WJM  Vol.2 No.4 , August 2012
The Effect of Carotid Plaque Morphology on Longitudinal Fibrous Cap Stress Levels
ABSTRACT
Background and Purpose: Rupture of vulnerable carotid atherosclerotic plaques is a major cause of stroke. Stress levels may reflect risk of rupture in patients with carotid atherosclerotic plaques. Features thought to influence the risk of plaque rupture include the degree of stenosis, lipid-rich necrotic core (LR-NC) size, and thickness of the protective fibrous caps. We used computational models to investigate the effect of these variables on fibrous cap stress levels. Methods: Two-way coupled fluid-structure interaction longitudinal 2D simulations were performed on a bifurcation model based on idealized geometry derived from a symptomatic patient. Models with varying degrees of stenosis (50%-95%), fibrous cap thicknesses (0.05-1 mm), and LR-NC sizes (2 × 1 mm-6 × 3 mm) were simulated. The stress distribution for each model was calculated and peak principal stresses extracted. Regression analysis was used for assessing the relationship between the variables and stress levels. Results: Mechanical stresses increased with decreasing fibrous cap thicknesses ( β= -0.905, p < 0.001) and increasing LR-NC sizes (β = 0.262, p < 0.001). The degree of steno-sis (β = 0.024, p = 0.344) and LR-NC placement (ß = -0.001, p = 0.979) had insignificant effects on mechanical stress levels. Conclusions: Thin-capped plaques with large atheromas, known predictors of plaque vulnerability, were shown to exhibit the greatest mechanical stress levels.

Cite this paper
nullS. Thrysoe, A. Stegmann, N. Eldrup, A. Klærke, W. Paaske, W. Kim and J. Nygaard, "The Effect of Carotid Plaque Morphology on Longitudinal Fibrous Cap Stress Levels," World Journal of Mechanics, Vol. 2 No. 4, 2012, pp. 216-223. doi: 10.4236/wjm.2012.24026.
References
[1]   G. C. Cheng, H. M. Loree, R. D. Kamm, M. C. Fishbein, and R. T. Lee, “Distribution of Circumferential Stress in Ruptured and Stable Atherosclerotic Lesions,” A structural analysis with histopathological correlation,” Circulation, Vol. 87, No. 4, 1993, pp. 1179-1187. doi:10.1161/01.CIR.87.4.1179

[2]   D. Lloyd-Jones, R. J. Adams, T. M. Brown, M. Carnethon, S. Dai, et al., “Heart Disease and Stroke Statistics—2010 Update: A Report from the American Heart Association,” Circulation, Vol. 121, No. 7, 2010, pp. e46e215. doi:10.1161/CIRCULATIONAHA.109.192667

[3]   Z.-Y. Li, S. P. S. Howarth and J. H. Gillard, “How Critical is Fibrous Cap Thickness to Carotid Plaque Stability? A Flow-Plaque Interaction Model,” Stroke, Vol. 37, No. 5, 2006, pp. 1195-1199. doi:10.1161/01.STR.0000217331.61083.3b

[4]   Z.-Y. Li, S. P. S. Howarth, M. J. Graves, J. U-King-Im, et al., “Structural Analysis and Magnetic Resonance Imaging Predict Plaque Vulnerability: A Study Comparing Symptomatic and Asymptomatic Individuals,” Journal of Vascular Surgery, Vol. 45, No. 4, 2007, pp. 768-775. doi:10.1016/j.jvs.2006.12.065

[5]   C. Yuan and W. S. Kerwin, “MRI of Atherosclerosis,” Journal of Magnetic Resonance Imaging, Vol. 19, No. 6, 2004, pp. 710-719. doi:10.1002/jmri.20070

[6]   H. J. Barnett, D. W. Taylor, M. Eliasziw, A. J. Fox, G. G. Ferguson, et al., “Benefit of Carotid Endarterectomy in Patients with Symptomatic Moderate or Severe Stenosis,” North American Symptomatic Carotid Endarterectomy Trial Collaborators. The New England Journal of Medicine, Vol. 339, No. 20, 1998, pp. 1415-1425. doi:10.1056/NEJM199811123392002

