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Atheroma is a disease of the intima of arteries

Atheroma is the accumulation of lipid-rich material in the intima of arteries associated with cellular reactions. The lesions are termed 'plaques'. Although atheroma is essentially a disease of the tunica intima, it has an impact on the structure and function of the media.

The macroscopic appearance of atheroma 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.

Understanding of risk factors for atheroma is largely based on epidemiological studies.

Atheroma 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 atheroma development. These can be grouped into:

Constitutional factors

Hard risk factors

Soft risk factors.

(a) The pathogenesis of atheroma 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 atheroma is still uncertain

There have been many hypotheses as to the pathogenesis of atheroma, 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 atheroma 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 atheroma 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 atheromatous plaque 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.

Clinicopathological consequences of atheroma

Atheroma produces disease in several ways:

Reduction of blood flow through arteries. When atheroma affects small arteries, the enlargement of an intimal atheromatous plaque may severely reduce the size of the lumen. The main clinical implications are ischaemic heart disease. peripheral vascular disease. and cerebrovascular disease.

Predisposition to thrombosis. If the fibrous cap over an atheromatous plaque breaks down, collagen fibres in the abnormal intima are exposed to the circulating blood, and this initiates the formation of thrombus In small-bone vessels, such as the coronary or cerebral arteries, this thrombus may suddenly complete the occlusion of an already narrowed artery. In larger vessels, such as the aorta, a plaque of mural thrombus is formed, which may embolize to distal vessels.

Bleeding into a plaque. If there is breakdown of the fibrous cap of a plaque, blood may dissect into the centre of the plaque, causing it to balloon into the vessel lumen and reducing blood flow. This is occasionally seen in coronary arteries, leading to myocardial infarction.

Weakening of vessel wall and aneurys formation. Severe atheroma in the intima eventually leads to thinning of the media, loss of smooth muscle cells and elastic fibres, and progressive replacement by non contractile inelastic collagen. The media becomes functionally incompetent and this leads to generalized dilatation of the artery over a period of some years to form an aneurysm. The abdominalaorta is the most common site for aneurysms secondary to atherosclerosis.

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Revised: 02-11-2014.