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Research Papers

Hydrodynamic Effects of Compliance Mismatch in Stented Arteries

[+] Author and Article Information
N. K. C. Selvarasu, Pavlos P. Vlachos

Department of Mechanical Engineering, Virginia Polytechnic Institute and State University, 114-I Randolph Hall, Mail Code 0238, Blacksburg, VA 24061

Danesh K. Tafti1

Department of Mechanical Engineering, Virginia Polytechnic Institute and State University, 114-I Randolph Hall, Mail Code 0238, Blacksburg, VA 24061dtafti@vt.edu

1

Corresponding author.

J Biomech Eng 133(2), 021008 (Jan 31, 2011) (11 pages) doi:10.1115/1.4003319 History: Received May 31, 2010; Revised November 24, 2010; Posted December 22, 2010; Published January 31, 2011; Online January 31, 2011

Cardiovascular diseases are the number one cause of death in the world, making the understanding of hemodynamics and development of treatment options imperative. The most common modality for treatment of occlusive coronary artery diseases is the use of stents. Stent design profoundly influences the postprocedural hemodynamic and solid mechanical environment of the stented artery. However, despite their wide acceptance, the incidence of stent late restenosis is still high (Zwart, 2010, “Coronary Stent Thrombosis in the Current Era: Challenges and Opportunities for Treatment,” Current Treatment Options in Cardiovascular Medicine, 12(1), pp. 46–57), and it is most prevailing at the proximal and distal ends of the stent. In this work, we focus our investigation on the localized hemodynamic effects of compliance mismatch due to the presence of a stent in an artery. The compliance mismatch in a stented artery is maximized at the proximal and distal ends of the stent. Hence, it is our objective to understand and reveal the mechanism by which changes in compliance contribute to the generation of nonphysiological wall shear stress (WSS). Such adverse hemodynamic conditions could have an effect on the onset of restenosis. Three-dimensional, spatiotemporally resolved computational fluid dynamics simulations of pulsatile flow with fluid-structure interaction were carried out for a simplified coronary artery with physiologically relevant flow parameters. A model with uniform elastic modulus is used as the baseline control case. In order to study the effect of compliance variation on local hemodynamics, this baseline model is compared with models where the elastic modulus was increased by two-, five-, and tenfold in the middle of the vessel. The simulations provided detailed information regarding the recirculation zone dynamics formed during flow reversals. The results suggest that discontinuities in compliance cause critical changes in local hemodynamics, namely, altering the local pressure and velocity gradients. The change in pressure gradient at the discontinuity was as high as 90%. The corresponding changes in WSS and oscillatory shear index calculated were 9% and 15%, respectively. We demonstrate that these changes are attributed to the physical mechanism associating the pressure gradient discontinuities to the production of vorticity (vorticity flux) due to the presence of the stent. The pressure gradient discontinuities and augmented vorticity flux are affecting the wall shear stresses. As a result, this work reveals how compliance variations act to modify the near wall hemodynamics of stented arteries.

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Copyright © 2011 by American Society of Mechanical Engineers
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Figures

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Figure 1

(a) Applied coronary artery inlet velocity and outlet pressure waveforms with the region of interest (ROI) indicated. (b) Change in compliance due to stent effects that are applied to the stented cases as compared with the unstented baseline case. The velocity and pressure shown are normalized using a∗ω∗ and ρ(a∗ω∗)2 as the characteristic scales, respectively.

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Figure 2

Flow field evolution at the distal end located at 2.8 units, starting from T=5.768 for the unstented vessel: (a) T=5.768, (b) T=5.798, (c) T=5.818, (d) T=5.828, (e) T=5.858, and (f) T=5.888

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Figure 3

Flow field evolution at the distal end located at 2.8 units, starting from T=5.768 for the stented vessel with Es/Eus=10.0: (a) T=5.768, (b) T=5.798, (c) T=5.818, (d) T=5.828, (e) T=5.858, and (f) T=5.888

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Figure 4

(a) Percentage change in time-averaged WSS with respect to the unstented vessel, (b) percentage change in OSI of the stented vessel with respect to the unstented vessel, and (c) gradient of shear stress ratio versus axial distance at different times when the velocity peaks

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Figure 5

(a) Percentage change in pressure and (b) change in pressure gradient between the stented vessel and the unstented vessel

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Figure 6

(a) Time-averaged vorticity flux density ratio versus axial distance and (b) time-averaged vorticity change near wall with respect to the stented and unstented vessels

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Figure 7

(a) Time-averaged peak pressure gradient difference at the proximal end versus stent stiffness ratio and (b) peak pressure gradient difference at the proximal end versus stent authority. The pressure gradient shown is normalized using ρa∗(ω∗)2 as the characteristic scale.

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Figure 9

(a) Comparison of analytical solution due to Womersley and the current numerical solution at T=0.000, 1.884, 3.768, and 5.652 time units. (b) Comparison of analytical solution due to Zamir (41) and the current numerical solution at T=0.000, 1.884, and 5.652 time units. The symbols are due to the analytical solution and the solid lines are due to the current numerical solution. The velocity is normalized using a∗ω∗ as the characteristic scale.

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Figure 8

Variation of intimal thickness based on histological measurements due to Vernhet (32) in ten animals and the absolute percentage change in WSS from the present study. Both the plots are normalized by the maximum value, which occurs at the proximal location.

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