Circulation. 2002;105:939-943
Published online before print January 28, 2002, doi: 10.1161/hc0802.104327
Published online before print January 28, 2002, doi: 10.1161/hc0802.104327
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(Circulation. 2002;105:939.)
© 2002 American Heart Association, Inc.
Clinical Investigation and Reports |
Relationship Between Coronary Artery Remodeling and Plaque Vulnerability
From the Department of Cardiology, London Chest Hospital (A.M.V., P.G.M.), and the British Heart Foundation Department of Cardiovascular Pathology (M.J.D.), St George’s Hospital Medical School, London, UK.
Correspondence to Dr A. Varnava, Department of Cardiology, London Chest Hospital, Bonner Road, London E29JX, UK. E-mail avarnava{at}sghms.ac.uk
Background— In vivo studies with intravascular ultrasound have shown that complex plaque anatomy and plaque rupture are more frequent in the presence of marked outward remodeling. A large lipid core and a high macrophage count are recognized histological markers for plaque vulnerability. The link between plaque vulnerability in terms of these markers and remodeling in coronary arteries has not been explored.
Methods and Results— In 88 male subjects who died suddenly with coronary artery disease, 108 plaques were studied. The percent remodeling was calculated. Lesions with remodeling 
0% were considered to have positive remodeling, and those in which remodeling was <0% were considered to have negative remodeling. Percent lipid core and macrophage count at the plaque were assessed. Of 108 plaque sites, 64 (59.2%) had undergone no remodeling or positive remodeling, and 44 (40.7%) had negative remodeling (vessel shrinkage). Lesions with positive remodeling, compared with lesions with vessel shrinkage, had a larger lipid core (percent mean lipid core was 39.0±21.0% versus 22.3±23.1%, respectively; P<0.0001) and a higher macrophage count (mean macrophage count was 15.6±12.3 versus 8.9±11.6, respectively; P=0.005).
Conclusions— We have shown that coronary artery plaques with positive remodeling have a higher lipid content and macrophage count, both markers of plaque vulnerability. These results may explain why plaque rupture is often apparent at sites with only modest luminal stenoses (but marked positive remodeling).
Key Words: coronary disease • remodeling • plaque
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B. D. MacNeill, H. C. Lowe, M. Takano, V. Fuster, and I.-K. Jang Intravascular Modalities for Detection of Vulnerable Plaque: Current Status Arterioscler Thromb Vasc Biol, August 1, 2003; 23(8): 1333 - 1342. [Abstract] [Full Text] [PDF]
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P. H. Stone, A. U. Coskun, S. Kinlay, M. E. Clark, M. Sonka, A. Wahle, O. J. Ilegbusi, Y. Yeghiazarians, J. J. Popma, J. Orav, et al. Effect of Endothelial Shear Stress on the Progression of Coronary Artery Disease, Vascular Remodeling, and In-Stent Restenosis in Humans: In Vivo 6-Month Follow-Up Study Circulation, July 29, 2003; 108(4): 438 - 444. [Abstract] [Full Text] [PDF]
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J. J. Wentzel, E. Janssen, J. Vos, J. C.H. Schuurbiers, R. Krams, P. W. Serruys, P. J. de Feyter, and C. J. Slager Extension of Increased Atherosclerotic Wall Thickness Into High Shear Stress Regions Is Associated With Loss of Compensatory Remodeling Circulation, July 8, 2003; 108(1): 17 - 23. [Abstract] [Full Text] [PDF]
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F. Prati, T. Pawlowski, R. Gil, A. Labellarte, A. Gziut, E. Caradonna, A. Manzoli, A. Pappalardo, F. Burzotta, and A. Boccanelli Stenting of Culprit Lesions in Unstable Angina Leads to a Marked Reduction in Plaque Burden: A Major Role of Plaque Embolization?: A Serial Intravascular Ultrasound Study Circulation, May 13, 2003; 107(18): 2320 - 2325. [Abstract] [Full Text] [PDF]
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J. F. Bentzon, G. Pasterkamp, and E. Falk Expansive Remodeling Is a Response of the Plaque-Related Vessel Wall in Aortic Roots of ApoE-Deficient Mice: An Experiment of Nature Arterioscler Thromb Vasc Biol, February 1, 2003; 23(2): 257 - 262. [Abstract] [Full Text] [PDF]
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P. Schoenhagen, E. M. Tuzcu, and S. G. Ellis Plaque Vulnerability, Plaque Rupture, and Acute Coronary Syndromes: (Multi)-Focal Manifestation of a Systemic Disease Process Circulation, August 13, 2002; 106(7): 760 - 762. [Full Text] [PDF]
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