3-D Simulation for Blood Flow and Artery Compression in Asymmetric Stenotic Arteries With Axial Stretch

D. Tang, Chun Yang, S. Kobayashi
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Abstract

There has been increasing evidence that severe stenosis may cause artery compression and plaque cap rupture leading to heart attack and stroke. The physiological conditions under which that may occur and mechanisms involved are not well understood. It has been known that severe stenosis causes critical flow and wall mechanical conditions such as flow limitation, flow separation, low and oscillating shear stress distal to the stenosis, high shear stress and low or even negative flow pressure at the throat of stenosis, artery compression or even collapse. Those conditions are related to limitation of blood supply, intimal thickening and thrombosis formation, endothelism damage, platelet activation and aggregation, plaque cap rupture (for review, see [1,2]). Due to the complexity of the problem and lack of experimental data for mechanical properties of arteries under both expansion and compression, previous models were limited primarily to flow behaviors and with various limitations (axisymmetry, rigid wall, small strain, small pressure gradient). In this paper, experimental data for artery mechanical properties under physiological conditions were measured and a 3-d computational model is introduced to investigate flow behaviors and wall stress and strain distributions with fluid-structure interactions to better understand the mechanism involved in artery compression and plaque cap rupture.
不对称狭窄动脉轴向拉伸血流和动脉压迫的三维模拟
越来越多的证据表明,严重的狭窄可能导致动脉受压和斑块帽破裂,从而导致心脏病发作和中风。可能发生这种情况的生理条件和相关机制尚不清楚。已知严重狭窄会引起临界流动和壁面力学条件,如流动受限、流动分离、狭窄远端低且振荡的剪切应力、狭窄喉部高剪切应力、低甚至负流压、动脉受压甚至塌陷等。这些情况与血液供应受限、内膜增厚和血栓形成、内皮损伤、血小板活化和聚集、斑块帽破裂有关(回顾,见[1,2])。由于问题的复杂性和缺乏动脉在膨胀和压缩下力学性能的实验数据,以往的模型主要局限于流动行为,并且有各种局限性(轴对称、刚性壁面、小应变、小压力梯度)。本文测量了生理条件下动脉力学性能的实验数据,并引入三维计算模型来研究流固相互作用下的流动行为和壁面应力应变分布,以更好地了解动脉受压和斑块帽破裂的机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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