A parameterized analysis of the mechanical stress for co-ronary plaque fibrous caps

DOI: 10.4236/jbise.2013.612A006   PDF   HTML     2,391 Downloads   3,788 Views   Citations


The fibrous cap is a protective layer of connective tissue that covers the core of an atherosclerotic plaque. The rupture of this layer has been commonly associated with acute myocardial infarctions. The thickness of the fibrous cap, the percentage of stenosed area, and the stiffness of the core were studied (commonly associated with vulnerable plaque characteristics) to quantify their effects on the cap’s mechanical stress state by performing analyses using computational fluid-structure interaction (FSI) methods. The mechanical stress levels are significantly increased within the fibrous cap structure at the upstream side of the plaque. As expected, the highest stresses occurred for a severe stenosis and a thin fibrous cap. Interestingly, a weak structural support such as a soft lipid pool beneath the fibrous cap allowed for the hemodynamic pressure gradient forces to displace the fibrous cap in the direction of the flow, resulting in higher strains and thus higher mechanical stresses in the upstream portion of the plaque cap, potentially increasing the risk of cap rupture. The peak stress behavior of the most critical cases (thin fibrous cap and soft lipid core) at various degrees of stenosis was analyzed. For mid-range stenosis from 43% to 75%, there was a plateau region revealing that mild and moderate plaques were quickly exposed to the high stress condition of severe plaques. In conclusion, the particular combination of a mild to severe stenosis, a thin fibrous cap and a soft lipid core resulted in the highest mechanical stresses calculated at the proximal side of the plaque. Mild and moderate plaques can be subjected to stresses similar to severe plaques, possibly contributing to their rupture.


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Galaz, R. , Pagiatakis, C. , Gaillard, E. and Mongrain, R. (2013) A parameterized analysis of the mechanical stress for co-ronary plaque fibrous caps. Journal of Biomedical Science and Engineering, 6, 38-46. doi: 10.4236/jbise.2013.612A006.

Conflicts of Interest

The authors declare no conflicts of interest.


