Simulation of stent deployment in a realistic human coronary artery

Frank JH Gijsen¹ , Francesco Migliavacca² , Silvia Schievano³ , Laura Socci² , Lorenza Petrini² , Attila Thury¹ , Jolanda J Wentzel¹ , Anton FW van der Steen¹ , Patrick WS Serruys¹ and Gabriele Dubini²

¹Department of Biomedical Engineering, Thoraxcentre Ee2322, Erasmus Medical Center Rotterdam, P.O. Box 2040, 3000 CA, Rotterdam, The Netherlands

²Laboratory of Biological Structure Mechanics, Structural Engineering Department, Politecnico di Milano, Milan, Italy

³Cardiothoracic Unit, University College of London Institute of Child Health and Great Ormond Street Hospital for Children, London, UK

author email corresponding author email

BioMedical Engineering OnLine 2008, 7:23doi:10.1186/1475-925X-7-23


Published:	6 August 2008

Abstract

Background

The process of restenosis after a stenting procedure is related to local biomechanical environment. Arterial wall stresses caused by the interaction of the stent with the vascular wall and possibly stress induced stent strut fracture are two important parameters. The knowledge of these parameters after stent deployment in a patient derived 3D reconstruction of a diseased coronary artery might give insights in the understanding of the process of restenosis.

Methods

3D reconstruction of a mildly stenosed coronary artery was carried out based on a combination of biplane angiography and intravascular ultrasound. Finite element method computations were performed to simulate the deployment of a stent inside the reconstructed coronary artery model at inflation pressure of 1.0 MPa. Strut thickness of the stent was varied to investigate stresses in the stent and the vessel wall.

Results

Deformed configurations, pressure-lumen area relationship and stress distribution in the arterial wall and stent struts were studied. The simulations show how the stent pushes the arterial wall towards the outside allowing the expansion of the occluded artery. Higher stresses in the arterial wall are present behind the stent struts and in regions where the arterial wall was thin. Values of 200 MPa for the peak stresses in the stent strut were detected near the connecting parts between the stent struts, and they were only just below the fatigue stress. Decreasing strut thickness might reduce arterial damage without increasing stresses in the struts significantly.

Conclusion

The method presented in this paper can be used to predict stresses in the stent struts and the vessel wall, and thus evaluate whether a specific stent design is optimal for a specific patient.