Carotid Plaque Fibrous Cap Thickness Measurement by ARFI Variance of Acceleration: <i>In Vivo</i> Human Results

Torres, Gabriela; Czernuszewicz, Tomasz J.; Homeister, Jonathon W.; Caughey, Melissa C.; Gallippi, Caterina M.

doi:10.1109/tmi.2020.3019184

Cited by 8 publications

(2 citation statements)

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“…When the "outer FC" is pulled away from the artery wall, an additional cavity is formed through which blood flows -arterial dissection or aortic dissection (Figures 1.4-1.7, 3.1-3.6). [129][130][131][132][133]21,[23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42] Coincidence 9.…”

Section: Coincidencementioning

confidence: 99%

“…-ASL (Animal) -artificial hypertension in the experiment; artificial damage to the endothelium in the experiment; artificial diet high in cholesterol in rabbits, monkeys, chickens and rats; selection of animals with a gene mutation that ensures a permanent increase in the level of LDL in the blood (Figures 1.8-1.10) [125][126][127][128][129][130][131][132][133][134][135][136][137]43,46,47 ; -ASL IV -not known; presumably, long-term average compression of the vessel due to stimulation from the autonomic nervous system, and the appearance of an inflammatory process in the middle and outer shells of the artery (Figures 1.1-1.3); -ASL V -prolonged strong compression of the vessel due to stimulation from the autonomic nervous system, accumulation of LDL in front of the constriction site, and further fastening of LDL between each other by fibrous filaments (Figures 1.4, 1.5, 2.6). 20,21 There are two separate types of ASL in humans that have no connection with each other, and one type in animals.…”

Section: Coincidence 13mentioning

confidence: 99%

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Atherosclerosis in Animals is a Separate Type of Atherosclerosis that has Nothing to do with the Two Types of Atherosclerosis in Humans

Rusanov¹

2022

MRAJ

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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 in humans. A contemporary vision is refuted that animal models of atherosclerosis are completely similar to the two types of human atherosclerotic lesions. The use of incorrect information about the etiology and pathogenesis of atherosclerotic lesions in humans reduces and even completely interferes with the possibility to carry out effective treatment and prevention of cardiovascular diseases associated with atherosclerosis. The two types of human atherosclerotic plaques have very different characteristics compared to atherosclerotic plaques in animals. They have a completely different etiology, pathogenesis, have a completely different appearance and location relative to the artery wall, have a different structure of the fibrous cap, a different pathway of LDL and macrophages, a different location of lipid core, a different way and time of arterial occlusion, a different type of endothelial dysfunction, they interact in totally different way with the walls of the artery and still have many additional differences that make both human atherosclerotic lesions completely different from atherosclerotic lesion in animals. Types IV atherosclerotic lesions consist of one lipid core with molten extracellular lipid. Type V atherosclerotic lesions type is a long, concentric, soft, strong, elastic, yellow, uniform structure. Due to the large number of inconsistencies between atherosclerotic lesions in animals and the two types of atherosclerotic lesions in humans, it is neither possible nor reasonable to use animal models to study the development of atherosclerotic lesions in humans. The plaques appear in the lumen of the artery in just a few days, in places of a sharp narrowing of the artery caused by hyperstimulation of the nervous system. The plaques consist of LDL, which were glued together with fibrin filaments. It also doesn't allow to detect a very simple mechanism accountable for the pathological increase in LDL levels in people who do not have genetic abnormalities. This mechanism proposed by the author is described in the first article dedicated to the type V atherosclerotic lesions (“Cylindrical cholesterol plaque”).

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