only approximately 120 beats/min in octogenarians. The maximal cardiac index therefore decreases approximately 30% over six decades. Older cardiomyocytes secrete more stress-related products, such as atrial natriuretic factor and opioid peptides. Moreover, ambient plasma catecholamine levels are elevated, and the production of nitric oxide is reduced, which all contribute to increased afterload and a lowered cardiac output. These age-related changes often diminish the normal response to stressors, such as standing up rapidly, volume loss, or exercise, which results in orthostatic hypotension and syncope.
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