ArticleEuropean radiology2008
A rabbit model of atherosclerosis at carotid artery: MRI visualization and histopathological characterization.
Article in European radiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- A novel rabbit model of atherosclerotic vulnerable plaque established by cryofluid-induced endothelial injury.Scientific reports · 2024Article
- Longitudinal effects of common carotid artery stenosis on ocular hemodynamics assessed using laser speckle flowgraphy in a rabbit model.Scientific reports · 2020Article
- Angiotensin II-accelerated vulnerability of carotid plaque in a cholesterol-fed rabbit model-assessed with magnetic resonance imaging comparing to histopathology.Saudi journal of biological sciences · 2017Article
- Non-invasive imaging of carotid arterial restenosis using 3T cardiovascular magnetic resonance.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2014Article
- In vivo serial MR imaging of magnetically labeled endothelial progenitor cells homing to the endothelium injured artery in mice.PloS one · 2011Article
- Developing a rabbit model of neointimal stenosis and atherosclerotic fibrous plaque rupture.The journal of Tehran Heart Center · 2011Article
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Authors and funding
6 authors.
Funding
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Abstract
To induce a rabbit model of atherosclerosis at carotid artery, to visualize the lesion evolution with magnetic resonance imaging (MRI), and to characterize the lesion types by histopathology. Atherosclerosis at the right common carotid artery (RCCA) was induced in 23 rabbits by high-lipid diet following balloon catheter injury to the endothelium. The rabbits were examined in vivo with a 1.5-T MRI and randomly divided into three groups of 6 weeks (n=6), 12 weeks (n=8) and 15 weeks (n=9) for postmortem histopathology. The lesions on both MRI and histology were categorized according to the American Heart Association (AHA) classifications of atherosclerosis. Type I and type II of atherosclerotic changes were detected at week 6, i.e., nearly normal signal intensity (SI) of the injured RCCA wall without stenosis on MRI, but with subendothelial inflammatory infiltration and proliferation of smooth muscle cells on histopathology. At week 12, 75.0% and 62.5% of type III changes were encountered on MRI and histopathology respectively with thicker injured RCCA wall of increased SI on T(1)-weighted and proton density (PD)-weighted MRI and microscopically a higher degree of plaque formation. At week 15, carotid atherosclerosis became more advanced, i.e., type IV and type V in 55.6% and 22.2% of the lesions with MRI and 55.6% and 33.3% of the lesions with histopathology, respectively. Statistical analysis revealed a significant agreement (p<0.05) between the MRI and histological findings for lesion classification (r=0.96). A rabbit model of carotid artery atherosclerosis has been successfully induced and noninvasively visualized. The atherosclerotic plaque formation evolved from type I to type V with time, which could be monitored with 1.5-T MRI and confirmed with histomorphology. This experimental setting can be applied in preclinical research on atherosclerosis.
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