Three-dimensional numerical simulation of plaque formation in arteries

Atherosclerosis develops from oxidized low-density lipoprotein (LDL) molecules. When oxidized LDL evolves in plaque formation within an artery wall, a series of reactions occur to repair the damage to the artery wall caused by oxidized LDL. The body’s immune system responds to damage to the artery wall caused by oxidized LDL by sending specialized white blood cells-macrophages (Mphs) to absorb the oxidized-LDL and form specialized foam cells. Macrophages accumulate inside arterial intima. Also smooth muscle cells accumulate in the atherosclerotic arterial intima, where they proliferate and secrete extracellular matrix to generate a fibrous cap. In this study, a model of plaque formation on the pig left anterior descending (LAD) coronary artery is simulated numerically using a specific animal data obtained from IVUS and histological recordings. The 3D bloodflow is described by the Navier–Stokes equations, together with the continuity equation. Mass transfer within the blood lumen and through the arterial wall is coupled with the blood flow and is modeled by a convection-diffusion equation. The LDL transports in lumen of the vessel and through the vessel tissue (which has a mass consumption term) are coupled by Kedem–Katchalsky equations. The inflammatory process is modeled using three additional reaction-diffusion partial differential equations. A full three-dimensional model was created which includes blood flow and LDL concentration, as well as plaque formation. Matching of IVUS and histological animal data is performed using a 3D histological image reconstruction and 3D deformation of elastic body.Computed concentration of macrophages indicates that there is a newly formed matter in the intima, especially in the LAD 15mm region from bifurcation. Understanding and prediction of the evolution of atherosclerotic plaques either into vulnerable or stable plaques are major tasks for the medical community.