Stenting coronary arteries is one of the safest and most efficient procedures for restoring the normal lumen diameter in atherosclerotic arterial segments. A stent is a metal mesh which is deployed in the affected arterial segment to open it up and keep it from narrowing again. After deployment the stent naturally becomes covered by smooth muscle cells and endothelial lining, but in some cases a restenosis develops. A restenosis is a complication caused by excessive smooth muscle proliferation inside the lumen, which narrows the artery again. Currently, the causes of restenosis are being studied, and research is conducted to optimize stent geometries and treatment procedures to decrease the frequency of restenosis and other complications.
We have developed a model for in-stent restenosis, which is based on directly modelling the cell growth and proliferation in tunica media and tunica intima of coronary arteries. The process of smooth muscle cell proliferation is governed by mechanical shear stress on the vessel wall, which is caused by blood flowing through the lumen, and also by the concentrations of growth factors and inhibitors. The full model of restenosis is a multiscale multiphysics model, and includes, in addition to the biological model of tissue, a rheological model of vessel wall, a hydrodynamic model of blood flow, and a model for the diffusion of biologically active substances inside the vessel wall.
Our model allows us to study and analyse the process of restenosis and to compare the pathogenicity of different stent geometries.
The function of this model is illustrated by modelling restenosis in a coronary stent 3×8 mm (diameter and length). The computation corresponds to two weeks of growth.
An in silico study on the role of smooth muscle cell migration in neointimal formation after coronary stenting // Journal of The Royal Society Interface. — 2015. — Vol. 12., Issue 108. Article number 0358.
Modelling the effect of a functional endothelium on the development of in-stent restenosis // PLoS One. — 2013. — Vol. 8., Issue 6. Article number e66138.