Structural changes with aging involve the myocardium, the endocardium and the cardiac conduction system,.

There is a progressive degeneration of the cardiac structures with aging, including: a) A loss of elasticity.

b) Fibrotic changes in the valves of the heart. c) And infiltration with amyloid.

The age-associated structural characteristics that have the greatest impact involve :

1- The contractility of the heart's left ventricular wall . 2- The ability of the arteries to distend in response to the heart's pumping action (aorta).

with resultant reduction in pumping capacity of the heart. The heart's left ventricular wall affects the heart's pumping capacity because of:

- Its ability to contract quickly. - It fully determines the force and rate at which blood is pumped into the arteries.

For decades, it was thought that the heart undergoes atrophy with advancing age. The use of echocardiography has made it possible to measure accurately left ventricular wall thickness and chamber size. An age-related increase in the left ventricular posterior wall thickness ,of approximately 25%, has been found between the second and the seventh decades. An increase in heart mass with aging, for the most part, is due to an increase in the average myocyte size, whereas the number of myocardial cells declines. A. Increases in myocardial collagen, fibrosis, and lipofuscin take place with aging. 1- Collagen content within the myocardium increases, and there is a change in physical properties of collagen (due to altered cross-linking); The pericardium, composed of bundles of collagen, becomes stiffer, which contributes to the decrease in compliance of the left ventricular wall. 2- Lipofuscin, a brownish lipid-containing substance, accumulates at the poles of the nuclei of myocardial cells.

Lipofuscin is thought to arise by the peroxidation of lipid/protein mixtures

(Lipid peroxidation refers to the oxidative degradation of lipids producing free

radicals resulting in cell damage), and its size in the myocardium increases.

B. The progressive deposition of amyloid (amyloidosis) in the

myocardium, usually in the atria, occurs in up to one third of elderly people.

This histologic feature of aging is observed in the vasculature and many

organs, This protein infiltrates tissue, rending it dysfunctional.

C. Adipose deposition between muscle cells is also common, resulting

in fattier heart tissue in the ventricles and the interatrial septum. Fat deposits in

the interatrial septum may displace conduction tissue in the sino-atrial node and

lead to conduction disturbances .

Stimulus for Ventricular Hypertrophy (Increased Mass) In younger adults, ventricular hypertrophy occurs in response to an increased

cardiac volume or pressure work load, e.g., during high-resistant weight training. However, the stimulus for the increase in left ventricular wall thickness in the

older adult is unclear. Age-associated ventricular hypertrophy may result from altered systolic blood

pressure and aortic compliance that occur with aging. For example, with age the volume of blood in the ascending aorta increases due to

age-related aortic dilatation. This increase in volume of blood must be advanced by the heart for ejection to occur; thus there is an increase in work load (afterload) that has to be performed by the heart. The increase in work load acts as the stimulus for muscle hypertrophy.

An age-related increase in valvular circumference has been reported in

all four cardiac valves, with the greatest changes occurring in the aortic valve .

The age-associated increase in valvular circumference does not appear to

be associated with valvular incompetence.

Other valvular changes with aging include thickening and calcification of

the cusps and leaflets. These changes do not usually cause significant

dysfunction, although in some older adults, severe aortic valvular stenosis and

mitral valvular insufficiency are related to degenerative changes with age.

Clinical heart murmurs are detected more frequently.

Subcellular changes take place within the myocardial cells. 1-The nucleus, containing DNA, becomes larger and may show invagination of its membrane.

2-Nucleoli (the dense body within the nucleus that contains a high concentration of RNA) increase in size and number.

3-The mitochondria show alterations in size, shape, cristal pattern, and matrix density, which reduce their functional surface.

4-The cytoplasm is marked by fatty infiltration or degeneration, and a progressive accumulation of pigments such as lipofuscin.

The combined age related changes in the subcellular compartments of the cells result in decreased cellular activities such as altered homeostasis, protein synthesis, and degradation rates.

In general, the walls of the heart become less compliant with age.

a) The decreased capacity of the left ventricular wall to expand during diastole

results in a reduced and delayed filling of the left ventricle. Subsequently, during

the systolic (emptying) phase of the cardiac cycle, the left ventricle contracts less

and ejects less blood (Frank-Starling relationship).

b) Increased left atrial size is another age-related change that is thought to be

related to an age-related decrease in left ventricular compliance, resulting in a

decreased rate of left ventricular filling.

c) The decline in left ventricular compliance provides an increase work load on

the atria, resulting in hypertrophy of the atria.

1-Heart Rate :Resting heart rate: - Heart rate is determined by the influence of the autonomic nervous system on the intrinsic pacemaker activity of the sinoatrial node. - The parasympathetic and sympathetic nervous systems interact in controlling heart rate, the parasympathetic system acting through the vagus to slow the heart and the sympathetic system acting to increase heart rate. - A shift in the balance of autonomic control of the heart from vagal to sympathetic occurs with age. - The number of pacemaker cells in the sinoatrial node declines with age, so that by the age of 70 years only about 10% of the number found in young adults are present. This decline in pacemaker cell number may, in part, explain the decreased heart rate. - Supine resting heart rate is widely reported to be unchanged by aging. In contrast, sitting-position heart rate decreases with age.

