[ath-uh-roh-skluh-roh-sis, ath-] 
| a common form of arteriosclerosis in which fatty substances form a deposit of plaque on the inner lining of arterial walls. |
ath·er·o·scle·ro·sis (āth'ə-rō-sklə-rō'sĭs)  (click for larger image in new window) n. A form of arteriosclerosis characterized by the deposition of atheromatous plaques containing cholesterol and lipids on the innermost layer of the walls of large and medium-sized arteries. [athero(ma) + sclerosis.] ath'er·o·scle·rot'ic (-rŏt'ĭk) adj., ath'er·o·scle·rot'i·cal·ly adv. |
A form of arteriosclerosis in which the arteries become clogged by the buildup of fatty substances, which eventually reduces the flow of blood to the tissues. These fatty substances, called plaque, are made up largely of cholesterol. (Compare arteriosclerosis; see circulatory system.)
atherosclerosis ath·er·o·scle·ro·sis (āth'ə-rō-sklə-rō'sĭs)
n.
A form of arteriosclerosis characterized by the deposition of atheromatous plaques containing cholesterol and lipids on the innermost layer of the walls of large and medium-sized arteries.
atherosclerosis
chronic disease caused by the deposition of fats, cholesterol, calcium, and other substances in the innermost layer of endothelium of the large and medium-sized arteries. Atherosclerosis is the most common arterial abnormality characterized as arteriosclerosis, which is defined by the loss of arterial elasticity due to vessel thickening and stiffening. The precise mechanisms of atherosclerosis are not completely understood, but there is evidence that in some people the condition can begin in childhood with the formation of tiny "fatty streaks," or streaks of fat deposition, in the arteries. As the endothelium is infiltrated by more and more fatty materials-primarily low-density lipoproteins (LDLs), protein-lipid complexes that serve as a vehicle for delivering cholesterol to the body-immune cells called macrophages are drawn to the site to scavenge the materials. When filled with lipids the macrophages become known as "foam cells," which later die and accumulate in the endothelial lining. Other materials are also deposited in the lining, including salts of calcium and other minerals, smooth muscle cells, and cellular debris of varying composition. This causes the initially tiny lesions to enlarge and thicken to form atheromas, or atherosclerotic plaques. These plaques may narrow the vessel channel, interfering with the flow of blood. Endothelial injury, either as a result of lipid deposition or as a result of another cause, may also be accompanied by the formation of fibrous caps of scar tissue. These areas of scar tissue make the vessel walls less elastic, with one consequence being an increase in blood pressure. Thick plaques that severely occlude an artery can significantly decrease the flow of blood to vascular beds in tissues served by the artery, thereby causing severe tissue damage. In addition, a disturbance to the endothelium may result in the formation of a blood clot (thrombus) at the site of a plaque, likewise obstructing the channel or breaking loose from the site and causing a catastrophic blockage elsewhere.
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