Editing Atherosclerosis (section)

===Components===
The plaque is divided into three distinct components:
# The [[atheroma]] ("lump of gruel", {{ety|gre|''ἀθήρα'' (athera)|[[gruel]]}}), which is the nodular accumulation of a soft, flaky, yellowish material at the center of large plaques, composed of macrophages nearest the [[lumen (anatomy)|lumen]] of the artery{{citation needed|date=December 2020}}
# Underlying areas of cholesterol crystals{{citation needed|date=December 2020}}
# Calcification at the outer base of older or more advanced [[lesions]]. Atherosclerotic lesions, or atherosclerotic plaques, are separated into two broad categories: Stable and unstable (also called vulnerable).<ref>{{cite journal | vauthors = Ross R | title = Atherosclerosis--an inflammatory disease | journal = The New England Journal of Medicine | volume = 340 | issue = 2 | pages = 115–126 | date = January 1999 | pmid = 9887164 | doi = 10.1056/NEJM199901143400207 }}</ref> 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 cell]]s, and the extracellular matrix separating the lesion from the arterial lumen (also known as the [[fibrous cap]]) is usually weak and prone to rupture.<ref>{{cite journal | vauthors = Finn AV, Nakano M, Narula J, Kolodgie FD, Virmani R | title = Concept of vulnerable/unstable plaque | journal = Arteriosclerosis, Thrombosis, and Vascular Biology | volume = 30 | issue = 7 | pages = 1282–1292 | date = July 2010 | pmid = 20554950 | doi = 10.1161/ATVBAHA.108.179739 | doi-access = free }}</ref> Ruptures of the fibrous cap expose thrombogenic material, such as [[collagen]],<ref>{{cite journal | vauthors = Didangelos A, Simper D, Monaco C, Mayr M | title = Proteomics of acute coronary syndromes | journal = Current Atherosclerosis Reports | volume = 11 | issue = 3 | pages = 188–195 | date = May 2009 | pmid = 19361350 | doi = 10.1007/s11883-009-0030-x }}</ref> 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]].{{citation needed|date=December 2020}}

Apart from thromboembolism, chronically expanding atherosclerotic lesions can cause complete closure of the lumen. Chronically expanding lesions are often asymptomatic until the 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 the death of the tissues fed by the artery in approximately five minutes. This event is called an [[infarction]].{{citation needed|date=December 2020}}