Myocardial collagen content increases with age.5,6 Collagen is the principal noncontractile protein occupying the cardiac interstitium.⁷ Increased myocardial collagen content renders the myocardium less compliant; therefore a decrease in myocardial compliance can adversely affect diastolic filling (through decreased distensibility and dilation) and myocardial relaxation. Consequently, the left ventricle must develop a higher filling pressure for a given increase in ventricular volume. Decreased left ventricular compliance may be evident in the older adult by the presence of an S₄ heart sound.⁸

The functional consequence of these changes could be an increase in myocardial oxygen consumption. Under normal physiological conditions, an increase in myocardial oxygen demand is met with a corresponding increase in coronary artery blood flow. However, in the presence of coronary artery disease, coronary artery blood flow can be limited because of atherosclerotic-mediated narrowing of the coronary arteries. Hence the older patient is at risk for developing myocardial ischemia and/or infarction. Clinical manifestations of myocardial ischemia include electrocardiographic (ECG) changes and chest pain. However, the sensation of chest pain may be altered in the older adult. Atypical symptoms, such as dyspnea, confusion, and failure to thrive are frequently the only symptoms associated with myocardial infarction in this high-risk population.⁹

The aging heart also undergoes a modest degree of hypertrophy that is similar to pressure overload-induced hypertrophy. Such hypertrophy entails a thickening of the left ventricular wall without appreciable changes in left ventricular cavity size.¹⁰ However, increases in left ventricular cavity size associated with aging occur only in men.⁹ The increase in left ventricular wall thickness is a result primarily of an increase in muscle cell size. In older individuals the myocardial hypertrophy may be caused by corresponding increases in aortic impedance and systemic vascular resistance.¹¹

Myocardial contractility depends on numerous factors. However, the most important determinants of myocardial contraction are the intracellular level of free calcium and the sensitivity of the contractile proteins for calcium.^11,12 Because peak contractile force in the senescent myocardium is unaltered, this suggests that neither the amount of intracellular free calcium during systole nor the sensitivity of the contractile proteins for calcium is altered. The prolonged duration of contraction (systole) is caused in part by a slowed or delayed rate of myocardial relaxation, which may be an adaptive mechanism to preserve contractile function compromised by age-related increases in afterload.^3,12

Resting (supine) heart rate decreases with age.13,14 Cinelli et al¹³ reported a decrease in the resting heart rate from 78.8 beats/min in young adults to 62.3 beats/min in older adults. Heart rate is an important determinant of cardiac output (CO), and the normal resting heart beats approximately 70 times a minute. At rest or with minimal activity, the older adult probably will not experience any untoward cardiovascular effect (i.e., a decrease in CO) with a heart rate of 62 beats/min. However, if the heart rate response is attenuated during exercise, the older person’s capacity for exercise may be limited.

Resting CO and stroke volume (SV) are not changed with advancing age. At rest, left ventricular end-diastolic volume (LVEDV, preload), end-systolic volume, and the ejection fraction are not affected by age.¹⁵ In the older human myocardium, the early diastolic filling period and isovolumic phase of myocardial relaxation are prolonged.^15–17 However, these changes, although suggestive of diastolic dysfunction, do not translate into decreases in end-diastolic volume or stroke volume.^16,17 Finally, aging is associated with a moderate increase in pulmonary artery pressure.¹⁸

Advancing age produces changes in the ECG. R-wave and S-wave amplitude significantly decrease in persons older than 49 years, whereas QT duration increases¹⁹ (Table 7-2). The incidence of asymptomatic cardiac dysrhythmias increases in older patients.²⁰ The most common dysrhythmia occurring in older individuals is the premature ventricular contraction (PVC). Carom et a1²¹ and Fleg and Kennedy²² report that 70% to 80% of all patients older than 60 years experience PVCs. Other common types of dysrhythmias are sinus node dysfunction (atrial fibrillation, atrial flutter, or paroxysmal supraventricular tachycardia) and atrioventricular conduction disturbances.^15,19,20 Because the majority of patients are asymptomatic, the use of antidysrhythmics is generally not recommended. The side effects and toxic effects of antidysrhythmics impose more of a risk, as compared with the risk of mortality or morbidity related to the dysrhythmia.^20,23 In contrast, for patients who are symptomatic and have malignant ventricular dysrhythmias (sustained ventricular tachycardia and/or fibrillation), pharmacological therapy is warranted.^20,23

