What is "atherosclerosis"

atherosclerosis \ath`er*o*scle*ro"sis\ ([a^]th`[~e]r*[-o]*skl[-e]*r[=o]"s[i^]s), n. [Gr. ? + -logy.] (Med.) a form of arteriosclerosis characterized by irregular fatty deposits on the inner surface of large and medium-sized arteries; the deposits are associated with fibrosis and calcification of the inner layer of the arteries. Similar conditions may be found in swine and fowl. The deposits may become large enough to impede the blood circulation and in some cases may restrict the blood supply to the heart.
--Stedman

1908, from atherosklerose, coined in German 1904; see atheroma + sclerosis.

n. (context pathology English) The clogging or hardening of artery or blood vessels caused by plaques (accumulations of fat deposits, usually cholesterol).

1. n. a stage of arteriosclerosis involving fatty deposits (atheromas) inside the arterial walls [syn: coronary artery disease]

2. [also: atheroscleroses (pl)]

Atherosclerosis (also known as arteriosclerotic vascular disease or ASVD) is a specific form of arteriosclerosis in which an artery-wall thickens as a result of invasion and accumulation of white blood cells (WBCs) (foam cell) and proliferation of intimal-smooth-muscle cell creating a fibrofatty plaque.

The accumulation of the white blood cells is termed "fatty streaks" early on because of the appearance being similar to that of marbled steak. These accumulations contain both living, active WBCs (producing inflammation) and remnants of dead cells, including cholesterol and triglycerides. The remnants eventually include calcium and other crystallized materials within the outermost and oldest plaque. The "fatty streaks" reduce the elasticity of the artery walls. However, they do not affect blood flow for decades because the artery muscular wall enlarges at the locations of plaque. The wall stiffening may eventually increase pulse pressure; widened pulse pressure is one possible result of advanced disease within the major arteries.

Atherosclerosis is therefore a syndrome affecting arterial blood vessels due to a chronic inflammatory response of WBCs in the walls of arteries. This is promoted by low-density lipoproteins (LDL, plasma proteins that carry cholesterol and triglycerides) without adequate removal of fats and cholesterol from the macrophages by functional high-density lipoproteins (HDL). It is commonly referred to as a "hardening" or furring of the arteries. It is caused by the formation of multiple atheromatous plaques within the arteries.

The plaque is divided into three distinct components:

1. The atheroma ("lump of gruel", ), which is the nodular accumulation of a soft, flaky, yellowish material at the center of large plaques, composed of macrophages nearest the lumen of the artery
2. Underlying areas of cholesterol crystals
3. Calcification at the outer base of older or more advanced lesions.

Atherosclerosis is a chronic disease that remains asymptomatic for decades. Atherosclerotic lesions, or atherosclerotic plaques, are separated into two broad categories: Stable and unstable (also called vulnerable). The pathobiology of atherosclerotic lesions is very complicated, but generally, stable atherosclerotic plaques, which tend to be asymptomatic, are rich in extracellular matrix and smooth muscle cells. On the other hand, unstable plaques are rich in macrophages and foam cells, and the extracellular matrix separating the lesion from the arterial lumen (also known as the fibrous cap) is usually weak and prone to rupture. Ruptures of the fibrous cap expose thrombogenic material, such as collagen, to the circulation and eventually induce thrombus formation in the lumen. Upon formation, intraluminal thrombi can occlude arteries outright (e.g., coronary occlusion), but more often they detach, move into the circulation, and eventually occlude smaller downstream branches causing thromboembolism. Apart from thromboembolism, chronically expanding atherosclerotic lesions can cause complete closure of the lumen. Chronically expanding lesions are often asymptomatic until lumen stenosis is so severe (usually over 80%) that blood supply to downstream tissue(s) is insufficient, resulting in ischemia.

These complications of advanced atherosclerosis are chronic, slowly progressive and cumulative. Most commonly, soft plaque suddenly ruptures (see vulnerable plaque), causing the formation of a thrombus that will rapidly slow or stop blood flow, leading to death of the tissues fed by the artery in approximately five minutes. This catastrophic event is called an infarction. One of the most common recognized scenarios is called coronary thrombosis of a coronary artery, causing myocardial infarction (a heart attack). The same process in an artery to the brain is commonly called stroke. Another common scenario in very advanced disease is claudication from insufficient blood supply to the legs. Atherosclerosis affects the entire artery tree, but mostly larger, high-pressure vessels such as the coronary, renal, femoral, cerebral, and carotid arteries. These are termed " clinically silent" because the person having the infarction does not notice the problem and does not seek medical help, or when they do, physicians do not recognize what has happened.

Atherosclerosis is a monthly peer-reviewed scientific journal established in 1970 and published by Elsevier. It is the official journal of the European Atherosclerosis Society and is affiliated with both the International Atherosclerosis Society and the Society of Atherosclerosis Imaging and Prevention. The editor-in-chief is S. Humphries. According to the Journal Citation Reports, the journal has a 2012 impact factor of 3.706.