[7]   L. A. Crowe, J. Keegan, P. D. Gatehouse, R. H. Mohiaddin, A. Varghese, et al., “3D Volume-Selective Turbo Spin Echo for Carotid Artery Wall Imaging with Navigator Detection of Swallowing,” Journal of Magnetic Resonance Imaging, Vol. 22, No. 4, 2005, pp. 583-588. doi:10.1002/jmri.20424

[8]   ECST, “Randomised Trial of Endarterectomy for Recently Symptomatic Carotid Stenosis: Final Results of the MRC European Carotid Surgery Trial (ECST),” Lancet, Vol. 351, No. 9113, 1998, pp. 1379-1387. doi:10.1016/S0140-6736(97)09292-1

[9]   V. L. Yarnykh, M. Terashima, C. E. Hayes, A. Shimakawa, N. Takaya, et al., “Multicontrast Black-Blood MRI of Carotid Arteries: Comparison between 1.5 and 3 Tesla Magnetic Field Strengths,” Journal of Magnetic Resonance Imaging, Vol. 23, No. 5, 2006, pp. 691-698. doi:10.1002/jmri.20562

[10]   M. Titi, C. George, D. Bhattacharya, A. Rahi, P. Woodhead, et al., “Comparison of Carotid Doppler Ultrasound and Computerised Tomographic Angiography in the Evaluation of Carotid Artery Stenosis,” Surgeon, Vol. 5, No. 3, 2007, pp. 132-136. doi:10.1016/S1479-666X(07)80039-4

[11]   I. Koktzoglou and D. Li, “Submillimeter Isotropic Resolution Carotid Wall MRI with Swallowing Compensation: Imaging Results and Semiautomated Wall Morphometry,” Journal of Magnetic Resonance Imaging, Vol. 25, No. 4, 2007, pp. 815-823. doi:10.1002/jmri.20849

[12]   S. Glagov, E. Weisenberg, C. K. Zarins, R. Stankunavicius and G. J. Kolettis, “Compensatory Enlargement of Human Atherosclerotic Coronary Arteries,” The New England Journal of Medicine, Vol. 316, No. 22, 1987, pp. 1371-1375. doi:10.1056/NEJM198705283162204

[13]   M. Naghavi, P. Libby, E. Falk, S. Casscells, S. Litovsky, et al., “From Vulnerable Plaque to Vulnerable Patient: A Call for New Definitions and Risk Assessment Strategies: Part I,” Circulation, Vol. 108, No. 14, 2003, pp. 16641672. doi:10.1161/01.CIR.0000087480.94275.97

[14]   I. Sipahi, E. Tuzcu, K. Moon, S. Nicholls, P. Schoenhagen, et al., “Does the Extent and Direction of Arterial Remodeling Predict Subsequent Progression of Coronary Atherosclerosis? A Serial Intravascular Ultrasound Study,” Heart (British Cardiac Society), Vol. 94, No. 5, 2007, pp. 623-627

[15]   A. H. Chau, R. C. Chan, M. Shishkov, B. MacNeill, N. Iftimia, et al., “Mechanical Analysis of Atherosclerotic Plaques Based on Optical Coherence Tomography,” Annals of Biomedical Engineering, Vol. 32, No. 11, 2004, pp. 1494-1503. doi:10.1114/B:ABME.0000049034.75368.4a

[16]   D. Tang, C. Yang, J. Zheng, P. K. Woodard, G. A. Sicard, et al., “3D MRI-Based Multicomponent FSI Models for Atherosclerotic Plaques,” Annals of Biomedical Engineering, Vol. 32, No. 7, 2004, pp. 947-960. doi:10.1023/B:ABME.0000032457.10191.e0

[17]   S. A. Kock, J. V. Nygaard, N. Eldrup, E.-T. Fründ, A. Klaerke, et al., “Mechanical Stresses in Carotid Plaques Using MRI-Based Fluid-Structure Interaction Models,” Journal of Biomechanics, Vol. 41, No. 8, 2008, pp. 16511658. doi:10.1016/j.jbiomech.2008.03.019

[18]   S. A. Thrys?e, M. Oikawa, C. Yuan, N. Eldrup, A. Klaerke, et al., “Longitudinal Distribution of Mechanical Stresses in Carotid Plaques of Symptomatic Patients,” Stroke, Vol. 41, No. 5, 2010, pp. 1041-1043. doi:10.1161/STROKEAHA.109.571588

