Table 2.
Aging and the cardiovascular system.
| Cardiovascular abnormalities | |
|---|---|
| Site | Main findings |
| Heart: structural changes | (i) Mild increase in heart weight (ii) Age-dependent change in cardiac shape (iii) Rightward shift in the ascending aorta (iv) Proximal bulge in the interventricular septum (v) Increased cardiomyocyte dimensions (vi) Decreased number of cardiomyocytes (vii) Quantitative and qualitative changes in collagen (viii) No increase in the collagen-to-myocyte ratio (ix) Partial degeneration of cardiac sympathetic nerve supply |
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| Heart: functional changes | (i) In the resting aging heart, no alterations on LV systolic function as resting heart rate if anything minimally reduced with aging and cardiac output is preserved (ii) LV diastolic function undergoes significant age-related changes, with a reduction in early diastolic filling compensated for by increased end-diastolic filling and a consequent progressive reduction of the echocardiographic early wave/atrial wave (E/A) velocity ratio (iii) Both the catecholamine- or exercise-induced increases in heart rate and myocardial contractility are definitely blunted in elderly subjects (iv) Peak cardiac output attained in response to maximal effort is blunted by some 20–30% in elderly compared with young healthy subjects (v) Aging is accompanied by a blunted inotropic but preserved chronotropic response, and although LV filling reserve declines with age, relaxation reserve does not. |
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| Vasculature: structural changes | (i) Large arteries are elongated and tortuous (ii) Enlarged lumen and a thickened walls (iii) Thickening mainly affecting the intima and the media (iv) Endothelial cells might become irregular in shape and have increased height (v) Migration and/or proliferation of vascular smooth muscle cells (vi) Exaggerated deposition of collagen, elastin, and proteoglycans, along with abnormal abundance of leukocytes and macrophages (vii) More abundant number of adhesion molecules, matrix metalloproteinases, transforming growth factor-β, and proinflammatory cytokines |
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| Vasculature: functional changes | (i) Impaired distensibility (ii) Enhanced pulse wave velocity (iii) Increased stiffness (iv) Abnormal humoral and endothelial regulation of vascular smooth muscle tone (v) Increased endothelial permeability and a reduced nitric oxide-dependent vasodilator response to acetylcholine (vi) Moderate increase in total peripheral resistance (vii) Vessel wall hypertrophy |
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| Arterial baroreflexes | (i) Age-related decline in the ability to modulate cardiac chronotropic activity (ii) Age-related depression of the baroreceptor-heart rate reflex (iii) Aging is associated with a blunted reflex changes in R-R interval in response to a change in BP (iv) Increased levels of oxidative stress and decreased cardiac cholinergic responsiveness with age (v) Increased levels of BP variability (vi) Impaired ability to respond to acute challenges to the maintenance of BP (vii) Increased risk of sudden cardiac death (viii) In contrast, baroreflex control of sympathetic outflow is not impaired with age |
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| Cardiopulmonary reflexes | (i) Less attention given to these reflexes (ii) They control plasma renin activity and renal function (iii) Blunt hemodynamic and humoral component of the cardiopulmonary reflex with aging (iv) Preserved rather than attenuated cardiopulmonary reflex control of forearm vascular resistance |