As we grow older, the heart tends to increase in size and becomes less efficient at distributing blood to body tissues. It is forced to work harder.
Artery walls progressively harden with age, and the gap through which blood flows is narrowed. This results in an increase in blood pressure.
The development of heart disease
Heart disease is caused by two processes, atherosclerosis and thrombosis. Atherosclerosis occurs over a period of time and is the underlying cause of angina, whereas coronary thrombosis can occur spontaneously, leading to a heart attack.
Atherosclerosis, not to be confused with arteriosclerosis (gradual loss of elasticity in artery walls), is the condition in which the lining of the arteries is thickened in places by raised plaques. This leads to the narrowing and hardening of arteries, which can ultimately result in a blockage.
This proceeds through the accumulation of material known as atheroma in the inner arterial lining, which is effectively a combination of cholesterol and modified fatty material (lipids) surrounded by fibrous material.
| The process occurs in stages: - Damage to the artery wall is accompanied by the build-up of a plaque of atheroma, most harm occurring where the arteries split or branch to form new ones - for example vessels of the neck, limbs and the heart itself. The damage is principally due to free radical action that occurs over time, causing oxidation of cholesterol and other lipids (veins are not susceptible to this process, as the oxygen has been removed from the blood)
- At the site of damage, lipid material accumulates, especially the oxidised low-density lipoprotein (LDL) cholesterol that develops into fatty streaks
- Our repair system attempts to heal the lesion (the wound), by forming a cap composed of fibrous material, resulting in atherosclerotic plaques
- These plaques grow through the combination of continuing lipid deposition and through the accumulation of fibrin and blood clot (thrombus)
- The result is damage and distortion of the inner arterial wall and greater tendency to form clots.
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Symptoms arise when the coronary arteries are markedly narrowed or when a thrombus forms. A blockage occurs when around 90% of the artery becomes narrowed.
Thrombosis
The development of thrombosis is different in its occurrence to atherosclerosis as it happens more or less spontaneously rather than over a period of time.
The process results in the formation of a thrombus, a stationery blood clot, which forms at the site of damage. In the majority of cases, a thrombus is initiated by a tear or split through the plaque. These plaques can then block the artery completely, preventing blood flow to the heart, depriving the muscle of its oxygen supply. The end result is the death of heart muscle, leading to a heart attack.
The lack of blood flow to a part of the body is known as ischaemia, hence the term ischaemic heart disease, when the supply of blood to the heart is significantly reduced or cut off altogether.
Coronary heart disease
Besides ischaemic heart disease, the other term commonly encountered is coronary heart disease.
This term covers: - stable angina
- unstable angina
- myocardial infarction
- sudden death (with or without the history of previous infarction or pain)
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Angina is the cardiac pain that people experience on exertion due to lack of oxygen from narrowing of coronary arteries. Unstable angina refers to angina that occurs more frequently with decreasing activity and may even occur at rest.
Myocardial infarction, a heart attack, is when part of the heart muscle stops functioning due to lack of oxygen. The blood supply is usually stopped by a thrombus or an embolus. A thrombus develops at the site of injury to the artery. An embolus is a travelling thrombus in a different part of the circulatory system.
Sudden death is usually caused by ventricular fibrillation - abnormal heart rhythms. This happens when the ventricles of the heart twitch rapidly, resulting in circulatory arrest, causing the heart to stop beating. It is fatal unless it can be controlled rapidly.
20/05/2009