Circulation, Vol 87, 1179-1187, Copyright © 1993 by American Heart Association
GC Cheng, HM Loree, RD Kamm, MC Fishbein and RT Lee
BACKGROUND. Although rupture of an atherosclerotic plaque is considered to
be the cause of most acute coronary syndromes, the mechanism of plaque
rupture is controversial. METHODS AND RESULTS. To test the hypothesis that
plaque rupture occurs at sites of high circumferential stress in the
diseased vessel, the distribution of stress was analyzed in 24 coronary
artery lesions. Histological specimens from 12 coronary artery lesions that
caused lethal myocardial infarction were compared with those from 12 stable
control lesions. A finite element model was used to calculate the stress
distributions at a mean intraluminal pressure of 110 mm Hg. The maximum
circumferential stress in plaques that ruptured was significantly higher
than maximum stress in stable specimens (4,091 +/- 1,199 versus 1,444 +/-
485 mm Hg, p < 0.0001). Twelve of 12 ruptured lesions had a total of 31
regions of stress concentration of more than 2,250 mm Hg (mean, 2.6 +/- 1.4
high stress regions per lesion); only one of 12 control lesions had a
single stress concentration region of more than 2,250 mm Hg. In seven of 12
lethal lesions (58%), rupture occurred in the region of maximum
circumferential stress; in 10 of the 12 lethal lesions (83%), rupture
occurred in a region where computed stress was more than 2,250 mm Hg.
CONCLUSIONS. These data suggest that concentrations of circumferential
tensile stress in the atherosclerotic plaque may play an important role in
plaque rupture and myocardial infarction. However, plaque rupture may not
always occur at the region of highest stress, suggesting that local
variations in plaque material properties contribute to plaque rupture.
ARTICLES
Distribution of circumferential stress in ruptured and stable atherosclerotic lesions. A structural analysis with histopathological correlation
Department of Mechanical Engineering, Massachusetts Institute of Technology, Cambridge.
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G. C. Cheng, W. H. Briggs, D. S. Gerson, P. Libby, A. J. Grodzinsky, M. L. Gray, and R. T. Lee Mechanical Strain Tightly Controls Fibroblast Growth Factor-2 Release From Cultured Human Vascular Smooth Muscle Cells Circ. Res., January 1, 1997; 80(1): 28 - 36. [Abstract] [Full Text]
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M. J. Davies Stability and Instability: Two Faces of Coronary Atherosclerosis: The Paul Dudley White Lecture 1995 Circulation, October 15, 1996; 94(8): 2013 - 2020. [Full Text]
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L. Wexler, B. Brundage, J. Crouse, R. Detrano, V. Fuster, J. Maddahi, J. Rumberger, W. Stanford, R. White, and K. Taubert Coronary Artery Calcification: Pathophysiology, Epidemiology, Imaging Methods, and Clinical Implications: A Statement for Health Professionals From the American Heart Association Circulation, September 1, 1996; 94(5): 1175 - 1192. [Full Text]
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R. T. Lee, F. J. Schoen, H. M. Loree, M. W. Lark, and P. Libby Circumferential Stress and Matrix Metalloproteinase 1 in Human Coronary Atherosclerosis: Implications for Plaque Rupture Arterioscler Thromb Vasc Biol, August 1, 1996; 16(8): 1070 - 1073. [Abstract] [Full Text]
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J. A. Ambrose and M. Weinrauch Thrombosis in Ischemic Heart Disease Arch Intern Med, July 8, 1996; 156(13): 1382 - 1394. [Abstract] [PDF]
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N. D. Wong, R. C. Detrano, D. Abrahamson, J. M. Tobis, and J. M. Gardin Coronary Artery Screening by Electron Beam Computed Tomography : Facts, Controversy, and Future Circulation, August 1, 1995; 92(3): 632 - 636. [Full Text]
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E. Falk, P. K. Shah, and V. Fuster Coronary Plaque Disruption Circulation, August 1, 1995; 92(3): 657 - 671. [Full Text]
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D. Recchia, D. R. Abendschein, J. E. Saffitz, and S. A. Wickline The Biologic Behavior of Balloon Hyperinflation–Induced Arterial Lesions in Hypercholesterolemic Pigs Depends on the Presence of Foam Cells Arterioscler Thromb Vasc Biol, July 1, 1995; 15(7): 924 - 929. [Abstract] [Full Text]
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M. O'Rourke Mechanical Principles in Arterial Disease Hypertension, July 1, 1995; 26(1): 2 - 9. [Full Text]
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P. Libby Molecular Bases of the Acute Coronary Syndromes Circulation, June 1, 1995; 91(11): 2844 - 2850. [Full Text]
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G. N. Levine, J. F. Keaney, and J. A. Vita Cholesterol Reduction in Cardiovascular Disease -- Clinical Benefits and Possible Mechanisms N. Engl. J. Med., February 23, 1995; 332(8): 512 - 521. [Full Text] [PDF]
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R. T. Lee, F. Berditchevski, G. C. Cheng, and M. E. Hemler Integrin-Mediated Collagen Matrix Reorganization by Cultured Human Vascular Smooth Muscle Cells Circ. Res., February 1, 1995; 76(2): 209 - 214. [Abstract] [Full Text]
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T. J. Vogl, N. D. Abolmaali, T. Diebold, K. Engelmann, M. Ay, S. Dogan, G. Wimmer-Greinecker, A. Moritz, and C. Herzog Techniques for the Detection of Coronary Atherosclerosis: Multi-detector Row CT Coronary Angiography Radiology, April 1, 2002; 223(1): 212 - 220. [Abstract] [Full Text] [PDF]
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D. Sorescu, D. Weiss, B. Lassegue, R. E. Clempus, K. Szocs, G. P. Sorescu, L. Valppu, M. T. Quinn, J. D. Lambeth, J. D. Vega, et al. Superoxide Production and Expression of Nox Family Proteins in Human Atherosclerosis Circulation, March 26, 2002; 105(12): 1429 - 1435. [Abstract] [Full Text] [PDF]
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