[1] Kolodgie, F., Virmani, R., Burke, A., Farb, A., Weber, D., Kutys, R., Finn, A. and Gold, H. (2004) Pathologic assess-ment of the vulnerable human coronary plaque. Heart, 90, 1385-1391.
[2] Burke, A., Farb, A., Malcolm, G., Liang, Y., Smialek, J. and Virmani, R. (1997) Coronary risk factors and plaque morphology in patients with coronary disease dying suddenly. New England Journal of Medicine, 336, 1276-1282. http://dx.doi.org/10.1056/NEJM199705013361802
[3] Libby, P. and Theroux P. (2005) Pathophysiology of coro-nary artery disease. Circulation, 111, 3481-3488.
[4] Falk, E. (1989) Morphologic features of unstable atherothrombotic plaques underlying acute coronary syndromes. American Journal of Cardiology, 63, 114E-120E.
[5] Davies, M. (1992) Anatomic features in victims of sudden coronary death. Coronary artery pathology. Circulation, 85, 119-124.
[6] Richardson, P., Davies, M. and Born, G. (1989) Influence of plaque configuration and stress distribution of coronary atherosclerotic plaques. Lancet, 2, 941-944.
[7] Lee, R., Schoen, F., Loree, H., Lark, M. and Libby, P. (1996) Circumferential stress and matrix metalloproteinase-1 in human coronary atherosclerosis: Implications for plaque rupture. Arteriosclerosis, Thrombosis, and Vascular Biology, 16, 1070-1073.
[8] Finet, G., Ohayon, J. and Rioufol, G. (2004) Biomechanical interaction between cap thickness, lipid core composition and blood pressure in vulnerable coronary plaque: Impact on stability or instability. Coronary Artery Disease, 15, 13-20.
[9] Williamson, S., Lam, Y., Younis, H., Patel, S., Kaazempur-Mofrad, M. and Kamm, R. (2003) On the sensitivity of wall stresses in diseased arteries to variable material properties. Journal of Biomechanical Engineering, 125, 147-155. http://dx.doi.org/10.1115/1.1537736
[10] Lovett, J. and Rothwell, P. (2003) Site of carotid plaque ulceration in relation to direction of blood flow: An angiographic and pathological study. Cerebrovascular Diseases, 16, 369-375. http://dx.doi.org/10.1159/000072559
[11] Li, Z., Howarth, S., Tang, T. and Gillard, J. (2006) How critical is fibrous cap thickness to carotid plaque stability? A flow-plaque interaction model. Stroke, 37, 1195-1199.
[12] Burke, A., Farb, A., Malcom, G.T., Liang, Y.-h, Smialek, J.E. and Virmani, R. (1999) Plaque rupture and sudden death related to exertion in men with coronary artery disease. Journal of the American Medical Association, 281, 921-926. http://dx.doi.org/10.1001/jama.281.10.921
[13] Falk, E., Shah, P. and Fuster, V. (1995) Coronary plaque disruption. Circulation, 92, 657-671.
[14] Mattsson, E., Kohler, T., Vergel, S. and Clowes, A. (1997) Increased blood flow induces regression of intimal hyperplasia. Arteriosclerosis, Thrombosis, and Vascular Biology, 17, 2245-2249.
[15] Wang, J., Normand, S., Mauri, L. and Kuntz, R. (2004) Coronary artery spatial distribution of acute myocardial infarction occlusions. Circulation, 110, 278-284.
[16] Berne, R.M. and Levy, M.N. (1967) Cardiovascular physiology. Mosby, St. Louis.
[17] Tang, D., Yang, C., Zheng, J., Woodard, P.K., Sicard, G.A., Saffitz, J.E. and Yuan, C. (2004) 3D MRI-based multicomponent FSI models for atherosclerotic plaques. Annals of Biomedical Engineering, 32, 947-960.
[18] Virmani, R., Kolodgie, F.D., Burke, A.P., Farb, A. and Schwartz, S.M. (2000) Lessons from sudden coronary death: A comprehensive morphological classification scheme for atherosclerotic lesions. Arteriosclerosis, Thrombosis, and Vascular Biology, 20, 1262-1275.
[19] Cheng, G.C., Loree, H.M., Kamm, R.D., Fishbein, M.C. and Lee, R.T. (1993) Distribution of circumferential stress in ruptured and stable atherosclerotic lesions. A structural analysis with histopathological correlation. Circulation, 87, 1179-1187.
[20] Imoto, K., Hiro, T., Fujii, T., Murashige, A., Fukumoto, Y., Hashimoto, G., Okamura, T., Yamada, J., Mori, K. and Matsuzaki, M. (2005) Longitudinal structural determinants of atherosclerotic plaque vulnerability. A computational analysis of stress distribution using vessel models and three dimensional intravascular ultrasound imaging. Journal of the American College of Cardiology, 46, 1507-1515. http://dx.doi.org/10.1016/j.jacc.2005.06.069
[21] Groen, H.C., Gijsen, F.J.H., van der Lugt, A., Ferguson, M.S., Hatsukami, T.S., van der Steen, A.F., Yuan, C. and Wentzel, J.J. (2007) Plaque rupture in the carotid artery is located at the high shear stress region. A case report. Stroke, 38, 2379-2381.
[22] Fujii, K., Kobayashi, Y., Mintz, G., Takebayashi, H., Dangas, G., Moussa, I., Mehran, R., Lansky, A.J., Kreps, E., Collins, M., Colombo, A., Stone, G.W., Leon, M.B. and Moses, J.W. (2003) Intravascular ultrasound assessment of ulcerated ruptured plaques: A comparison of culprit and nonculprit lesions of 15 patients with acute coronary syndromes and lesions in patients without acute coronary syndromes. Circulation, 108, 2473-2478.
[23] Hiro, T., Fujii, T., Yoshitake, S., Kawabata, T., Yasumoto, K. and Matsuzaki, M. (2000) Longitudinal visualization of spontaneous coronary plaque rupture by 3D intravascular ultrasound. Circulation, 101, e114.
[24] Tang, D., Yang, C., Zheng, J., Woodard, P.K., Saffitz, J.E., Petruccelli, J.D., Sicard, G.A. and Yuan, C. (2005) Local maximal stress hypothesis and computational plaque vulnerability index for atherosclerotic plaque assessment. Annals of Biomedical Engineering, 33, 1789-1801.
[25] Tang, D., Teng, Z., Canton, G., Yang, C., Ferguson, M., Huang, X., Zheng, J., Woodard, P.K. and Yuan, C. (2009) Sites of rupture in human atherosclerotic carotid plaques are associated with high structural stresses: An in vivo MRI-based 3D fluid-structure interaction study. Stroke, 40, 3258-3263.
[26] Lee, R.T., Loree, H.M., Cheng, G.C., Lieberman, E.H., Jaramillo, N. and Schoen, F.J. (1993) Computational structural analysis based on intravascular ultrasound imaging before in vitro angioplasty: Prediction of plaque fracture locations. Journal of the American College of Cardiology, 21, 777-782.
[27] Doriot, P. (2003) Estimation of the supplementary axial wall stress generated at peak flow by an arterial stenosis. Physics in Medicine and Biology, 48, 127-138.
[28] Yang, C., Tang, D., Kobayashi, S., Zheng, J., Woodard, P.K., Teng, Z., Back, R. and Ku, D.N. (2008) Cyclic bending contributes to high stress in human coronary atherosclerotic plaque and rupture risk. Molecular & Cellular Biomechanics, 5, 259-274.
[29] Virmani, R., Burke, A., Farb, A. and Kolodgie, F. (2002) Cardiovascular plaque rupture. Marcel Dekker Publishers Inc., New York.
[30] Loree, H.M., Kamm, R.D., Stringfellow, R.G. and Lee, R.T. (1992) Effects of fibrous cap thickness on peak circumferential stress in model atherosclerotic vessels. Circulation Research, 71, 850-858.

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