https://wiki.tiffa.net/w/index.php?action=history&feed=atom&title=Translations%3AAtherosclerosis%2F43%2Fen 2026-05-26T12:34:22Z Revision history for this page on the wiki MediaWiki 1.43.0 https://wiki.tiffa.net/w/index.php?title=Translations:Atherosclerosis/43/en&diff=124909&oldid=prev 2024-03-05T13:10:03Z

<p>Importing a new version from external source</p> <p><b>New page</b></p><div>===Components===<br /> The plaque is divided into three distinct components:<br /> # The [[atheroma]] (&quot;lump of gruel&quot;, {{ety|gre|&#039;&#039;ἀθήρα&#039;&#039; (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<br /> # Underlying areas of cholesterol crystals<br /> # 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). 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. 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]].</div>

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