Patients & CaregiversHealthcare Professionals - Opens new windowWorldwide - Opens new window
HomeAbout Merck Products Newsroom Investor Relations CareersResearchLicensingThe Merck Manuals

The Merck Manual of Geriatrics logo
red line
click here to go to the Contents page of The Merck Manual of Geriatrics
click here to go to the title page of The Merck Manual of Geriatrics
click here to search The Merck Manual of Geriatrics
click here to go to the Index of The Merck Manual of Geriatrics
red line
Section 11. Cardiovascular Disorders
Chapter 83. Aging and the Cardiovascular System
Topics:    Introduction | Cardiovascular Structure | Cardiovascular Function | Effects of Lifestyle

red line

Cardiovascular Structure

The Heart

With age, the heart can atrophy, remain unchanged, or develop moderate or marked hypertrophy. Atrophy usually coincides with various wasting diseases and is not observed during aging in healthy persons. A modest increase in left ventricular wall thickness is normal with age; an exaggerated increase occurs in persons with hypertension. Other normal age-associated changes may include enlargement of the left atrium and slight enlargement of the left ventricular cavity and of the cardiac silhouette, seen on chest x-ray.

The amount of fibrous tissue within the myocardium increases with age but does not contribute appreciably to cardiac mass. Rather, myocardial wall thickening occurs largely because cardiac myocytes increase in size. Some myocytes are replaced by fibrous tissue, so that the number of myocytes probably decreases with age. However, cardiac myocytes are probably able to reenter the cell cycle and proliferate, thereby partly offsetting cell loss due to necrosis or apoptosis.

In nearly half of persons > 70 years, amyloid can be detected in the heart, and the incidence increases sharply with age. About half of these persons have only small amounts of amyloid confined to the atria. Whether cardiac amyloidosis is part of normal aging is debatable; it is not present in all elderly persons, not even in centenarians.

The Vasculature

With age, the walls of large distributing arteries (eg, the aorta) thicken, and the arteries become dilated and elongated. The thickening results mainly from an increase in intimal thickness due to cellular accumulation and to matrix deposition; fragmentation of the internal elastic membrane also occurs. These changes may partly explain the elderly's increased likelihood of developing atherosclerosis. With age, increases in collagen and changes in the cross-linking of collagen within the vascular media may make the media less elastic. Glycoprotein eventually disappears from elastin fibrils, and elastin becomes frayed. An age-associated increase in elastase activity and in Ca++ and cholesterol deposition on elastin may contribute to elastin fragmentation or to a reduction in elastin content. The total mucopolysaccharide content (ground substance) of the interstitial matrix is unaltered with age, but the amount of dermatan and heparan sulfate contained in the matrix increases and that of hyaluronate and chondroitin sulfate decreases.

Contact Merck Site MapPrivacy PolicyTerms of UseCopyright 1995-2008 Merck & Co., Inc.