Age-related Changes in the Cardiovascular System

Original Editor ­ Andeela Hafeez Top Contributors - Andeela Hafeez, Kim Jackson, Adam Vallely Farrell, Tony Lowe and Lauren Lopez


Even without the presence of disease, a person's body will undergo changes in it's structure and function[1]. Aging is an independent risk factor for cardiovascular disease. The effects of aging are widely diverse and can be identified at the molecular, cellular, tissue, organ, and system levels as contributing to the altered function of the cardiovascular system.

Age Related Structural changes:

Structural changes with aging involve the myocardium, the cardiac conduction system, and the endocardium. There is a progressive degeneration of the cardiac structures with aging, including a loss of elasticity, fibrotic changes in the valves of the heart, and infiltration with amyloid.The age-associated structural characteristics that have the greatest impact involve the contractility of the heart's left ventricular wall. The pumping capacity of the heart is reduced with age due to a variety of changes affecting the structure and function of the heart muscle.[2]
For decades, it was thought that the heart undergoes atrophy with advancing age, but evidence suggests that,An age-related increase in the left ventricular posterior wall thickness of approximately 25% has been found between the second and the seventh decade. 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.


An age-related increase in valvular circumference has been reported in all four cardiac valves (aortic semilunar valve, semilunar valve, bicuspid valve, tricuspid valve),with the greatest changes occurring in the aortic valve (the valve between the left ventricle and the aorta) Calcific deposits frequently are present .[3]
one or more aortic valve cusp.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.

Myocardial Sub-cellular Changes

The nucleus, containing DNA, becomes larger and may show invagination of its membrane.The mitochondria show alterations in size, shape, cristal pattern, and matrix density, which reduce their functional surface.The cytoplasm is marked by fatty infiltration or degeneration, vacuole formation, and a progressive accumulation of pigments such as lipofuscin. The combined age related changes in the sub-cellular compartments of the cells result in decreased cellular activities such as altered homeostasis, protein synthesis, and degradation rates.

Cardiac Muscle Compliance

Again, the decline in left ventricular compliance provides an increase work load on the atria, resulting in hypertrophy of the atria.

Age-Related Changes in the Blood Vessels

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. Factors that contribute to the increased wall thickening and stiffening in aging include increased collagen, reduced elastin, and calcification.[4]
One important set of changes involves the aorta, the wall of the aorta becomes less flexible, or shows an increase in wall stiffness, so that the blood leaving the left ventricle of the heart is faced by more resistance and cannot travel as far into the arteries.Age-associated changes also occur in the more peripheral vessels the walls of the arteries throughout the body become thicker so that they, too, are less flexible and stiffer.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.

Age-Related Changes in the Electrical Conduction System of the Heart

First, cardiac conduction is affected by the decrease in the number of pacemaker cells in the sinoatrial node with age.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.With advancing age, there is an increase in elastic and collagenous tissue in all parts of the conduction system. Fat accumulates around the sinoatrial node, sometimes producing a partial or complete separation of the node from the atrial musculature.The conduction time from the bundle of His to the ventricle is not altered. There is a leftward shift of the QRS axis with advancing age, perhaps reflecting a variable degree of fibrosis in the anterior fascicle of the left bundle branch as well as mild left ventricular hypertrophy. The S-T segment becomes flattened, and the amplitude of the T wave diminishes.

Change in Cardiac Output,Stroke Volume,Blood Pressure

Cardiac output

Cardiac output at rest is unaffected by age. Maximum cardiac output and aerobic capacity are reduced with age.

Stroke volume

Stroke volume is changed little by aging; at rest in healthy individuals, there may even be a slight increase.

Blood pressure

Blood pressure is a measure of cardiovascular efficiency. Although blood pressure is characteristically heightened among older adults, there is evidence suggesting that there are no effects of aging on this index of cardiovascular.[2] Receptors called baroreceptors, monitor the blood pressure and make adjustments to help maintain a fairly constant blood pressure when a person changes their position or is doing more strenuous activities. The baroreceptors are believed to become less sensitive with aging. This may explain why older people have orthostatic hypotension, in which the blood pressure falls when a person goes from lying or sitting to standing. This causes dizziness because there is less blood flow to the brain.

Age-Related Cardiovascular Response During Exercise

The maximum achievable heart rate with exercise decreases linearly with age and may be calculated empirically, using 220 beats per minute as the maximum in the adult. The age changes can be calculated by subtracting the age of the individual from the 220 values.In older adults, there is a consistent smaller tachycardia (increase in heart rate) during both isometric and dynamic exercise compared with younger adults.[2]
One possibility for the lower response in heart rate in the older adult is that there is a reduction in cardiac vagal influence on heart rate under resting conditions and that this limits the degree of reduction in vagal tone possible in response to exercise. Cardiac output increases similarly with increasing work loads in various age groups; however, the mechanism of augmentation of cardiac output is different between the age groups. The young adults demonstrate a large increase in heart rate from rest to exercise. In young adults, stroke volume increases with exercise because of a large decrease in end-systolic volume compared to rest.with aging under resting conditions but is reduced even in healthy older subjects during strenuous exercise. Thus the impaired "pump" performance during exercise appears to be mediated, at least in part, by age-associated reductions in f3adrenergic function or responsiveness on the heart.

Cardiovascular Exercises For elderly


  1. Chodzko-Zajko WJ, Proctor DN, Fiatarone Singh MA, Minson CT, Nigg CR, Salem GJ, Skinner JS. Exercise and Physical Activity for Older Adults.  Medicine & Science in Sports & exercise: Official Journal of the American College of Sports Medicine. Med Sci Sports Exerc. 2009. 41 (7): 1510-1530. Available from
  2. 2.0 2.1 2.2 geriatric physical therapy Dale L. Avers, PT, MSEd Vice President of Academic Affairs Rocky Mountain University of Health Professions Los Angeles, California
  3. Section of Cardiovascular Pathology, Department of Pathology, Indiana University School of Medicine, Indianapolis,fckLRIndiana, USA
  4. Clinical Hypertension and Vascular Diseases: Hypertension in the ElderlyfckLREdited by: L. M. Prisant © Humana Press Inc., Totowa, NJ