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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.