Baroreceptor reflex function is altered with aging.24 Baroreceptors, located at the bifurcation of the common carotid artery and aortic arch, are mechanoreceptors that respond to stretch and other changes in the blood vessel wall.²⁵ Impulses arising in the baroreceptor region project to the vasomotor center (nucleus of tractus solitarius) in the medulla. Abrupt changes in blood pressure caused by increases in peripheral resistance, CO, or blood volume are sensed by the baroreceptors, resulting in an increase in the impulse frequency to the vasomotor center within the medulla. This increase inhibits vasoconstrictor impulses arising from the vasoconstrictor region within the medulla.²⁵ The result is a decrease in heart rate (HR) and peripheral vasodilation; both these effects return the blood pressure to within normal limits.

Postural hypotension was once thought to occur more frequently in older persons and to be related to age. However, recent studies have shown that the prevalence of postural hypotension is quite low in older persons.^26,27 The prevalence of orthostatic hypotension is greater in institutionalized older patients who are receiving antihypertensive medications.²⁸

In most individuals, aging is associated with a decline in exercise performance. The thickening of the left ventricular wall along with stiffening of the aortic and mitral valves makes the aging heart less able to provide adequate contractile strength.29 With advancing age the maximal HR achieved during exercise is attenuated; however, the decreased HR response is accompanied by an increase in LVEDV and SV. This augmentation in LVEDV and SV offsets the attenuated HR response and maintains CO in exercise.

Healthy older persons have no age-associated decline in CO during exercise, but other factors (e.g., neural functioning, skeletal/joint functioning, pulmonary function) may limit an older individual’s ability to exercise.

The effects of aging on the peripheral vascular system are reflected in the gradual but linear rise in systolic blood pressure.30,31 Diastolic blood pressure is less affected by age and generally remains the same or decreases.³¹

Important determinants of systolic blood pressure include the compliance of the vasculature and the blood volume within the vascular system. Similar to the heart, the compliance of the vasculature is determined by its cell type and tissue composition. With advancing age the intimal layer thickens, principally because of an increase in smooth muscle cells that have migrated from the medial layer, and the amount of connective tissue (collagen, elastic tissue) increases.³⁰ These changes occur in the intima of the large and distal arteries. This gradual decrease in arterial compliance, or “stiffening of the arteries,” is known as arteriosclerosis. Arteriosclerotic and atherosclerotic processes cause the arteries to become progressively less distensible, altering the vascular pressure-volume relationship. These changes are clinically significant because small changes in intravascular volume are accompanied by disproportionate increases in systolic blood pressure. The decrease in arterial compliance and disproportionate increase in systolic blood pressure may lead to an increase in afterload and the development of concentric (pressure-induced) ventricular hypertrophy in the elderly patient.³²

Arterial pressure is also governed by the amount of blood volume, which in turn is regulated by plasma levels of sodium and water and the activity of the renin-angiotensin system.³³ Plasma renin activity declines with age, and aging per se has no appreciable effect on sodium and water homeostasis.^34,35 As noted later, however, age-related changes occur in renal tubular function, and the glomerular filtration rate (GFR) decreases, both of which can affect overall sodium and water homeostasis. Circulating levels of sodium-regulating hormones, such as natriuretic hormone, aldosterone, and antidiuretic hormone (ADH), are not appreciably altered by advancing age.^35,36 However, a delayed natriuretic response after sodium loading and plasma volume expansion and a diminished renal response to ADH secretion have been reported in older persons.³⁶