A computational framework for atherosclerotic plaque growth simulations

研究人员开发了一个计算框架，用于大动脉中动脉粥样硬化斑块的生长。特别强调的是动脉壁的非线性本构模型，包括残余应力，并在高度分离的时间尺度，管理这个过程的桥接。这项研究的重点是不可压缩的Navier-Stokes方程描述的血液流动，再加上非线性弹性方程，管理的反应，患病的动脉壁。实际的斑块生长过程在斑块的生长（其发生在数年的过程中）和心率（其为秒的量级）之间表现出时间尺度的大分离。研究人员开发了一种方法，将增长模型与流体-结构相互作用问题耦合起来，解决了时间尺度分离所带来的根本挑战。此外，计算框架允许纳入可变的行为因素，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可导致心脏病发作，但动脉斑块的实际生长过程远未得到很好的理解。在该项目中，开发了一个计算框架，该框架将斑块生长和心率之间高度分离的时间尺度连接起来，并且允许将弹性动脉壁的精确模型结合起来。这个新的框架可以产生对动脉粥样硬化的长期原因的基本见解，以及疾病对行为因素的依赖性，如体力活动，胆固醇摄入量和烟草使用。此外，在这个项目中开发的方法可以在弹性材料损伤的建模中找到应用，其他在很长时间跨度内发展的疾病，如腹主动脉瘤和内膜增生，以及生物现象，如通道流动中藻类的生长和运输以及生物膜的生长。该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.