In silico experiments of intimal hyperplasia development: disendothelization in an axisymmetric idealized artery.

We use in silico experiments to study the role of the hemodynamics and of the type of disendothelization on the physiopathology of intimal hyperplasia. We apply a multiscale bio-chemo-mechanical model of intimal hyperplasia on an idealized axisymmetric artery that suffers two kinds of disendothelizations. The model predicts the spatio-temporal evolution of the lesions development, initially localized at the site of damages, and after few days displaced downstream of the damaged zones, these two stages being observed whatever the kind of damage. Considering macroscopic quantities, the model sensitivity to pathology-protective and pathology-promoting zones is qualitatively consistent with experimental findings. The simulated pathological evolutions demonstrate the central role of two parameters: (a) the initial damage shape on the morphology of the incipient stenosis, and (b) the local wall shear stresses on the overall spatio-temporal dynamics of the lesion.

Multiscale bio-chemo-mechanical model of intimal hyperplasia.

We consider a computational multiscale framework of a bio-chemo-mechanical model for intimal hyperplasia. With respect to existing models, we investigate the interactions between hemodynamics, cellular dynamics and biochemistry on the development of the pathology. Within the arterial wall, we propose a mathematical model consisting of kinetic differential equations for key vascular cell types, collagen and growth factors. The luminal hemodynamics is modeled with the Navier-Stokes equations. Coupling hypothesis among time and space scales are proposed to build a tractable modeling of such a complex multifactorial and multiscale pathology. A one-dimensional numerical test-case is presented for validation by comparing the results of the framework with experiments at short and long timescales. Our model permits to capture many cellular phenomena which have a central role in the physiopathology of intimal hyperplasia. Results are quantitatively and qualitatively consistent with experimental findings at both short and long timescales.

Comparison between a generalized Newtonian model and a network-type multiscale model for hemodynamic behavior in the aortic arch: Validation with 4D MRI data for a case study.

Blood is a complex fluid in which the presence of the various constituents leads to significant changes in its rheological properties. Thus, an appropriate non-Newtonian model is advisable; and we choose a Modified version of the rheological model of Phan-Thien and Tanner (MPTT). The different parameters of this model, derived from the rheology of polymers, allow characterization of the non-Newtonian nature of blood, taking into account the behavior of red blood cells in plasma. Using the MPTT model that we implemented in the open access software OpenFOAM, numerical simulations have been performed on blood flow in the thoracic aorta for a healthy patient. We started from a patient-specific model which was constructed from medical images. Exiting flow boundary conditions have been developped, based on a 3-element Windkessel model to approximate physiological conditions. The parameters of the Windkessel model were calibrated with in vivo measurements of flow rate and pressure. The influence of the selected viscosity of red blood cells on the flow and wall shear stress (WSS) was investigated. Results obtained from this model were compared to those of the Newtonian model, and to those of a generalized Newtonian model, as well as to in vivo dynamic data from 4D MRI during a cardiac cycle. Upon evaluating the results, the MPTT model shows better agreement with the MRI data during the systolic and diastolic phases than the Newtonian or generalized Newtonian model, which confirms our interest in using a complex viscoelastic model.