Published online before print December 12, 2002, doi: 10.1161/01.ATV.0000051387.70962.79
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© 2003 American Heart Association, Inc.
Atherosclerosis and Lipoproteins |
Expansive Remodeling Is a Response of the Plaque-Related Vessel Wall in Aortic Roots of ApoE-Deficient Mice
An Experiment of Nature
From the Department of Cardiology (J.F.B., E.F.), Skejby University Hospital, Aarhus, Denmark; the Experimental Cardiology Laboratory (G.P.), Heart Lung Institute, Utrecht University Medical Center, and the Interuniversity Cardiology Institute of the Netherlands (G.P.), Utrecht, the Netherlands.
Correspondence to Jacob F. Bentzon, Department of Cardiology, Research Unit, Skejby University Hospital, Brendstrupgaardsvej, Aarhus, Denmark. E-mail jab{at}studmed.au.dk
Objective— In the present study, we (1) evaluated the apolipoprotein E–deficient (apoE-/-) mouse aortic root as a model for expansive remodeling in atherosclerosis and (2) examined whether remodeling at this site was due to dilation of the vessel wall beneath or flanking the plaque.
Methods and Results— Plaque area and length of the internal elastic lamina (IEL) were measured in aortic roots of apoE-/- mice at 11 weeks, 6 months, and 13 months of age. Expansive remodeling, indicated by IEL lengthening exceeding that of normal growth in wild-type C57BL/6 mice, was evident at 6 months of age and showed overcompensation (luminal enlargement) by 13 months of age. When the left coronary (LC), right coronary (RC), and noncoronary (NC) sinuses of the aortic root were looked at individually, remodeling was located to the LC at 6 months of age and to the LC and RC at 13 months of age. The remodeling response was closely related to local plaque area but unrelated to plaque formation in flanking sinuses.
Conclusions— The aortic root of the apoE-/- mouse features a consistent remodeling response. In this model, expansive remodeling was a strictly local response of the plaque-related vessel wall.
Key Words: atherosclerosis • remodeling • apolipoprotein E–deficient mice • animal model • media degeneration
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