This term, derived from Greek, meaning porridge and hardening, means that the flow of blood through the nary arteries that supply oxygen and nutrients to heart muscles get blocked resulting in damage to them or even death.
With the modern life style in vogue more and more men and women are falling prey to this.
This process is said to start at any stage in one’s life; it goes on year after year without the patient being unaware of it and ultimately, when it is detected, it is tcn late.
Medical experts differ on the theory of its development. One of the opinions is that it began as a result of injury to the cells covering the inner wall of artery—the arterial endothelium.
In order to get an answer to this question we have to take into consideration the growing age, the sex difference, the striking geographic and national differences, variation in severity among individuals of comparable age and the role of the major risk factors. Also, we must account for the presence of cholesterol within the atheromatous lesions and the manner by which hyperlipidemia predisposes to atherosclerosis.
There have been many theories put forth by medical men. But not all fully answer the question.
One theory called the ‘imbibation hypothesis’ holds that a principal factor in progression of a patch or eruption of skin due to damage is increased passage from the arterial cavity and accumulation in the arterial intima of
What is atherosclerosis? 13
plasma constituents (mainly fat). The second (encrustation theory) tells that small thrombi composed of a disk of protoplasm in blood and involved in clotting, fibrin and white blood cells—all constituents of the blood collected over the areas of injury of the blood vessel lining, and the organization of such thrombi and their gradual growth—resulted in plaque formation.
The modern theory is that the morbid change in the texture are initiated as a response to some form of injury to arterial lining (endothelium). Sites of injury lead to increased permeability to plasma constituents such as fatcarrying proteins and permit platelets to adhere to the subendothelial tissue, aggregate and release the contents of their granules.
The process starts with the weakening of the GAG layer, the protecting arm of endothelial cells. The weakening damages the cells. The cells get damaged by various factors such as virus, immunisation, chemicals or drugs, and once this happens, it is easier for lipoproteins to enter. The inner lining of arteries becomes raised, yellow or pearly white due to deposition of soft fatty material, largely cholesterol. When enough damage has been done, large white blood cells and patches stick to the spot. Lipoproteins, monocytes and platelets drive away smooth muscle cells from the media into the intima where they increase rapidly. The cells dump debris into the intima which results in more deposits of patches.
The plaque or deposits lead to further worsening of the functioning of the arteries. The plaque continues to grow until at last it completely blocks the artery. When symptoms of atherosclerosis come up, the blockage reaches generally more than 85 per cent level. The symptoms come to the surface only after cholesterol level exceeds 160 mg/ 100 ml.
The plaques, which stick to the surface of artery, are normally small in size—O.3 to cm in diameter. It is only occasionally that they are in the form of large deposits.
Blood pressure & heart attack
In the whole process the damages in the abdomjnal aorta are more prominent near the opening of major
branches. The most heavily pressed vessels are the coronary arteries, the lower thoracic aorta and the vessels of the circle of willis in the brain.
Atheromatous plaques may undergo changes constantly alid create further complications in the following ways:
Atheromas may undergo calcification. In severe atherosclerotic disease, arteries may be converted into virtual pipe stems, and the aorta may assume an eggshell brittleness.
Ulceration of the luminal surface and rupture of the atheromatous plaques may result in discharge of the debris into the bloodstream, producing microemboli.
What is atherosclerosis ?
Superimpoge€l thrombosis may occur on ulcerated lesions. Thrombi may either occlude the lumen or become incorporated within the plaque.
Haemorrhage into the plaque may occur, especially into the coronary arteries, from rupture of either the linIng membrance or the thin-walled capillaries. The collection of blood may remain localized or rupture into the lumen.
Although atherosclerosis is basically a disease of the lining membrane of the blood vessels, in severe cases the underlying vessel wall undergoes considerable pressure, atrophy and loss of elastic tissue, causing sufficient weakness to permit ancurysmal dilatation.
In case of coronary arteries, atherosclerotic patches are most prominent in the main stems, the highest incidence being a short distance beyond the aortic opening. Atherosolcrosis is nearly always found in the portions of the vessels which are not embedded inside the heart musCle. And once the process develops, the whole lining of the vessel is usually involved.