Circulation. 2002;105:297-303
doi: 10.1161/hc0302.102610
doi: 10.1161/hc0302.102610
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(Circulation. 2002;105:297.)
© 2002 American Heart Association, Inc.
Clinical Investigation and Reports |
Morphological Predictors of Arterial Remodeling in Coronary Atherosclerosis
From the Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC.
Correspondence to Renu Virmani, MD, Chairperson, Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC 20306-6000. E-mail virmani{at}afip.osd.mil
Background— Although arterial remodeling in atherosclerotic arteries affects luminal patency, the role of plaque components has not been systematically studied.
Methods and Results— Coronary segments (n=2885) were harvested from the hearts of 36 patients who died of severe coronary artery disease after perfusion fixation. Remodeling was determined by morphometric analysis of 657 sections selected as reference segments and 1318 segments with atheromatous plaques. Atherosclerotic plaques were identified as fibroatheroma, thin-cap fibroatheroma, intraplaque hemorrhage with or without rupture or erosion, or total occlusion. Plaque components consisted of calcification, lipid core, macrophage burden, and fibrosis. There was no correlation between plaque area and lumen size in proximal arteries, unlike middle and distal segments, which demonstrated a significant correlation. Marked expansion of the internal elastic lamina (IEL) occurred in plaque hemorrhages with or without and thin-cap fibroatheroma (vulnerable plaque), whereas in erosions and total occlusions there was shrinkage of the IEL. Macrophage burden, lipid core size, calcium (in fibrous plaque and lipid core), and medial atrophy were all associated with positive remodeling; fibrous areas, however, were negatively associated with remodeling.
Conclusions— Inflammation, calcification, and medial thinning are primary determinants of positive remodeling, which appears to be a feature of plaque instability.
Key Words: remodeling • coronary disease • thrombosis • inflammation • atherosclerosis
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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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 L. S. Babiarz, D. M. Yousem, B. A. Wasserman, C. Wu, W. Bilker, and N. J. Beauchamp Jr. Cavernous Carotid Artery Calcification and White Matter Ischemia AJNR Am. J. Neuroradiol., May 1, 2003; 24(5): 872 - 877. [Abstract] [Full Text] [PDF]
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F. Bea, E. Blessing, B. Bennett, M. Levitz, E. P. Wallace, and M. E. Rosenfeld Simvastatin Promotes Atherosclerotic Plaque Stability in ApoE-Deficient Mice Independently of Lipid Lowering Arterioscler Thromb Vasc Biol, November 1, 2002; 22(11): 1832 - 1837. [Abstract] [Full Text] [PDF]
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W. Y. Kim, M. Stuber, P. Bornert, K. V. Kissinger, W. J. Manning, and R. M. Botnar Three-Dimensional Black-Blood Cardiac Magnetic Resonance Coronary Vessel Wall Imaging Detects Positive Arterial Remodeling in Patients With Nonsignificant Coronary Artery Disease Circulation, July 16, 2002; 106(3): 296 - 299. [Abstract] [Full Text] [PDF]
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P. Schoenhagen and S. Nissen Understanding coronary artery disease: tomographic imaging with intravascular ultrasound Heart, July 1, 2002; 88(1): 91 - 96. [Full Text] [PDF]
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P. R. Moreno, K. R. Purushothaman, V. Fuster, and W. N. O'Connor Intimomedial Interface Damage and Adventitial Inflammation Is Increased Beneath Disrupted Atherosclerosis in the Aorta: Implications for Plaque Vulnerability Circulation, May 28, 2002; 105(21): 2504 - 2511. [Abstract] [Full Text] [PDF]
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