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Mathematical Modeling of Intravascular Blood Coagulation under Wall Shear Stress

机译:壁剪切应力作用下血管内血液凝固的数学模型

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摘要

Increased shear stress such as observed at local stenosis may cause drastic changes in the permeability of the vessel wall to procoagulants and thus initiate intravascular blood coagulation. In this paper we suggest a mathematical model to investigate how shear stress-induced permeability influences the thrombogenic potential of atherosclerotic plaques. Numerical analysis of the model reveals the existence of two hydrodynamic thresholds for activation of blood coagulation in the system and unveils typical scenarios of thrombus formation. The dependence of blood coagulation development on the intensity of blood flow, as well as on geometrical parameters of atherosclerotic plaque is described. Relevant parametric diagrams are drawn. The results suggest a previously unrecognized role of relatively small plaques (resulting in less than 50% of the lumen area reduction) in atherothrombosis and have important implications for the existing stenting guidelines.
机译:剪切应力的增加(例如在局部狭窄处观察到的)可能会导致血管壁对促凝剂的渗透性发生剧烈变化,从而引发血管内血液凝结。在本文中,我们提出了一个数学模型来研究剪切应力诱导的渗透性如何影响动脉粥样硬化斑块的血栓形成潜能。该模型的数值分析揭示了系统中存在两个激活血液凝结的流体动力学阈值,并揭示了血栓形成的典型情况。描述了凝血发展对血流强度的依赖性,以及对动脉粥样硬化斑块的几何参数的依赖性。绘制了相关的参数图。结果表明,动脉粥样硬化中相对较小的斑块(导致管腔面积减少不到50%)以前未被认识到,并且对现有的支架置入指南具有重要意义。

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