MRI of early- and late-stage arterial remodeling in a low-level cholesterol-fed rabbit model of atherosclerosis

被引:10
作者
Ronald, John A.
Walcarius, Rhonda
Robinson, John F.
Hegele, Robert A.
Rutt, Brian K.
Rogers, Kern A.
机构
[1] Robarts Res Inst, Dept Imaging, London, ON N6A 5K8, Canada
[2] Univ Western Ontario, Dept Med Biophys, London, ON, Canada
[3] Robarts Res Inst, Dept Vasc Biol, London, ON N6A 5C1, Canada
[4] London Hlth Sci Ctr, Dept Radiol, London, ON, Canada
[5] Univ Western Ontario, Dept Med, London, ON, Canada
[6] Univ Western Ontario, Dept Anat & Cell Biol, London, ON, Canada
关键词
rabbit model; low-level cholesterol-feeding; arterial remodeling; MRI;
D O I
10.1002/jmri.21113
中图分类号
R8 [特种医学]; R445 [影像诊断学];
学科分类号
1002 ; 100207 ; 1009 ;
摘要
Purpose: To monitor early- and late-stage arterial remodeling following low-level cholesterol (CH) feeding in rabbits using a standardized MRI protocol. Materials and Methods: New Zealand White rabbits were fed a CH diet (0.25% w/w) (n = 15) or normal chow (n = 6) and imaged either at 0, 2, 6, 8, and 11 months ("early-stage") or 12, 14, 16, 18, and 20 months ("late-stage"). T2-weighted fast-spin-echo images (approximate to 200 mu m in-plane resolution) of aortic lesions were collected using either a 1.5 or 3.0T MR scanner interfaced with a customized surface RF coil. Luminal (LA), outer vessel wall boundary (OVBA), and vessel wall areas (VWA) were assessed. Results: Among CH-fed animals in the early-stage group, increased VWA associated with decreased OVBA and a more pronounced decrease in LA was first detectable at 8 months. These changes became more evident between 8 and 11 months. In the late-stage group, lesions continued to grow in response to CH-feeding, as VWA significantly increased at regular 2-month intervals. Beyond 16 months, signal intensity differences (reflecting increased lesion complexity) within the vessel wall were noted. Conclusion: This often-overlooked rabbit model combined with customized MR technology holds tremendous promise for studying the natural progression, regression, and remodeling of atherosclerotic lesions.
引用
收藏
页码:1010 / 1019
页数:10
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