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TECHNICAL PAPERS: Fluids/Heat/Transport

Developing Pulsatile Flow in a Deployed Coronary Stent

[+] Author and Article Information
Divakar Rajamohan, Ashraf A. Ibrahim, Milind A. Jog

Department of Mechanical Engineering,  University of Cincinnati, Cincinnati, OH 45221

Rupak K. Banerjee1

Department of Mechanical Engineering, and Department of Biomedical Engineering,  University of Cincinnati, 688 Rhodes Hall, PO Box 210072, Cincinnati, OH 45221rupak.banerjee@uc.edu

Lloyd H. Back

Jet Propulsion Laboratory,  California Institute of Technology, Pasadena, CA 91109

1

Corresponding author.

J Biomech Eng 128(3), 347-359 (Nov 09, 2005) (13 pages) doi:10.1115/1.2194067 History: Received August 06, 2004; Revised November 09, 2005

A major consequence of stent implantation is restenosis that occurs due to neointimal formation. This patho-physiologic process of tissue growth may not be completely eliminated. Recent evidence suggests that there are several factors such as geometry and size of vessel, and stent design that alter hemodynamic parameters, including local wall shear stress distributions, all of which influence the restenosis process. The present three-dimensional analysis of developing pulsatile flow in a deployed coronary stent quantifies hemodynamic parameters and illustrates the changes in local wall shear stress distributions and their impact on restenosis. The present model evaluates the effect of entrance flow, where the stent is placed at the entrance region of a branched coronary artery. Stent geometry showed a complex three-dimensional variation of wall shear stress distributions within the stented region. Higher order of magnitude of wall shear stress of 530dyncm2 is observed on the surface of cross-link intersections at the entrance of the stent. A low positive wall shear stress of 10dyncm2 and a negative wall shear stress of 10dyncm2 are seen at the immediate upstream and downstream regions of strut intersections, respectively. Modified oscillatory shear index is calculated which showed persistent recirculation at the downstream region of each strut intersection. The portions of the vessel where there is low and negative wall shear stress may represent locations of thrombus formation and platelet accumulation. The present results indicate that the immediate downstream regions of strut intersections are areas highly susceptible to restenosis, whereas a high shear stress at the strut intersection may cause platelet activation and free emboli formation.

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Copyright © 2006 by American Society of Mechanical Engineers
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Figures

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Figure 1

Mesh plot of coronary artery with deployed coronary stent (A) and geometry of the stent struts (B)

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Figure 2

Pulse cycles from basal to hyperemic flows; S-systole, D-diastole (A) and variation of blood viscosity with shear rate (Cho and Kensey (19)) (B)

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Figure 3

Finite volume mesh of stented artery (A) and validation of wall shear stress (B)

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Figure 4

Variation of axial velocity along the radius of artery at intersection 1 and intersection 4 at times of accelerating, peak and decelerating flows

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Figure 5

Variation of axial velocity along the radius of artery at midpoint 1 and midpoint 3 at times of accelerating, peak and decelerating flows

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Figure 6

Temporal variation of axial wall shear stress at strut intersections (I) and midpoints (M)

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Figure 7

Temporal variation of axial wall shear stress at the vertices

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Figure 8

Comparison of arterial wall shear stress between stented wall and smooth wall at peak inlet flow (t=2.0s)

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Figure 9

Axial variation of wall shear stress along the artery wall at times of accelerating, peak and decelerating flows

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Figure 10

Variation of modified oscillatory shear index (MOSI) with flow rate at vertices

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Figure 11

Variation of recirculation length and height along the struts at times of accelerating, peak and decelerating flows

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Figure 12

Contour plot of axial wall shear stress showing the recirculation zones for hyperemic condition (200mL∕min) at times of accelerating, peak and decelerating flows

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Figure 13

Pressure drop along the stent for a pulse cycle (A) and a comparison between a developing time-averaged mean pressure drop for a deployed stent and smooth wall and steady state developing flow in an unstented coronary artery of same size (B)

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