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Simulation of Low Density Lipoprotein (LDL) permeation into multilayer coronary arterial wall: Interactive effects of wall shear stress and fluid-structure interaction in hypertension

机译:低密度脂蛋白(LDL)渗透到多层冠状动脉壁上的模拟:壁剪切应力的互动效应和高血压中的流体 - 结构相互作用

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Abstract Due to increased atherosclerosis-caused mortality, identification of its genesis and development is of great importance. Although, key factors of the origin of the disease is still unknown, it is widely believed that cholesterol particle penetration and accumulation in arterial wall is mainly responsible for further wall thickening and decreased rate of blood flow during a gradual progression. To date, various effective components are recognized whose simultaneous consideration would lead to a more accurate approximation of Low Density Lipoprotein (LDL) distribution within the wall. In this research, a multilayer Fluid-Structure Interaction (FSI) model is studied to simulate the penetration of LDL into the arterial wall. Distention impact on wall properties is taken into account by considering FSI and Wall Shear Stress (WSS) dependent endothelium properties. The results show intensified permeation of LDL whilst the FSI approach is applied. In addition, luminal distension prompted by FSI reduces WSS along lumen/wall interface, especially in hypertension. This effect leads to a lowered endothelial resistance against LDL permeation, comparing to the case in which WSS effect is overlooked. The results are in an acceptable consistency with the clinical researches on WSS effect on atherosclerosis development.
机译:摘要由于动脉粥样硬化导致的死亡率增加,鉴定其起源和发展具有重要意义。虽然,疾病起源的关键因素仍然未知,但普遍认为胆固醇颗粒渗透和动脉壁的积累主要负责进一步的壁厚和逐渐进展过程中的血流率降低。迄今为止,识别各种有效组分,其同时考虑将导致墙壁内的低密度脂蛋白(LDL)分布的更准确近似。在该研究中,研究了多层流体结构相互作用(FSI)模型以模拟LDL进入动脉壁的渗透。通过考虑FSI和壁剪切应力(WSS)依赖性内皮特性,考虑对墙壁性质的距离影响。结果表明,施加FSI方法的LDL的强化渗透。此外,FSI提示的腔扩散沿着腔/墙壁界面的WSS​​,特别是在高血压中。这种效果导致对LDL渗透的降低的内皮抗性,比较与WSS效应被忽视的情况相比。结果符合可接受的一致性,与对动脉粥样硬化发育的临床研究。

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