What Is Atherosclerosis;Diagnosis,Treatment And Prevention

Atherosclerosis is a condition where plaque builds up of fat, cholesterol and other substances in the walls of the arteries, which restricts blood flow and can lead to serious health complications.

What Is Atherosclerosis;Diagnosis,Treatment And Prevention

HISTORY of Atherosclerosis.

The antiquity’ of atherosclerosis has been established from studies of Egyptian mummies. The term atheroma, derived from the Greek word for porridge, was first used in the context of arterial disease in 1904. when Marchand coined the term atheroselerc*ts. This disease is lipid nch. as contrasted with arteriosclerosis, an older and more general term for thickening and stiffening of the vessel wall. Artenosclcrohc involvement of a blood vessel wall tends to be concentric and diffuse, whereas atherosclerotic lesions are more eccentric and focal. The interrelation among coronary disease, myocardial damage, and clinical syndromes was first appreciated in the latter part of the nineteenth century. Following the proposal by Herrick in 1918, a connection between clinically detected nonlethai heart damage and atherosclerotic coronary disease gained acceptance.

PATHOLOGY of  Atherosclerosis

Atherosclerosis tends to involve large and medium-sized arteries. Most commonly affected are the aorta and the iliac, femoral, coronary, and cerebral arteries. Clinical symptoms occur because the atherosclerotic plaque reduces blood flow through the involved artery and compromises tissue or organ function distal to it. Ischemia or necrosis of the per fused tissue results in characteristic clinical syndromes, and myocardial infarction and sudden death are common fatal outcomes.

By the time it is large enough to cause symptoms, the atherosclerotic plaque is a complicated mixture of three components: (1) cells, mostly smooth muscle in origin, (2) connective tissue (elastin, collagen, glycosaminoglycans), often concentrated as a “cap” on the lesion, and (3) lipid deposits, both intra- and extracellular, representing complex aggregates of cholestervl ester, cholesterol, triglyceride, and phospholipids. Cell necrosis contributes to the gruel-like nature of the lesion. Calcification is often present in advanced lesions, and hemorrhage from small ingrowing vessels frequently occurs. A slowly progressive increase in the plaque mass is usually responsible for its clinical sequelae. Sudden symptoms can be provoked by transient or progressive deposition of platelet clumps or thrombus on the irregular luminal surface, rupture of the plaque and release of its components, hemorrhage into a plaque, dissection of blood into the wall, and perhaps spasm.

Clinical events in middle age that are associated with the advanced plaque represent the culmination of decades of slow growth of the lesion beginning in childhood. In the first decade of life, blood vessels undergo structural remodeling, which mainly involves the intima. This takes the form of concentric fibromuscular intimal thickening and development of intimal cushions at branch sites. In all human populations studied, this thickening develops progressively throughout life. However, in populations with a predilection for development of atherosclerosis, this arteriosclerotic thickening is well developed long before lipid deposition is prominent. Enhanced intimal thickening of certain artery segments, especially in the male, also predicts patterns of subsequent atherosclerotic lesions. In human societies not vulnerable to atherosclerosis, this concentric intimal thickening, even when prominent, does not in itself compromise blood flow.

Upon this matrix, lipid accumulates in the form of fatty streaks in all populations. These yellow, soft, raised lesions may be transient, but their prevalence increases to a peak in the third decade of life. Microscopically, these consist largely of smooth muscle cells in the intimal layer that are filled with lipid deposits, mainly cholesterol and cholesteryl ester. In populations prone to atherosclerotic vascular disease, plaques, as described above, begin to be seen in the third decade and become more numerous with time in common disease sites, such as the proximal coronary vessels. The fibrous plaque is grayish white, focal, and raised and microscopically consists of a prominent extracellular matnx, with less prominence of visible lipid (although by biochemical analysis the lipid content is high). It is thought that these lesions usually develop from fatty streaks. The forces required for this transformation are not well understood, but hypertension seems to be one such shmulus.

Diagnosis of Atherosclerosis

The doctor will begin the diagnosis by a physical examination and with questions about the medical history of the patient and his / her family. Then ask for some tests. There are many of them that can help diagnose atherosclerosis. The doctor usually asks for more than one test to get an accurate diagnosis.

Tests for atherosclerosis may include:

  • Angiography / coronary arteriography, an invasive examination that evaluates the coronary arteries in X-rays
  • Echocardiogram
  • Electrocardiogram (ECG)
  • Angiotomography of the heart, to check the level of calcium inside the arteries. The more calcium, the greater the risk
  • It is also possible to use it to measure the degree of stenosis (Obstruction) of an artery
  • Physical exertion test
  • Magnetic resonance angiography
  • Nuclear stress test (myocardial scintigraphy)
  • Doppler ultrasonography (very important for evaluation of carotid and lower limb arteries).

PATHOGENESIS of  Atherosclerosis

Atherosclerosis is undoubtedly multifactonal in origin and progression. The sharp contrast between the frequent suddenness of clinical events and the slow progressiveness of vascular lesions suggests that different factors are responsible for each. Autopsy studies of advanced lesions generated the classic theories which invoked processes of vascular injury, lipid infiltration, thrombosis, and hemorrhage. These terms are now being incorporated into concepts more consonant with newer knowledge of cell biology. Vascular tissue is increasingly appreciated to be a dynamic responsive organ system of great complexity, rather than a simple conduit with limited responses. The normal blood vessel is a tightly organized, highly regulated, and closely integrated fibrocellular system. The two major cell types found in blood vessel walls are smooth muscle cells and endothelial cells. Each has characteristics and diverse metabolic capabilities.


Current treatment of clinical atherosclerotic complications revolves around coronary care units, replacement of diseased vascular segments with prosthetic or natural grafts, use of antiarrhythmic agents, anticoagulants, and plasma lipid lowering agents, and even heart transplantation. Remarkable as these accomplishments are, they are addressed to the late stages of a disease process for which prevention is clearly the best goal. Extreme manipulation of diets that result in great reductions in serum lipid levels and regression of established lesions in nonhuman primates are not usually possible in man. Although an occasional study suggests that progression of atherosclerotic lesions may be slowed or arrested by stringent diet control in man, results are not conclusive. The clinician might therefore encourage a “prudent” course that involves moderation of intake of cholesterol and saturated fat. This approach, together with reduction of elevated blood pressure and cigarette use, both of proved benefit, and control of obesity and other risk factors, reflects the best information now available for the prevention of atherosclerosis.

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