Research Papers

Quantifying Effect of Intraplaque Hemorrhage on Critical Plaque Wall Stress in Human Atherosclerotic Plaques Using Three-Dimensional Fluid-Structure Interaction Models

[+] Author and Article Information
Xueying Huang

School of Mathematical Sciences,
Xiamen University,
Xiamen, Fujian 361005, P. R. C.;
Mathematical Sciences Department,
Worcester Polytechnic Institute,
Worcester, MA 01609
e-mail: xhuang@xmu.edu.cn

Chun Yang

Mathematical Sciences Department,
Worcester Polytechnic Institute,
Worcester, MA 01609;
School of Mathematics,
Beijing Normal University, Beijing 100875, P. R. C.

Gador Canton

Department of Mechanical Engineering,
University of Washington,
Seattle, WA 98195

Chun Yuan

Deparment of Radiology,
University of Washington,
Seattle, WA 98195

Dalin Tang

Life Science and Biomedical Engineering Institute,
Southeast University,
Nanjing, Jiangsu 210096, P. R. C.;
Mathematical Sciences Department,
Worcester Polytechnic Institute,
Worcester, MA 01609

1Corresponding author. Present address: School of Mathematical Sciences, Xiamen University, Xiamen, Fujian 361005, P. R. C.

Contributed by the Bioengineering Division of ASME for publication in the JOURNAL OF BIOMECHANICAL ENGINEERING Manuscript received June 13, 2012; final manuscript received October 8, 2012; accepted manuscript posted October 25, 2012; published online November 27, 2012. Assoc. Editor: Ender A. Finol.

J Biomech Eng 134(12), 121004 (Nov 27, 2012) (9 pages) doi:10.1115/1.4007954 History: Received June 13, 2012; Revised October 08, 2012; Accepted October 25, 2012

Recent magnetic resonance studies have indicated that intraplaque hemorrhage (IPH) may accelerate plaque progression and play an important role in plaque destabilization. However, the impact of hemorrhage on critical plaque wall stress (CPWS) and strain (CPWSn) has yet to be determined. The objective of this study was to assess the effect of the presence and size of IPH on wall mechanics. The magnetic resonance image (MRI) of one patient with histology-confirmed IPH was used to build eight 3D fluid-structure interaction (FSI) models by altering the dimensions of the existing IPH. As a secondary end point, the combined effect of IPH and fibrous cap thickness (FCT) was assessed. A volume curve fitting method (VCFM) was applied to generate a mesh that would guarantee numerical convergence. Plaque wall stress (PWS), strain (PWSn), and flow shear stress (FSS) were extracted from all nodal points on the lumen surface for analysis. Keeping other conditions unchanged, the presence of intraplaque hemorrhage caused a significant increase (27.5%) in CPWS; reduced FCT caused an increase of 22.6% of CPWS. Similar results were found for CPWSn. Furthermore, combination of IPH presence, reduced FCT, and increased IPH volume caused an 85% and 75% increase in CPWS and CPWSn, respectively. These results show that intraplaque hemorrhage has considerable impact on plaque stress and strain conditions and accurate quantification of IPH could lead to more accurate assessment of plaque vulnerability. Large-scale studies are needed to further validate our findings.

Copyright © 2012 by ASME
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Fig. 1

TOF, PD, and T1-weighted MR images of a human carotid plaque sample with hemorrhage validated by histology

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Fig. 2

PD-weighted MR images and segmented contour plots showing Hemorrhage. (a) in vivo MR-images, (b) segmented contour plots showing plaque components, and (c) 3D geometry showing hemorrhage and other components.

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Fig. 3

Material curves and pressure conditions used in the multicomponent plaque model. (a) Material curves derived from the modified Mooney–Rivlin model; (b) Pressure conditions specified at the inlet (CCA) and outlet (ICA and ECA).

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Fig. 4

Component-fitting mesh-generation process. (a) Segmented contour data showing the components, (b) created lines connecting data points and dividing the slice into component-fitting areas, (c) two types of volumes to curve-fit components and complex geometry, and (d) component-fitting volumes formed by connection corresponding areas from stacking adjacent slices.

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Fig. 5

Illustration of the preshrink process to match in vivo MRI images: (a) segmented in vivo contour of Slice 7 (ICA), (b) the no-load contour after 8% shrinking in lumen and 4% expanding in outer-boundary (the expansion of outer-boundary was needed because the vessel was shortened), and (c) contour after stretch and pressurization

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Fig. 6

Schematic drawing demonstrating the method for reducing the fibrous cap thickness. (a) Original image and (b) plaque with reduced fibrous cap thickness.

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Fig. 7

Schematic drawing demonstrating the node-type assignment method for nodal point on lumen surfaces. Zone 1 and 3: Lipid nodes; Zone 2: Hemorrhage nodes; Zone 4: Normal Wall nodes.

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Fig. 8

Band plots of plaque wall stress (maximum principle stress) and flow maximum shear stress. (a) Wall stress on stacked cross-section slices, (b) wall stress on bifurcation cut surface, and (c) flow shear stress on bifurcation cut surface.

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Fig. 9

Comparison of PWS on slice 4 and slice 7 showing critical point from the models with lipid, fresh hemorrhage, the model where Lipid was replaced by fresh hemorrhage, and chronic hemorrhage




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