Description, Causes and Risk Factors:
Atheromatosis is the phenomenon of fatty deposits in the inner lining of arteries, constricting their lumen which may result in obstruction of blood flow. Atheromatosis which consists of cholesterol and inflammatory cells, occurs as part of a pathological process called atherosclerosis. It is a significant pathological condition which may result in potentially life-threatening problems.
In pathology, an atheromatosis is an accumulation and swelling in artery walls made up of (mostly) macrophage cells, or debris, and contain lipids (cholesterol and fatty acids), calcium and a variable amount of fibrous connective tissue. Atheromatosis occurs in atherosclerosis, which is one of the three subtypes of arteriosclerosis; atherosclerosis, Monckeberg's arteriosclerosis and arteriolosclerosis.
Atheromatosis is mainly seen in middle aged or older individuals. Older individuals are more commonly afflicted with this condition. However its incidence has been increasing in young adults in recent times. Men are more predisposed to atheroma formation as compared with women.
Atheromatosis is almost ubiquitous in the Western world, virtually all adults developing the disease to some degree. Fatty streaks can be seen in childhood, small fibrofatty atheromatous plaques in teenagers and young adults, and complicated atheroma lesions in early middle age; atheromatous lesions increase in number with age.
Epidemiological studies have identified risk factors associated with atheromatosis development. These can be grouped into:
Hard risk factors.
Soft risk factors.
(a) The pathogenesis of atheromatosis is believed to be damage to the endothelium associated with a variety of risk factors as coming later. This allows entry of cholesterol-rich low-density lipoproteins (LDLs) into the intima.
(b) The lipid is taken up by macrophages in the intima. Normal receptor-mediated uptake of lipid can be bypassed by oxidization of LDL, which is taken up by a receptor-independent pathway. In this way, excessive lipid accumulates in intimal macrophages to form a visible pale bulge termed a 'fatty streak'.
(c) With development and increased accumulation of lipid, macrophages release lipid into the intima. Cytokines secreted by macrophages stimulate proliferation of intimal cells with features of myofibroblasts. These cells secrete collagen and the plaque starts to become fibrotic. At this stage lesions are raised and yellow (lipid plaques). As the lesion develops, there is pressure atrophy of the media and the elastic lamina is disrupted.
(d) Increased secretion of collagen forms a dense fibrous cap to the plaque which is now hard and white (fibrolipid plaque). The advanced plaque shows free lipid as well as lipid in macrophages. Collagenization also affects the media, weakening the arterial wall. The endothelium is fragile and often ulcerates, allowing platelet aggregation and thrombosis. It is possible that platelet-derived growth factor causes further development of plaques by stimulating cell proliferation.
The pathogenesis of atheromatosis is still uncertain
There have been many hypotheses as to the pathogenesis of atheromatosis, which must explain the origin of the lipid seen in plaques, the reason for development of the cellular elements of plaques and the relation to known risk factors for atheromatosis development.
The thrombogenic hypothesis proposes that thrombus is incorporated into the intima of vessels, lipid being derived from platelet membranes and cells stimulated to proliferate by platelet-derived growth factors (PDGFs).
The clonal proliferation hypothesis is based on observations that smooth muscle cells in plaques are derived from one clone of cells, raising the possibility that atheromatosis is caused by a primary abnormality in cell growth.
The lipid insudation hypothesis proposes that LDLs are taken up into the intima, where they become chemically oxidized to act as toxic, pro-inflammatory and chemotactic factors. This is supported by the fact that antioxidant drugs can inhibit atherogenesis in animals. The response to injury hypothesis proposes that the atheromatosis is a response to chronic low-grade injury to the endothelium. Metabolic disturbance to endothelial cells (as a result of haemodynamic stresses and toxic effects of LDL) allows platelet adhesion, diffusion of plasma proteins, and migration of monocytes into the intima of arteries. Platelets release PDGF and this stimulates proliferation of intimal smooth muscle cells (myointimal cells). These, in turn, synthesize excess collagen and elastin in the intima. Oxidization of LDL facilitates its uptake into monocytes by non-receptor-mediated pathways.
Several risk factors trigger this event of atheromatosis, of which aging and family history, are most significant. Other risk factors include high blood pressure, diabetes, high blood cholesterol, obesity, physical inactivity, emotional stress and smoking.
Lifestyle modifications like maintaining optimal weight and regular physical exercises like running, brisk walking, cycling and swimming are helpful in preventing the progression of this pathogenic process. Appropriate dietary habits help not only in shedding excess weight but also reduce blood cholesterol and lipids. Low salt along with low fat diet is advisable. Increased consumption of fruits and vegetables is advisable. Smoking cessation provides immediate benefit by drastically reducing risk of heart disease and stroke.
