Cardiovascular System

The aging process is associated with primary and secondary changes in the heart, as well as primary changes in the blood vessels and alterations in autonomic control (see Chapter 18 ). As the heart ages, changes in morphology occur. For instance, myocyte number decreases, left ventricular wall thickening occurs, and both conduction fiber density and sinus node cell number decrease.^[7] Functionally, these changes translate to decreased contractility, increased myocardial stiffness and ventricular filling pressure, and decreased β-adrenergic sensitivity.^[7] Vascular stiffness increases with advancing age. Specifically, breakdown of elastin and collagen leads to changes in the vascular wall matrix that result in increased medial and intimal thickness. Morphologically, one sees an increase in the diameter and stiffness of large elastic arteries. Functionally, these changes are readily observed in terms of an elevated mean arterial pressure and increased pulse pressure. ^[8] Increased vascular stiffness leads to important secondary responses in the heart.

The vascular system functions as both a cushion and a conduit to ensure mechanically efficient and smooth delivery of blood to the periphery. In youth, the cardiac pump and the blood vessels are optimally coupled to maximize efficiency.^[9] With increased resistance in blood vessels, the velocity of conduction of pulse waves down the vascular tree increases. Increased pulse wave velocity results in earlier reflection of pulse waves from the periphery. In younger humans, wave reflection occurs later because of slower propagation such that reflected waves reach the heart after aortic valve closure. In the setting of increased pulse wave velocity and early wave reflection, reflected pulse waves reach the heart during the latter phases of ejection, thereby imposing an

Figure 62-1 Pressure wave pattern as seen in young human adults and in experimental animals (left) contrasted to pressure wave pattern as seen in mature human adults (right). (Reprinted with permission from O'Rourke MF, Kelly RP, Avolio AP [eds]: The Arterial Pulse. Philadelphia, Lea & Febiger, 1992.)

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The two most important changes in the autonomic system with aging are a decrease in response to β-receptor stimulation and an increase in sympathetic nervous system activity. Decreased β-receptor responsiveness is secondary to both decreased receptor affinity and alterations in signal transduction.^[11] Decreased β-receptor responsiveness assumes functional importance when increased flow demands are placed on the heart. Normally, β-receptor-mediated mechanisms act to increase the heart rate, venous return, and systolic arterial pressure while preserving preload reserve. In contrast, the attenuated β-receptor response in the elderly during exercise/stress is associated with a decreased maximal heart rate and decreased peak ejection fraction. Such decreases cause the increased peripheral flow demand to be met primarily by preload reserve, thereby making the heart more susceptible to cardiac failure.^[7] It is well known that sympathetic nervous system activity increases with aging. Although changes in β-receptor responsiveness are well defined, it is controversial whether the aging process alters the α-receptor response. Increased resting sympathetic nervous system activity may contribute to increases in systemic vascular resistance along with mechanical stiffening of the peripheral vasculature.^[7] Clinically, these autonomic changes lead to a greater likelihood of intraoperative hemodynamic lability and a decreased ability to meet the metabolic demands of surgery.

Although the age-related changes in cardiovascular physiology are generally well tolerated, several pathophysiologic states deserve mention. For one, impairment of diastolic relaxation leads to diastolic dysfunction in the aging heart. In its severest form, diastolic dysfunction may be manifested as diastolic heart failure. Predisposing disease states for this condition include hypertension with left ventricular hypertrophy, ischemic heart disease, hypertrophic cardiomyopathy, and valvular heart disease. The problem occurs when decreased left ventricular compliance during diastole results in greatly increased left ventricular diastolic pressure. If this pressure is conducted retrogradely to the pulmonary circulation, pulmonary venous congestion and pulmonary edema result. Diastolic dysfunction/failure is often related to systemic blood pressure and does not necessarily imply volume overload. The diagnosis can be difficult to make because the clinical picture appears identical to left ventricular systolic failure. Making the correct diagnosis is important in that interventions commonly used in systolic failure such as diuretics and inotropes may exacerbate diastolic dysfunction. Echocardiography is the diagnostic modality of choice.^[12] Classically, echocardiography will demonstrate preserved or hyperdynamic left ventricular systolic function and characteristic changes in flow velocity at the mitral valve.

Aortic valve sclerosis and mitral annular calcification are common echocardiographic findings in the elderly. They represent non-flow-limiting calcifications around the aortic and mitral valves, respectively. Otto and coworkers demonstrated that aortic valve sclerosis is common in the elderly and is associated with a 50% increase in the risk of cardiovascular death.^[13] Hence, it has been suggested that aortic valve sclerosis may represent a marker for coronary artery disease. A similar association has been postulated for mitral annular calcification.^[14]