2-Stroke Volume Stroke volume is changed little by aging. Earlier studies note a decrease in left ventricular end-diastolic volume, in contrast, left ventricular end-diastolic volume may increase slightly with age when no cardiovascular disease is present. With increasing age, there is a reduction in the rate of left ventricular filling during early diastole as reflected by the rate of closure of the mitral valve. This impairment of left ventricular filling may derive at least in part from age-related increases in left ventricular wall thickness, which diminish ventricular diastolic compliance. Because of these changes a greater proportion of blood must enter in late diastole. These changes do not have an impact at rest, whereas they have a significant impact during exercise, limiting maximum cardiac output in exercise when diastole will be shortened and limiting coronary blood flow.

3-Cardiac Output: Cardiac output at rest is unaffected by age. Maximum cardiac output and aerobic capacity are reduced with age. There is a linear decline through the adult years, so the average 65-year-old has 30% to 40% the aerobic capacity of a young adult.

4-Resting Blood Pressure: Blood pressure is determined by cardiac output and by total peripheral resistance. Since cardiac output is little altered by age in the healthy older adults, blood pressure increases with age are likely to reflect mainly alterations in total peripheral resistance and diminished aortic compliance. Remember the equation: Blood Pressure = Cardiac Output X Total Peripheral Resistance.

5-Systolic Blood Pressure vs. Diastolic Blood Pressure: Both systolic and mean blood pressures significantly increase from 20 to 80 years. Specifically, systolic blood pressure tends to increase with age throughout life, whereas diastolic pressure increases until the age of about 60 years and then stabilizes or even falls. The main cause of isolated systolic hypertension in the elderly is a decreased arterial compliance . The compliance of the aorta falls by a factor of three to four over the age range of 20 to 80. In summary, increased left ventricular stiffness, diminished compliance with resulting prolongation of relaxation, and a reduced rate of early diastolic rapid filling occur with age. Ventricular diastolic function, therefore, is compromised by aging changes, and diastolic filling becomes more dependent on atrial contraction in older persons.

Schematic representation of the effects of age on the heart.

With aging, the heart's conduction system (such that the frequency and regularity of cardiac impulses) may become abnormal (dysrhythmia).

Cardiac conduction is affected by :

1-The decrease in the number of pacemaker cells in the sinoatrial node with age:

a) Beginning by age 60 there is a pronounced "falling out:' or decrease, in the number of pacemaker cells in the sinoatrial node, and by age 75 less than 10%

of the cell number found in the young adult remains. b) A less dramatic cellular decrease is noted in the atrioventricular node and

the intraventricular bundle.

2-Fibrotic changes in the specialized nerve conduction system.

3-Increase in elastic and collagenous tissue in all parts of the conduction system.

4- Fat accumulates around the sinoatrial node, sometimes producing a partial or complete separation of the node from the atrial musculature.

5- A variable degree of calcification of the left side of the cardiac skeleton, which includes the aortic and mitral anuli. Because of their proximity to these

structures, the atrioventricular node, A-V bundle may be damaged or destroyed by this process, resulting in so-called primary or idiopathic block.

Several features of the electrocardiogram are altered by normal aging based on the structural changes with age .

a- The P-R and Q-T intervals show small increases with age. b- There is a leftward shift of the QRS axis with advancing age.

c- The S-T segment becomes flattened, and the amplitude of the T wave diminishes.

The electrocardiogram age-related changes.

The forward motion of blood on the arterial side of the circulation is a function of the elastic recoil of the vessel walls and the progressive loss of pressure energy down the vascular tree. The peripheral vasculature provides the delivery system by which blood pumped by the heart reaches the various body tissues, therefore age-related changes in the blood vessels may limit the maximal perfusion of these tissues and affect cardiac performance as well. The decrease of elasticity of the arterial vessels with aging may result in chronic or residual increases in vessel diameter and vessel wall rigidity, which impair the function of the vessel

I. One important set of changes involves the aorta, the chamber into which blood is ejected at each contraction of the heart muscle. In general, the wall of the aorta becomes less flexible, or shows an increase in wall stiffness, there is a decrease in the amount of elastic fibers and an increase in collagen fibers. So that the blood leaving the left ventricle of the heart is faced by more resistance and cannot travel as far into the arteries.. The aorta acts as a buffer for the total blood volume in the arterial system because about one half of the stroke volume is stored in the aorta. Up to the age of 60, the aortic buffering capacity is not decreased by the increased aortic wall stiffness. This is possible because the increase in aortic volume accommodates a given volume injected into it (volume elasticity). However, after the age of 60, there is a marked decrease in volume elasticity. As the aorta stiffens with age, less diastolic aortic recoil occurs and the aorta will not be able to propel the blood volume toward the systemic circulation.

II. The walls of the arteries throughout the body become thicker so that they, too, are less flexible and stiffer (altered elasticity). The stiffness of large arteries is associated with a loss in capacity to increase in diameter when needed to accommodate larger blood volumes. Thus, there is a decrease in arterial distensibility and compliance. Impedance of blood flow through the arteries is further influenced by the accumulation of lipids that occurs over the individual's lifetime. III. The walls of veins may become thicker with age because of an increase in connective tissue and calcium deposits. The valves also tend to become stiff and incompetent. Varicose veins develop. Because of low blood pressure in veins, these changes probably are not significant for cardiovascular function. They may be of concern because of the possibility of phlebitis and thrombus formation.