A computational framework for atherosclerotic plaque growth simulations

研究人员为大动脉中动脉粥样硬化斑块的生长开发了一个计算框架。特别强调的是动脉壁的非线性本构模型，包括残余应力，以及控制这一过程的高度分离的时间尺度的桥梁。这项研究的重点是描述血液流动的不可压缩的Navier-Stokes方程，以及控制病变动脉壁响应的非线性弹性方程。实际的斑块生长过程在斑块的生长(持续数年)和心率(以秒为量级)之间显示出很大的时间间隔。研究人员开发了一种方法，将增长模型与流固耦合问题结合起来，以解决时间尺度分离带来的根本挑战。此外，计算框架还允许纳入不同的行为因素，如体力活动和血液中的胆固醇浓度。虽然已知动脉粥样硬化斑块的破裂会导致心脏病发作，但动脉中斑块的实际生长过程远未被很好地了解。在这个项目中，开发了一个计算框架，它连接了斑块增长和心率之间高度分离的时间尺度，并允许纳入弹性动脉壁的准确模型。这个新的框架可以对动脉粥样硬化的长期原因以及疾病对行为因素的依赖产生基本的见解，如体力活动、胆固醇摄入量和吸烟。此外，该项目中开发的方法还可以应用于弹性材料损伤的建模，其他长时间发展的疾病，如腹主动脉瘤和内膜增生，以及生物现象，如渠道流中藻类的生长和运输以及生物膜的生长。这个项目涉及与工程师的合作，他们通过实验测量动脉中的残余应力。

The investigators develop a computational framework for the growth of atherosclerotic plaques in large arteries. Specific emphasis is placed on the nonlinear constitutive models for the arterial wall, including residual stresses, and on the bridging of the highly separated time scales that govern this process. This study focuses on the incompressible Navier-Stokes equations that describe the blood flow, coupled with nonlinear elasticity equations that govern the response of the diseased arterial walls. The actual plaque growth process exhibits a large separation of time scales between the growth of the plaque, which takes place over a course of years, and the heart rate, which is in the order of seconds. The investigators develop a methodology to couple a growth model with the fluid-structure interaction problem in a way that the fundamental challenges incurred by the separation of time scales are resolved. In addition, the computational framework allows for the incorporation of variable behavioral factors, such as physical activity and cholesterol concentration in the blood.While it is known that the rupturing of an atherosclerotic plaque can cause a heart attack, the actual growth process of plaques in arteries is far from well understood. In this project, a computational framework is developed that bridges the highly separated time scales between the plaque growth and the heart rate, and that allows for the incorporation of accurate models for the elastic arterial walls. This new framework can yield fundamental insights into the long-term causes of atherosclerosis, and the dependence of the disease on behavioral factors such as physical activity, cholesterol intake, and tobacco use. In addition, the methodologies developed in this project can find applications in the modeling of damage in elastic materials, other diseases that develop over a large time span such as abdominal aortic aneurysms and intimal hyperplasia, and biological phenomena such as the growth and transport of algae in channel flows and the growth of biofilms. This project involves a collaboration with engineers who measure residual stresses in arteries experimentally.