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Basic Science Investigations |
1 Department of Investigative Radiology, Research Institute, National Cardiovascular Center, Suita, Japan
2 Laboratory of Genome Bio-Photonics, Photon Medical Research Center, Hamamatsu University School of Medicine, Hamamatsu, Japan
3 Department of Pathofunctional Bioanalysis, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan
4 Department of Nuclear Medicine and Diagnostic Imaging, Graduate School of Medicine, Kyoto University, Kyoto, Japan
5 Institute for Experimental Animals, Kobe University School of Medicine, Kobe, Japan
The rupture of atherosclerotic plaques and the subsequent formation of thrombi are the main factors responsible for myocardial and cerebral infarctions. Thus, the detection of vulnerable plaques in atherosclerotic lesions is a desirable goal, and attempts to image these plaques with 18F-FDG have been made. In the present study, the relationship between the accumulation of 18F-FDG and the biologic characteristics of atherosclerotic lesions was investigated. Furthermore, PET imaging of vulnerable plaques was performed with an animal model of atherosclerosis, Watanabe heritable hyperlipidemic (WHHL) rabbits. Methods: WHHL (n = 11) and control (n = 3) rabbits were injected intravenously with 18F-FDG, and the thoracic and abdominal aortas were removed 4 h after injection. The accumulated radioactivity was measured, and the number of macrophages and the intimal area were investigated by examination of stained sections. PET and CT images were also acquired at 210 min after injection of the radiotracer. Results: 18F-FDG accumulated to a significantly higher level in the aortas of the WHHL rabbits (mean ± SD differential uptake ratio [DUR], 1.47 ± 0.90) than in those of the control rabbits (DUR, 0.44 ± 0.15); DUR was calculated as (tissue activity/tissue weight)/(injected radiotracer activity/animal body weight), with activities given in becquerels and weights given in kilograms. 18F-FDG uptake and the number of macrophages were strongly correlated in the atherosclerotic lesions of the WHHL rabbits (R = 0.81). In the PET analysis, intense 18F-FDG radioactivity was detected in the aortas of the WHHL rabbits, whereas little radioactivity was seen in the control rabbits. Conclusion: The results suggest that macrophages are responsible for the accumulation of 18F-FDG in atherosclerotic lesions. Because vulnerable plaques are rich in macrophages, 18F-FDG imaging should be useful for the selective detection of such plaques.
Key Words: 18F-FDG • atherosclerosis • vulnerable plaque • macrophage • Watanabe heritable hyperlipidemic rabbit
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