Abstract

Atherosclerosis is a progressive disease characterized by inflammation and lipid accumulation in the vascular wall. In this study, we analysed animal experiments and clinical data for plaque formation and progression. The first animal experiment examined cast model on the carotid artery (Cheng et al., 2006) [21]. The second animal experiment is related for pig on the left anterior descending coronary artery (LAD) after 2month of high fat diet. Experimental model of plaque formation on pig LAD is simulated numerically using specific animal data obtained from intravascular ultrasound (IVUS) and histological data. The 3D blood flow is governed 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 the convection–diffusion equation. LDL transport in lumen of the vessel is described by Kedem–Katchalsky equations. The inflammatory process is solved using three additional reaction–diffusion partial differential equations. Lipids concentration in the intimal area of the low shear stress was 16% and for oscillatory zone 10% which is in good agreement with experimental data. Computed concentration of macrophages for pig model indicates that there is a newly formed matter in the intima, especially at foam cell lipids area which varied from 12% to 20% and chemokine receptor type 4 (CXCR4) areas from 1.5% to 3.5%. Patients’ study predicts new plaque formation after 12months follow up which corresponds to size and plaque composition. Matching of plaque location, size and composition progression in time between experimental and computer model shows a potential benefit for future prediction of this vascular decease.

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