Abstract：Background Atherosclerotic plaque rupture is the primary mechanism of thrombosis which plays a key role in the onset of acute coronary syndromes. Detection of these plaques prone to rupture （vulnerable plaque） could be clinically significant for prevention of cardiac events. It has been shown that high metabolism cells have a high uptake of fluorine-18 fluorodeoxyglucose （18F-FDG）. The objective of this study was to investigate the correlation of FDG uptake and the immuno-histochemistry parameters of plaques, and the effect of atorvastatin on vulnerable atherosclerotic plaque in a rabbit model.Methods Ten male New Zealand White rabbits were divided into three groups as follows： （1） normal control group （n=2,C group）： the animals were fed a standard diet at 120 g/d and were given water ad labium; （2） atherosclerosis group （n=4,As group）： animals were fed with high fat diet for 5 months after aortic endothelia damage; （3） treatment group （atherosclerosis ＋ atorvastatin, n=4, Statin group）： animals were fed with high fat diet for 5 months and then changed into normal chow plus atorvastatin （2.5 mg·d-1·kg-1） treatment for another 4 months. Then these four rabbits were imaged with fluorine-18 fluorodexyglucose positron emission tomography/computed tomography （PET/CT） and sacrificed for pathohistologic studies. FDG uptake by the aorta was expressed as target-to-background ratio （TBR）. Maximal standardized uptake value （SUV） was measured over the thoracic and abdominal aortas. The aortic smooth muscle cell （SMC） number, CD-14 antibody positive cell （macrophage） number and the ratio of the thickness of fibrous cap to the thickness of lipid core （cap-to-core ratio） in atherosclerotic plaques were analyzed.Results As group showed significantly higher uptake of FDG than C group （SUVs： 0.746±0.172 vs. 0.286±0.073, P 〈0.001）. After 4 months of atorvastatin treatment and the modification of diet, SUVs decreased significantly （Statin
Background Noninvasive detection of vulnerable plaque has a significant implication for prevention and treatment of atherosclerotic disea±ses. The aim of this study is to investigate the difference between vulnerable plaques and stable plaques in magnetic resonance （MR） images. Methods Atherosclerosis was induced in twenty male New Zealand white rabbits by high cholesterol diet and balloon injury of the abdominal aorta. After baseline （pre-triggering） MR imaging （MRI） scan, the rabbits underwent pharmaceutical triggering with Russell＇s viper venom and histamine to induce atherothrombosis, followed by another MRI scan 48 hours later （post-triggering）. Rabbits were euthanized to obtain pathological and histological data. The results of MRI were compared with those of pathology and histology. Results MRI showed that abdominal aorta of the rabbits had pathological change of atherosclerosis in different degrees. Seventy-five plaques were analysed, among which 14 had vulnerable thrombi and 61 stable. Thrombosis was identified in 7 of 11 rabbits by post-triggering MRI, the sensitivity and K value of MR in detection of vulnerable plaque was 71% and 0.803 （P 〈0.05）. MRI data significantly correlated with the histopathological data in fibrous cap thickness （t=0.749） plaque area （t=0.853）, lipid core area （r=0.900）. Compared with stable plaques, vulnerable plaques had a significantly thinner fibrous cap （（0.58±0.27） mm vs. （0.95±0.22） mm）, larger lipid core area （（7.56±2.78） mm2 vs. （3.29±1.75） mm2）, and a higher ratio of lipid core area/plaque area （（55±16）% vs. （27±17）%）, but plaque area was comparable in two groups on MRI. The ratio of lipid core area/plaque area was a strong predictor of vulnerable plaques. Conclusion MRI could distinguish vulnerable plaques from stable plaques in a rabbit model of atherothrombosis and may thus be useful as a noninvasive modality for detection of vulnerable plaques in humans.
