Zhang Zhuangyu, Machac Josef, Helft Gerard, Worthley Stephen G, Tang Cheuk, Zaman Azfar G, Rodriguez Oswaldo J, Buchsbaum Monte S, Fuster Valentin, Badimon Juan J
Division of Nuclear Medicine, Department of Radiology, The Mount Sinai School of Medicine, New York, NY, USA.
BMC Nucl Med. 2006 May 25;6:3. doi: 10.1186/1471-2385-6-3.
Coronary atherosclerosis and its thrombotic complications are the major cause of mortality and morbidity throughout the industrialized world. Thrombosis on disrupted atherosclerotic plaques plays a key role in the onset of acute coronary syndromes. Macrophages density is one of the most critical compositions of plaque in both plaque vulnerability and thrombogenicity upon rupture. It has been shown that macrophages have a high uptake of 18F-FDG (FDG). We studied the correlation of FDG uptake with histopathological macrophage accumulation in atherosclerotic plaques in a rabbit model.
Atherosclerosis was induced in rabbits (n = 6) by a combination of atherogenic diet and balloon denudation of the aorta. PET imaging was performed at baseline and 2 months after atherogenic diet and coregistered with magnetic resonance (MR) imaging. Normal (n = 3) rabbits served as controls. FDG uptake by the thoracic aorta was expressed as concentration (muCi/ml) and the ratio of aortic uptake-to-blood radioactivity. FDG uptake and RAM-11 antibody positive areas were analyzed in descending aorta.
Atherosclerotic aortas showed significantly higher uptake of FDG than normal aortas. The correlation of aortic FDG uptake with macrophage areas assessed by histopathology was statistically significant although it was not high (r = 0.48, p < 0.0001). When uptake was expressed as the ratio of aortic uptake-to-blood activity, it correlated better (r = 0.80, p < 0.0001) with the macrophage areas, due to the correction for residual blood FDG activity.
PET FDG activity correlated with macrophage content within aortic atherosclerosis. This imaging approach might serve as a useful non-invasive imaging technique and potentially permit monitoring of relative changes in inflammation within the atherosclerotic lesion.
冠状动脉粥样硬化及其血栓形成并发症是整个工业化世界死亡率和发病率的主要原因。破裂的动脉粥样硬化斑块上的血栓形成在急性冠状动脉综合征的发病中起关键作用。巨噬细胞密度是斑块易损性和破裂后血栓形成性方面斑块的最关键组成部分之一。已表明巨噬细胞对18F-FDG（氟代脱氧葡萄糖）摄取量高。我们在兔模型中研究了FDG摄取与动脉粥样硬化斑块中组织病理学巨噬细胞积聚的相关性。
通过致动脉粥样硬化饮食和主动脉球囊剥脱术联合诱导兔（n = 6）发生动脉粥样硬化。在基线时以及致动脉粥样硬化饮食后2个月进行PET成像，并与磁共振（MR）成像进行配准。正常兔（n = 3）作为对照。胸主动脉的FDG摄取以浓度（μCi/ml）以及主动脉摄取与血液放射性的比值表示。分析降主动脉中的FDG摄取和RAM-11抗体阳性区域。
动脉粥样硬化主动脉显示出比正常主动脉显著更高的FDG摄取。尽管相关性不高，但通过组织病理学评估的主动脉FDG摄取与巨噬细胞区域的相关性具有统计学意义（r = 0.48，p < 0.0001）。当摄取以主动脉摄取与血液活性的比值表示时，由于对残留血液FDG活性进行了校正，其与巨噬细胞区域的相关性更好（r = 0.80，p < 0.0001）。
PET FDG活性与主动脉动脉粥样硬化内的巨噬细胞含量相关。这种成像方法可能作为一种有用的非侵入性成像技术，并有可能允许监测动脉粥样硬化病变内炎症的相对变化。
