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A phenomenological model for atherosclerotic plaque growth and rupture

机译：动脉粥样硬化斑块生长和破裂的现象学模型

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The objective of this communication is to develop a computer-based framework for the overall coupled phenomena leading to growth and rupture of atherosclerotic plaques. The modeling is purposely simplified to expose the dominant phenomenological controlling mechanisms, and their coupled interaction. The main ingredients of the present simplified modeling approach, describing the events that occur due to the presence and oxidation of excess low-density lipoprotein (LDL) in the intima, are: (i) adhesion of monocytes to the endothelial surface, which is controlled by the intensity of the blood flow and the adhesion molecules stimulated by the excess LDL, (ii) penetration of the monocytes into the intima and subsequent inflammation of the tissue, and (iii) rupture of the plaque accompanied with some degree of thrombus formation or even subsequent occlusive thrombosis. The set of resulting coupled equations, each modeling entirely different physical events, is solved using an iterative staggering scheme, which allows the equations to be solved in a computationally convenient decoupled fashion. Theoretical convergence properties of the scheme are given as a function of physical parameters involved. A numerical example is given to illustrate the modeling approach and an a priori prediction for time to rupture as a function of arterial geometry, diameter of the monocyte, adhesion stress, bulk modulus of the ruptured wall material, blood viscosity, flow rate and mass density of the monocytes. (C) 2003 Elsevier Ltd. All rights reserved.
机译：交流的目的是为导致动脉粥样硬化斑块生长和破裂的整体耦合现象开发一个基于计算机的框架。故意简化建模以暴露主要的现象学控制机制及其耦合的相互作用。本简化建模方法的主要成分描述了由于内膜中过量低密度脂蛋白（LDL）的存在和氧化而发生的事件，它们是：（i）单核细胞粘附于内皮表面，这是受控的通过血流的强度和过量LDL刺激的粘附分子，（ii）单核细胞渗透进入内膜并随后引起组织炎症，（iii）斑块破裂并伴有一定程度的血栓形成或甚至随后的闭塞性血栓形成。使用迭代交错方案求解每个建模完全不同的物理事件的结果耦合方程组，该迭代交错方案允许以计算方便的解耦方式求解方程。该方案的理论收敛性质是所涉及的物理参数的函数。给出了一个数值示例来说明建模方法以及根据动脉几何形状，单核细胞直径，粘附应力，破裂壁材料的体积模量，血液粘度，流速和质量密度而确定的破裂时间的先验预测单核细胞。 （C）2003 Elsevier Ltd.保留所有权利。

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