2015
DOI: 10.1016/j.jbiomech.2015.08.002
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Low-density lipoprotein accumulation within a carotid artery with multilayer elastic porous wall: fluid–structure interaction and non-Newtonian considerations

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Cited by 21 publications
(9 citation statements)
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“…Furthermore, the increased pressure suggests a lower risk of arterial wall compression and collapse in this area and the distal areas; however, increased pressure on the plaque, even in the short time, if the vulnerable (unstable) plaque is close to rupture, can increase stresses in the fibrous area and result in its rupture [76], which enhances the risk of clot formation. In addition, increased pressure in the stenotic region can increase the permeability of the plasma to the wall, thereby increasing the accumulation and penetration of low-density lipoprotein (LDL) particles into the wall [86], which can accelerate the growth of arterial plaques over time. In the post-stenotic area, if endothelial cells are not damaged, increased pressure over time can result in arterial regeneration [74].…”
Section: Resultsmentioning
confidence: 99%
“…Furthermore, the increased pressure suggests a lower risk of arterial wall compression and collapse in this area and the distal areas; however, increased pressure on the plaque, even in the short time, if the vulnerable (unstable) plaque is close to rupture, can increase stresses in the fibrous area and result in its rupture [76], which enhances the risk of clot formation. In addition, increased pressure in the stenotic region can increase the permeability of the plasma to the wall, thereby increasing the accumulation and penetration of low-density lipoprotein (LDL) particles into the wall [86], which can accelerate the growth of arterial plaques over time. In the post-stenotic area, if endothelial cells are not damaged, increased pressure over time can result in arterial regeneration [74].…”
Section: Resultsmentioning
confidence: 99%
“…In fact, once the luminal lesion is accompanied by a low WSS, it enhances luminal surface concentration of lipoproteins like albumin and low-density lipoprotein, and consequently infiltration to the vascular wall. 20 , 21 Moreover, hypertension intensifies penetration in the elderly, with consequences such as intimal thickening, stenosis, and plaque formation, 5 that increase the risk of ischaemic and thromboembolic strokes.…”
Section: Discussionmentioning
confidence: 99%
“…It may be assumed that such changes occur in vivo in the course of dyslipidaemia and contribute to arterial stiffening. Biochemical analyses have revealed that lipids accumulating on the membranes of atherosclerotic lesions are bonded with elastin already at the early stages of atherosclerosis [19,20].…”
Section: Discussionmentioning
confidence: 99%