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The macrophages release chemicals known as cytokines, which cause an inflammatory response. This results in the migration of smooth muscle cells, or myofibroblast, which lays a fibrous outer shell around the foam cells. The foams cells eventually die, resulting in the trapping of cholesterol and cellular debris inside the shell. The shell and its lipid core is known as a plaque, or atheroma. Occasionally cholesterol may crystallise within the plaque, forming cholesterol clefts.
The macrophages release chemicals known as cytokines, which cause an inflammatory response. This results in the migration of smooth muscle cells, or myofibroblast, which lays a fibrous outer shell around the foam cells. The foams cells eventually die, resulting in the trapping of cholesterol and cellular debris inside the shell. The shell and its lipid core is known as a plaque, or atheroma. Occasionally cholesterol may crystallise within the plaque, forming cholesterol clefts.
Over time, a number of plaques may form within the wall of an artery, some of which may combine to form larger plaques. This leads to a narrowing of the [[lumen]] of the artery, constricting the flow of blood. Depending on the artery affected, this may present as a variety of symptoms, including [[ischemic heart disease]] (coronary arteries), [[syncope]] (carotid arteries) or hypertension (renal arteries). Plaques can be either stable or unstable depending on the ratio of their shell thickness to liquid core, with a lower ratio corresponding to a less stable plaque. Unstable plaques may be eroded or rupture into the lumen of an atery, spelling their contents into the blood. This can lead to the formation of a [[thrombus]], which can further occlude the flow of blood. Large thrombi may completely prevent the passage of red blood cells, leading to [[ischemia]] and [[infarction]] of the supplied tissue.
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