[19]   H. C. Groen, L. Simons, Q. J. A. van den Bouwhuijsen, E. M. H. Bosboom, F. J. H. Gijsen, et al., “MRI-Based Quantification of Outflow Boundary Conditions for Computational Fluid Dynamics of Stenosed Human Carotid Arteries,” Journal of Biomechanics, Vol. 43, No. 12, 2010, pp. 2332-2338. doi:10.1016/j.jbiomech.2010.04.039

[20]   S. Lee and D. Steinman, “On the Relative Importance of Rheology for Image-Based CFD Models of the Carotid Bifurcation,” Journal of Biomechanical Engineering, Vol. 129, No. 2, 2007, pp. 273-278. doi:10.1115/1.2540836

[21]   J. Donea and S. Giuliani, “An Arbitrary Lagrangian-Eulerian Finite Element Method for Transient Dynamic Fluid-Structure Interactions,” Computer Methods in Applied Mechanics and Engineering, Vol. 33, No. 1-3, 1982, pp. 689-723. doi:10.1016/0045-7825(82)90128-1

[22]   J. N. Redgrave, P. Gallagher, J. K. Lovett and P. M. Rothwell, “Critical Cap Thickness and Rupture in Symptomatic Carotid Plaques: The Oxford Plaque Study,” Stroke, Vol. 39, No. 6, 2008, pp. 1722-1729. doi:10.1161/STROKEAHA.107.507988

[23]   P. M. Rothwell, M. Eliasziw, S. A. Gutnikov, A. J. Fox, D. W. Taylor, et al., “Analysis of Pooled Data from the Randomised Controlled Trials of Endarterectomy for Symptomatic Carotid Stenosis,” Lancet, Vol. 361, No. 9352, 2003, pp. 107-116. doi:10.1016/S0140-6736(03)12228-3

[24]   R. Virmani, F. Kolodgie, A. Burke, A. Finn, H. Gold, et al., “Atherosclerotic Plaque Progression and Vulnerability to Rupture: Angiogenesis as a Source of Intraplaque Hemorrhage,” Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 25, No. 10, 2005, pp. 2054-2061. doi:10.1161/01.ATV.0000178991.71605.18

[25]   M. Gronholdt, S. Ager-Pedersen and E. Falk, “Coronary Atherosclerosis: Determinants of Plaque Rupture,” European Heart Journal, Vol. 19, Suppl. C, 1998, pp. C24C29.

[26]   E. Falk, “Why Do Plaques Rupture?” Circulation, Vol. 86, No. 6, 1992, pp. III30-III42.

[27]   S. Z. Zhao, B. Ariff, Q. Long, A. D. Hughes, S. A. Thom, et al., “Inter-Individual Variations in Wall Shear Stress and Mechanical Stress Distributions at the Carotid Artery Bifurcation of Healthy Humans,” Journal of Biomechanics, Vol. 35, No. 10, 2002, pp. 1367-1377. doi:10.1016/S0021-9290(02)00185-9

[28]   A. Fernandez-Ortiz, J. J. Badimon, E. Falk, V. Fuster, B. Meyer, et al., “Characterization of the Relative Thrombogenicity of Atherosclerotic Plaque Components: Implications for Consequences of Plaque Rupture,” Journal of the American College of Cardiology, Vol. 23, No. 7, 1994, pp. 1562-1569. doi:10.1016/0735-1097(94)90657-2

[29]   G. Avril, M. Batt, R. Guidoin, M. Marois, R. HassenKhodja, et al., “Carotid Endarterectomy Plaques: Correlations of Clinical and Anatomic Findings,” Annals of Vascular Surgery, Vol. 5, No. 1, 1991, pp. 50-54. doi:10.1007/BF02021778

[30]   J. K. Lovett and P. M. Rothwell, “Site of Carotid Plaque Ulceration in Relation to Direction of Blood Flow: An Angiographic and Pathological Study,” Cerebrovascular Diseases, Vol. 16, No. 4, 2003, pp. 369-375. doi:10.1159/000072559

 
 
Top