Читать книгу Pathy's Principles and Practice of Geriatric Medicine - Группа авторов - Страница 56

In contrast to the general opinion that an enlarging heart is normal with age, there is no evidence supporting this opinion in the absence of a pathological condition. However, the fat composition in the pericardium, and thickness of the left ventricular wall, and collagen tissues in the endocardium and the walls of arteries all increase.^20‐21 Lipofuscin pigment accumulates in the myocardium with age. Cardiac valves, especially the mitral and tricuspid valves, become sclerotic and lose elasticity because of collagen production and oxidative damage. Thus, the prevalence of stenotic heart valves increases with age. Pacemaker cells in the sinoatrial node (SA) begin to decrease after the age of 60, as do cardiomyocytes in the atrioventricular (AV) node and the His bundle.^20‐22 All of these changes in the conduction system of the heart cause susceptibility to arrhythmia.

Another prominent feature of the ageing heart is decreased maximum heart rate. Reduced response to sympathetic stimuli may be one of the causes. Thus, it is best to choose endurance exercise rather than aerobic exercise in the elderly population. In a healthy elder, myocardial contractility is assumed to be normal. However, ventricular filling in diastole is mildly compromised in the elderly heart. Typically, ventricles are filled passively with blood flow from the atria in the early diastole, and the atrial contraction contributes little in young adults. But with age, ventricular compliance decreases, which increases the need for atrial contraction for ventricular blood flow. Preload of the atrium increases, and intra‐atrial pressure rises.²⁵ This is the primary mechanism responsible for atrial dilation in the elderly heart. Diastolic refilling into the ventricles takes longer in the elderly compared to younger adults, and thus the ejection fraction decreases. When the heart rate increases during exercise or stress, diastole time shortens. Thus, the cardiac output volume is reduced in the elderly population. In addition, with advanced age, exercise exacerbates slight arrhythmias such as premature or skipped beats. If an individual has atrial fibrillation, ventricular filling will be even more impaired. These situations may limit physical performance in elderly people.^23‐24

Endothelial function plays an important role in the health of vasculature. Beyond its structural role as a barrier between blood and the vascular muscle layer, the endothelium acts as a paracrine tissue by synthesizing nitric oxide (NO) in response to mechanical stimuli. When blood flow increases in the artery, shear stress on the endothelium causes NO production. As a result, NO acts on the vascular muscle layer, causing relaxation and thus arterial dilation via the intracellular cyclic guanosine monophosphate (cGMP) pathway.²⁶ The enzyme responsible for NO production is endothelial NO synthase, which loses its activity with age. The integrity of the endothelium is also essential to avoid endothelial damage. Smoking, obesity, and hypertension lead to endothelial damage, and a high LDL concentration in the blood accumulates in damaged areas, resulting in atheromatous plaque. When this happens in coronary arteries, the atheromatous plaque may lose its integrity and eventually rupture. A thrombotic cascade is triggered, causing a clot in the coronary artery, which results in a myocardial infarction.

Along with the decrease in NO concentration, atheromatous plaque contributes to arterial stiffness, leading to signs of elevated blood pressure and isolated systolic hypertension clinically.^28‐28 In the end, the compliance ability of the affected vascular segment is compromised, and the artery begins to stiffen. The carotid intima and media thickness increases threefold by age 90.^29‐30 Increases in collagen production, endothelial permeability, and smooth muscle cell infiltration to intima are major mechanisms responsible for increased arterial wall thickness. Regular exercise is a key factor in slowing the stiffening of arteries. Thickening is not specific to arteries but also happens to veins and capillaries. The thickening of veins and valves contributes to reduced venous return to the heart. Slow blood flow in veins facilitates disorders such as deep vein thrombosis, varicose veins, and thrombophlebitis.^31‐32