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We propose and study a nonlinear elimination preconditioned inexact Newton method for the numerical simulation of diseased human arteries with a heterogeneous hyperelastic model. We assume the artery is made of layers of distinct tissues and also contains plaque. Traditional Newton methods often work well for smooth and homogeneous arteries but suffer from slow or no convergence due to the heterogeneousness of diseased soft tissues when the material is quasi-incompressible. The proposed nonlinear elimination method adaptively finds a small number of equations causing the nonlinear stagnation and then eliminates them from the global nonlinear system. By using the theory of affine invariance of Newton method, we provide insight into why the nonlinear elimination method can improve the convergence of Newton iterations. Our numerical results show that the combination of nonlinear elimination with an initial guess interpolated from a coarse level solution can lead to the uniform convergence of Newton method for this class of very difficult nonlinear problems. 

Computational fluid dynamics (CFD) is increasingly used to study blood flows in patient-specific arteries for understanding certain cardiovascular diseases. The techniques work quite well for relatively simple problems but need improvements when the problems become harder when (a) the geometry becomes complex (eg, a few branches to a full pulmonary artery), (b) the model becomes more complex (eg, fluid-only to coupled fluid-structure interaction), (c) both the fluid and wall models become highly nonlinear, and (d) the computer on which we run the simulation is a supercomputer with tens of thousands of processor cores. To push the limit of CFD in all four fronts, in this paper, we develop and study a highly parallel algorithm for solving a monolithically coupled fluid-structure system for the modeling of the interaction of the blood flow and the arterial wall. As a case study, we consider a patient-specific, full size pulmonary artery obtained from computed tomography (CT) images, with an artificially added layer of wall with a fixed thickness. The fluid is modeled with a system of incompressible Navier-Stokes equations, and the wall is modeled by a geometrically nonlinear elasticity equation. As far as we know, this is the first time the unsteady blood flow in a full pulmonary artery is simulated without assuming a rigid wall. The proposed numerical algorithm and software scale well beyond 10 000 processor cores on a supercomputer for solving the fluid-structure interaction problem discretized with a stabilized finite element method in space and an implicit scheme in time involving hundreds of millions of unknowns. 

Simulation of blood flows in the pulmonary artery provides some insight into certain diseases by examining the relationship between some continuum metrics, e.g., the wall shear stress acting on the vascular endothelium, which responds to flow-induced mechanical forces by releasing vasodilators/constrictors. V. Kheyfets, in his previous work, studies numerically a patient-specific pulmonary circulation to show that decreasing wall shear stress is correlated with increasing pulmonary vascular impedance. In this paper, we develop a scalable parallel algorithm based on domain decomposition methods to investigate an unsteady model with patient-specific pulsatile waveforms as the inlet boundary condition. 

Nonlinear fluid–structure interaction (FSI) problems on unstructured meshes in 3D appear in many applications in science and engineering, such as vibration analysis of aircrafts and patient-specific diagnosis of cardiovascular diseases. In this work, we develop a highly scalable, parallel algorithmic and software framework for FSI problems consisting of a nonlinear fluid system and a nonlinear solid system, that are coupled monolithically.