International Elderly Day :"The Journey to Age Equality"
October 1st- International Elderly Day
Happy International Elderly Day. Let us review some cardiovascular related complications that elderly face.
Age related cardiac structural changes
• Increased left ventricular wall thickness, independent of any increase in blood pressure. This is attributed to hypertrophy of individual myocytes with a progressive loss of myocyte numbers. There is also an accumulation of interstitial connective tissue and, in the “old old”, accumulation of amyloid deposits.
• Increased fibrosis and calcification of the valves, particularly the mitral annulus and the aortic valve.Recently it has been shown that aortic sclerosis without outflow obstruction is not the benign condition once thought and is associated with significantly increased cardiovascular and total mortality.
• Loss of cells in the sinoatrial node. By 75 years of age, only 10% of the cells that were present at 20 years remain. There is loss of muscle cells and mild increases in fibrous tissue in the internodal tracts. The remainder of the conducting system is also affected but to a lesser extent. These changes occur in the absence of coronary artery disease.
Features of a normal aging process
• Universal within the species
• Intrinsic to the individual
• Deleterious to survival
• Progressive and irreversible
• Increased stiffness of peripheral and central arteries, caused by proliferation of collagen cross links, smooth muscle hypertrophy, calcification, and loss of elastic fibres.
• Increase in number of sites for lipid deposition cause endothelial changes that reduce laminar blood flow. These changes are independent of atherosclerosis.
• More diffuse coronary artery changes. The earliest changes usually appear in the left coronary artery during youth or adulthood, whereas the right and posterior coronary arteries do not usually become involved until after the age of 60 years.
Age related functional changes
Left ventricular systolic function
• In patients carefully screened to exclude coronary artery disease and hypertension, there is little change in left ventricular systolic function with increasing age, although cardiac output may decrease in parallel with a reduction in lean body mass. The determinants of cardiac output which may be influenced by age include heart rate, preload and afterload, muscle performance, and neurohormonal regulation.
• Increases in heart rate in response to exercise or stress caused by non-cardiovascular illnesses, particularly infections, are attenuated with increasing age. Stroke volume increases only by “moving up” the Frank Starling curve.Thus end diastolic volume increases. These age related changes in cardiac response to exercise are mimicked by β adrenergic blockade,but β adrenergic agonists do not reverse this aging process.The decline in exercise performance with age may additionally relate to peripheral factors, blood flow, and muscle mass rather than being solely the consequence of cardiac performance changes.
• The rate and volume of early diastolic filling decrease with age. The structural changes described above account for some of this decline, but recent findings of partial reversibility with calcium channel blockers or exogenous angiotensin II receptor antagonists illustrate the dynamic and therefore potentially reversible nature of the process.
• The aged heart requires atrial contraction to maintain adequate diastolic filling, so atrial fibrillation, so common in older people, has a disproportionate effect on cardiac function.
• Reduced ventricular compliance results in higher left ventricular diastolic pressures at rest and during exercise. As a result, pulmonary and systemic venous congestion may occur in the presence of normal systolic function.With increased afterload on the left ventricle, left ventricular hypertrophy occurs, even in the absence of hypertension or aortic stenosis.Diastolic dysfunction, at least in the early stages, may be a feature of normal aging. Later, however, it is a pathological process leading to significant left ventricular hypertrophy. At this stage coronary heart disease, hypertension or other pathology is probably involved.
• Age related decreases in capillary density and coronary reserve may cause myocardial ischaemia and thus further diastolic abnormalities in the absence of coronary atherosclerotic disease. Age associated decreases in the rate of maximal capacity of calcium sequestration by the sarcoplasmic reticulum and/or an age associated increase in net trans-sarcolemmal calcium influx may also contribute to diastolic ventricular abnormalities.
Chronic heart failure is a disease of “old old” people, and unlike coronary artery disease, the incidence continues to rise with increasing age. Only 17% of people with heart failure are less than 65 years of age, yet most of the interventional studies of the treatment of chronic heart failure have focused on this minority group and extrapolated the results to the older majority. “Diastolic” heart failure is probably the primary haemodynamic dysfunction in the elderly. Among patients over 80 years of age with clinically defined heart failure, up to 70% have preserved systolic function, whereas probably less than 10% of patients below 60 years of age have preserved systolic function. It is important to be aware of this high prevalence of diastolic dysfunction as it has implications for treatment. Over 75% of elderly patients with heart failure have hypertension and/or coronary artery disease, and patients with diastolic dysfunction may present with decompensated heart failure caused by uncontrolled blood pressure or progression of ischaemic heart disease