Clinical features may be seen when atheromatosis continuously grows and causes progressive narrowing of the artery. Arteries supplying the heart, the brain, the abdomen and the lower limbs are generally affected. If the coronary arteries supplying the heart get affected, it may lead to angina/chest pain along with breathlessness which typically improves on rest. Occasionally an angina may progress to a heart attack, also called myocardial infarction in which breathlessness and chest pain are not improved on rest. This is a potentially fatal condition which needs immediate medical attention. If atheromatosis affects the arteries supplying the brain, then it may hamper the functions of brain, thereby leading to a stroke. Sometimes, lower limbs may be involved when atheromatosis is lodged in arteries supplying the lower limbs. This is called peripheral vascular disorder which may be seen more frequently in smokers. It is characterized by pain in the calf muscles especially on walking or climbing stairs which is relieved on rest. Excruciating abdominal pain along with nausea may occur when presence of atheromatosis constricts the arteries supplying intestines and other abdominal organs.
Signs: The macroscopic appearance of atheromatosis varies according to the stage of evolution of a plaque.Histologically, plaques show varying amounts of free lipid, collagen, and macrophages containing lipid (foam cells).The earliest changes are small fatty streaks, visible as pale areas beneath the endothelium in the aortic segment on the left.The central segment shows pearly white fibrolipid plaques, and the segment on the right shows ulcerated advanced plaques with adherent fibrin-platelet thrombus.The plaque shows pale lipid-rich areas and pink-stained fibrous areas.Late in the fibrolipid plaque stage the media is thinned beneath the plaque.
Arterial wall fixation, staining and thin section: historically this has been the gold standard for detection and description of atheromatosis, though only done after autopsy. With special stains and examination, micro calcifications can be detected, typically with smooth muscle cells of the arterial media near the fatty streaks within a year or two of fatty streaks forming.
CIMT (carotid intima media thickness) as mentioned in the Evolution of Strategies and Changing Focus section, Interventional and non-interventional methods to detect atherosclerosis, specifically vulnerable plaque (non-occlusive or soft plaque), are widely used in research and clinical practice today; Carotid Intima-media thickness Scan (CIMT can be measured by B-mode ultrasonography) measurement has been recommended by the American Heart Association as the most useful method to identify atherosclerosis and may now very well be the gold standard for detection.
IVUS (intravascular ultrasound) is the current most sensitive method detecting and measuring more advanced atheroma within living individuals, though it is typically not used until decades after atheroma begin forming due to cost and body invasiveness.
CT Scans using state of the art higher resolution spiral, or the higher speed EBT, machines have been the most effective method for detecting calcification present in plaque. However, the atheroma have to be advanced enough to have relatively large areas of calcification within them to create large enough regions of ~130 Hounsfield units which the CT scanner software can recognize as distinct from the other surrounding tissues. Typically, such regions start occurring within the heart arteries about 2-3 decades after atheroma start developing. Hence the detection of much smaller plaques then previously possible is being developed by some companies, such as Image Analysis. The presence of smaller, spotty plaques may actually be the more dangerous culprit for progressing to acute myocardial infarction.
Arterial ultrasound, especially of the carotid arteries, with measurement of the thickness of the artery wall, offers a way to partially track the disease progression. As of 2006, the thickness, commonly referred to as IMT for intimal-medial thickness, is not measured clinically though it has used by some researchers since the mid 1990s to track changes in arterial walls. Traditionally, clinical carotid ultrasounds have only estimated the degree of blood lumen restriction, stenosis, a result of very advanced disease. The National Institute of Health did a five-year $5 million study, headed by medical researcher Kenneth Ouriel, to study intravascular ultrasound techniques regarding atherosclerotic plaque. More progressive clinicians have begun using IMT measurement as a way to quantify and track disease progression or stability within individual patients.
Angiography, since the 1960s, has been the traditional way of evaluating for atheroma. However, angiography is only motion or still images of dye mixed with the blood with the arterial lumen and never show atheroma; the wall of arteries, including atheroma with the arterial wall remain invisible. The limited exception to this rule is that with very advanced atheroma, with extensive calcification within the wall, a halo-like ring of radiodensity can be seen in most older humans, especially when arterial lumens are visualized end-on. On cine-floro, cardiologists and radiologists typically look for these calcification shadows to recognize arteries before they inject any contrast agent during angiograms.
The treatment includes certain medications like antihypertensives for controlling high blood pressure. Lipid lowering drugs are recommended in individuals with abnormal values of lipids in blood tests. Lifestyle modifications like weight management, good dietary habits smoking cessation and regular physical exercise are helpful in delaying the progression of the disease.
NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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