Balloon-stented angioplasty is a common treatment for carotid arterial atherosclerosis. Clinical studies have shown that within 6 months of the initial procedure, 25% of stented-angioplasty patients develop restenosis, a postoperative narrowing of the artery due to plaque accumulation onto the stent. While hemodynamics and more specifically low oscillatory wall-shear stress have been identified as key factors promoting atherogenesis, their role in restenosis following stent implantation remains unclear. We hypothesize that the implantation of a stent generates hemodynamic abnormalities consisting of low wall shear stresses in the vicinity of arterial wall regions prone to restenosis. The objective of this study was to compare computationally the hemodynamics in normal (healthy), stenosed (atherosclerotic) and stented carotid artery bifurcation models and to investigate potential correlations between regions presenting high hemodynamic abnormalities and regions prone to postoperative stent angioplasty restenosis. Realistic, three-dimensional models of normal, stenosed and stented human carotid bifurcations consisting of the common (CCA), external (ECA) and internal (ICA) carotid arteries were developed using the computer-assisted design software Solid Edge. The characteristic dimensions of the normal and stenosed models were obtained from previously published human data. The stented model was designed by modeling the inner surface of the ICA bulb region as a rigid cylindrical surface mimicking the presence of a stent. Fluid-structure interaction (FSI) simulations were carried out using the adaptive arbitrary Lagrangian Eulerian (ALE) approach of ANSYS 14 to simulate flow and arterial wall dynamics in each model subjected to physiologic pressure and flow rate. As expected, the atherosclerotic model resulted in higher velocity and wall shear stress (WSS) levels than the normal model due to the reduced ICA lumen. In addition, while stent implantation restored the hemodynamic performance of the vessel, it generated lower WSS than in the normal model, which may contribute to restenosis. This study provides new insights into the possible hemodynamic roots of postoperative stent angioplasty restenosis.

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