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Swine Model of Carotid Artery Atherosclerosis: Experimental Induction by Surgical Partial Ligation and Dietary Hypercholesterolemia

A. Ishiia, F. Viñuelaa, Y. Murayamaa, I. Yukia, Y.L. Niena, D.T. Yehb and H.V. Vintersb

a Division of Interventional Neuroradiology, UCLA Medical Center, David Geffen School of Medicine at UCLA, Los Angeles, California
b Departments of Pathology and Laboratory Medicine (Neuropathology) and Neurology, UCLA Medical Center, David Geffen School of Medicine at UCLA, Los Angeles, California


Figure 1
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  		Fig 1. A, Intraoperative photograph showing a ligated carotid artery with a spacer on the external surface of the artery. This spacer was subsequently removed, leaving a tight stenosis, but not occlusion.

B, Angiogram showing a partially ligated artery with approximately 80% stenosis immediately after the procedure.

C, Angiogram obtained 3 months after the procedure. Note luminal narrowing proximal and extensive dilation distal to the surgically created stenosis.


Figure 2
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  		Fig 2. Representative photographs of hematoxylin-eosin-stained cross-sections for carotid arteries from each group.

A, Group I (Ib; 6 months). Eccentric advanced atherosclerotic plaque located proximal to the surgical stenosis. Arrow indicates calcium deposits at the bottom of the plaque. Note that the entire plaque is covered by a fibromuscular cap, suggesting the similarity to human lesions.

B, Group II (IIb; 6 months). Concentric intimal thickening. Note that in contrast with A, no advanced features of atherosclerosis are seen.

C, Group III (6 months). No atherosclerotic change is observed. Scale bar, 500 µm.


Figure 3
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  		Fig 3. Histologic features of various atheromatous plaques in carotid arteries in group I. All sections are from 1 animal sacrificed at 6 months after the surgical procedure.

A, Low magnification micrograph (H-E-stained section) shows a large eccentric plaque in the portion proximal to the surgical stenosis featuring a fibromuscular cap, intra- and extracellular lipid deposition, and massive intraplaque hemorrhage (white arrowheads). Scale bar, 1 mm.

B, anti-SMA immunostaining clearly showing a fibromuscular cap covering a large collection of foamy macrophages at the bottom. Note that smooth muscle cells are scattered throughout the plaque and line its luminal surface (at the top). Scale bar, 100 µm.

C, Base of plaque immunostained with anti-SMA showing necrotic portion. Scale bar, 100 µm.

D, Anti-SMA immunostaining clearly showing calcification at the bottom of plaque (black arrowhead).

E, EVG-stained section of plaque shows abundant collagen deposition as well as focally defective internal elastic lamina (arrows). Scale bar, 100 µm. H-E, hematoxylin and eosin; SMA, smooth muscle actin; EVG, Van Gieson’s elastic


Figure 4
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  		Fig 4. Bar graphs of cross-sectional area stenosis (%) and plaque stage score.

A, Area stenosis (%) and plaque stage score versus groups.

B, Area stenosis (%) and plaque stage score versus subgroups.





Copyright © 2008 by the American Society of Neuroradiology. Print ISSN: 0195-6108 Online ISSN: 1936-959X