Abstract 17924: A Rabbit Model of Spontaneous Plaque Disruption and Thrombosis Induced by Lipopolysaccharide
Background: The aim of this study was to develop a rabbit model with spontaneous plaque disruption and secondary thrombosis that mimics the pathophysiologic and morphological characteristics of atherosclerotic plaques in humans. Inflammation plays a critical role in the development of atherosclerotic plaques. Lipopolysaccharide (LPS) is potentially an important inflammatory source.
Methods: Rabbits were randomized into 3 groups. Group A (n=10) a normal diet. Group B (n=15) a cholesterol-enriched diet following balloon injury to the right common carotid artery. Group C (n=15) injections of LPS once a week throughout the experiment in addition to a cholesterol diet and balloon injury. The morphological characteristics of the plaques were evaluated by optical coherence tomography (OCT) and histology.
Results: No significant atherosclerotic plaques were observed in group A. Group C, compared to Group B, showed higher incidence of the spontaneous plaque disruption (33.33% vs. 6.67%, P=0.2072) and the luminal thrombi (60% vs. 20%, P<0.05). The OCT images and the corresponding cross-sectional histopathology data revealed a close correlation for fibrous cap thickness and for detection of thrombus (Figure).
Conclusions: A rabbit model with spontaneous plaque disruption and secondary thrombosis induced by LPS was developed. OCT can be used to follow serial changes of plaque morphology in this model.
Key words: atherosclerosis, thrombosis, lipopolysaccharide, optical coherence tomography, rabbit Figure. Representative examples of OCT images and histological images with HE staining (B, D, F, H) or with Masson’s trichrome staining (J, L, N, P). The white arrow indicates thrombus.
- © 2012 by American Heart Association, Inc.