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(Stroke. 2007;38:2379.)
© 2007 American Heart Association, Inc.
Case Report |
From Biomedical Engineering (H.C.G., F.J.H.G., A.F.W.v.d.S., J.J.W.), Erasmus MC, Rotterdam, The Netherlands; Interuniversity Cardiology Institute of the Netherlands (H.C.G., A.F.W.v.d.S., J.J.W.), Utrecht, The Netherlands; Radiology (H.C.G., A.v.d.L.), Erasmus MC, Rotterdam, The Netherlands; and Radiology (M.S.F, C.Y.) and Surgery (T.S.H.), University of Washington, Seattle, Wash.
Correspondence to Jolanda Wentzel, Biomedical Engineering, Biomechanics Laboratory, Ee2322, Erasmus MC, PO Box 2040, 3000 CA Rotterdam, The Netherlands. E-mail j.wentzel{at}erasmusmc.nl
| Abstract |
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Summary of Case— We investigated a serial MRI data set of a 67-year-old woman with a plaque in the carotid artery at baseline and an ulcer at 10-month follow up. The lumen, plaque components (lipid/necrotic core, intraplaque hemorrhage), and ulcer were segmented and the lumen contours at baseline were used for WSS calculation. Correlation of the change in plaque composition with the WSS at baseline showed that the ulcer was generated exclusively at the high WSS location.
Conclusions— In this serial MRI study, we found plaque ulceration at the high WSS location of a protruding plaque in the carotid artery. Our data suggest that high WSS influences plaque vulnerability and therefore may become a potential parameter for predicting future events.
Key Words: carotid artery MRI shear stress ulceration
| Introduction |
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| Materials and Methods |
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MRI
The high-resolution, multisequence MRI protocol at baseline and follow up included 4 sequences: 3-dimensional time of flight, T1, T2, and proton density weightings. The in-plane resolution was 0.3x0.3 mm with a slice thickness of 2 mm. The image segmentation was based on the signal intensities relative to the adjacent sternocleidomastoid muscle. A validated scheme5 of hyper-, iso-, and hypointense signal intensities from the time of flight, T1, T2, and proton density images was used to identify the lumen, plaque components (lipid/necrotic core, intraplaque hemorrhage), and ulcer (Figure 1).
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Computational Fluid Dynamics
In preparation for the WSS calculation, the baseline lumen contours were imported into GAMBIT (Fluent Inc.) from which a 3-dimensional meshed volume was created. At the entrance and exit of the carotid bifurcation, circular segments were added to minimize the influence of the boundary conditions. A static parabolic inflow profile with a peak velocity of 0.6 m/s was chosen to obtain physiological shear stress values (1.2 Pa) at the common carotid artery. FIDAP (Fluent Inc.) was used to compute the flow velocities and WSS distribution by using free outflow for the internal and external arteries; no slip at the wall and blood was simulated as an incompressible Newtonian fluid (viscosity 3.5 mPa/s, density 1050 kg/m3).
Analysis
The segmentations at baseline and follow up were matched using the bifurcation as a marker to align the slices in the superior direction and the center of the lumen in the transversal direction. The slices containing plaque at baseline and/or follow up were selected for further analysis. For each slice, the wall was divided into 256 parts such that each baseline lumen contour was divided into 256 equidistant sections. In each part, the average baseline WSS and the baseline wall component volumes (ie, areaxslice thickness) were calculated using in-house created software. Subsequently, in each part, the volumes of the wall components at follow up were determined.
| Results |
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| Discussion |
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Assumptions were made for calculating the WSS distribution. Although the assumptions could have influenced the absolute WSS, several studies showed that they are of second order of importance. Moreover, we used the distribution rather than the absolute WSS so that the assumptions most likely did not influence the final conclusion of the study.
Intraplaque hemorrhage is known to be involved in plaque progression and cerebral events. The observed intraplaque hemorrhage at baseline could have accelerated the destabilization of the plaque; however, in this case, the site of rupture was precisely at the highest WSS region (Figures 2 and 3
). More patients will be required to confirm this preliminary finding that high WSS is involved in plaque destabilization leading to plaque rupture and to prove the value of this technology in risk prediction.
| Acknowledgments |
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Source of Funding
This study was supported by the Interuniversity Cardiology Institute of the Netherlands (H.C.G.).
Disclosures
None.
Received February 7, 2007; accepted February 28, 2007.
| References |
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2. Malek AM, Alper SL, Izumo S. Hemodynamic shear stress and its role in atherosclerosis. JAMA. 1999; 282: 2035–2042.
3. Slager CJ, Wentzel JJ, Gijsen FJ, Thury A, van der Wal AC, Schaar JA, Serruys PW. The role of shear stress in the destabilization of vulnerable plaques and related therapeutic implications. Nat Clin Pract Cardiovasc Med. 2005; 2: 456–464.[CrossRef][Medline] [Order article via Infotrieve]
4. Chu B, Yuan C, Takaya N, Shewchuk JR, Clowes AW, Hatsukami TS. Images in cardiovascular medicine. Serial high-spatial-resolution, multisequence magnetic resonance imaging studies identify fibrous cap rupture and penetrating ulcer into carotid atherosclerotic plaque. Circulation. 2006; 113: e660–661.
5. Saam T, Ferguson MS, Yarnykh VL, Takaya N, Xu D, Polissar NL, Hatsukami TS, Yuan C. Quantitative evaluation of carotid plaque composition by in vivo MRI. Arterioscler Thromb Vasc Biol. 2005; 25: 234–239.
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