The article is presented in the form of a review and analysis of the literature, which additionally helps to reveal the mechanisms of the pathogenesis of the development of atherosclerosis. This article provides a completely new understanding of the stages and sequence of atherosclerosis development. The modern vision is refuted, which states that all types of lesions in atherosclerosis are developed successively, one after another. The article sheds a light on a significant difference between type IV atherosclerotic lesions and between types V and VI atherosclerotic lesions. Type IV atherosclerotic lesions consists of one lipid core with molten extracellular lipid. Stretches the middle and outer layers of an artery from one side and protrudes beyond the anatomical artery dimensions over the years. In contrast, type V atherosclerotic lesions type is a long, concentric, soft, strong, elastic, yellow, uniform structure, in the form of a tube with a hole in the middle, located in the lumen, which is easily removed from the artery. This types V and VI atherosclerotic lesions - the author suggests calling “cylindrical cholesterol plaque”. Type V atherosclerotic lesions (cylindrical cholesterol plaque) has nothing to do with types I-V atherosclerotic lesions. There are many “coincidences” that make it impossible to see the difference between them. Type V atherosclerotic lesions (cylindrical cholesterol plaque) is an independent pathological structure that appears in a short period of time (few minutes) in the lumen of a healthy artery in case of artery spasm and appearance of a strong obstruction to blood flow. Low density lipoproteins are retained within the wall, in front of the site of arterial narrowing, and quickly create a CCP in the form of a hollow cylinder. All subsequent forms of types V and VI atherosclerotic lesions - concentric and eccentric, are the result of the destruction of the original concentric structure of the type V atherosclerotic lesions (cylindrical cholesterol plaque).
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Published on: Sep 29, 2021 Pages: 4-11
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DOI: 10.17352/ac.000018
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