Research Papers

Finite Element Analysis of the Implantation of a Self-Expanding Stent: Impact of Lesion Calcification

[+] Author and Article Information
Shijia Zhao

Department of Mechanical and Materials Engineering,  University of Nebraska-Lincoln, Lincoln, NE 68588-0656

Linxia Gu1

Department of Mechanical and Materials Engineering,  University of Nebraska-Lincoln, Lincoln, NE 68588-0656; Nebraska Center for Materials and Nanoscience, Lincoln, NE 68588-0656lgu2@unl.edu

Stacey R. Froemming

Hybrid Catheterization and Electrophysiology Laboratory, Children’s Hospital and Medical Center, Omaha, NE 68114-4133


Corresponding author.

J. Med. Devices 6(2), 021001 (Apr 06, 2012) (6 pages) doi:10.1115/1.4006357 History: Received January 11, 2011; Revised February 18, 2012; Published April 05, 2012; Online April 06, 2012

In this work, the deployment of a self-expanding stent in a stenosed artery was evaluated through finite element analysis. The three-layered structure of the artery and their material properties were measured and implemented in our computational models. The instant outcomes, including lumen gain, tissue prolapse, and stress distribution, were quantified, and the effect of plaque calcification was evaluated. Results showed that the peak wall stress occurred on the media layer regardless of plaque calcification. The calcified plaque mitigated the tissue prolapse and arterial wall stresses in general, compared with the soft plaque. However, the lesion calcification led to a more severe residual stenosis, dogboning effect, and corresponding edge stress concentrations after stenting, which requires pre- and/or post-surgical management.

Copyright © 2012 by American Society of Mechanical Engineers
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Figure 1

Computational model of a GPSTM stent, confined inside a sheath, inside a stenosed artery (top), photos of the GPSTM stent loaded in the tip of catheter and then self-expanded after the sheath removal (bottom)

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Figure 2

The stress-driven superelastic behavior of Nitinol

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Figure 3

Stress-stretch relationships for both artery and plaque

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Figure 4

The stented artery with soft plaque (cut view)

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Figure 5

The peak tissue prolapse distribution (top) located at central region of the plaque, and the cross section view (bottom)

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Figure 6

Stent induced maximum principal stress map on the intima (top), media (middle), and adventitia (bottom) layer of the artery with soft plaque (left) and calcified one (right)




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