Non-invasive imaging of atherosclerotic plaque macrophage in a rabbit model with F-18 FDG PET: a histopathological correlation

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 (μCi/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.Atherothrombosis, characterized by atherosclerotic lesion disruption with superimposed thrombosis, is the main cause of acute coronary syndromes (unstable angina, myocardial infarction and sudden death) [1]. It represents the major cause of morbidity and mortality in the industrialized world. Experimental, pathological and clinical studies have clearly demonstrated the heterogeneity of atherosclerotic lesions [2]. Typically, the mature atherosclerotic plaque contains two different components: soft lipid/macrophage-rich "atheromatous" material and hard smooth muscle cell-related sclerotic tissue. Significant advances have been made in understanding of mechanisms underlying this disease process. The progression of atherosclerotic plaques in coronary circulation is dependent on