Recently, Rudd et al.  investigated the detection of atherosclerotic lesions in the internal carotid artery by 18F-FDG PET in patients, and found that 18F-FDG was markedly accumulated in symptomatic plaques, but not in contralateral asymptomatic plaques. In addition, they incubated 3H-FDG with human atherosclerotic plaques in vitro, and detected high 3H-FDG uptake by macrophages. Ogawa et al.  reported that 18F-FDG accumulation in atherosclerotic lesions was correlated with the number of macrophages in the lesions in rabbits with spontaneous atherosclerosis. Tawakol et al.  found a high correlation between the accumulations of 18F-FDG and macrophages in 17 patients with severe carotid arterial stenosis who underwent carotid endarterectomy (CEA) within 1 month after 18F-FDG PET. Graebe et al.  reported that 18F-FDG uptake in carotid plaques was correlated to the gene expression of CD68 (a macrophage-specific marker) and other known molecular markers of inflammation and plaque vulnerability (interleukin [IL]-18, matrix metalloproteinase [MMP]-9). As data that demonstrated the high reproduc-ibility of 18F-FDG PET on plaque detection, Rudd et al.  imaged 20 patients twice, 14 days apart, and found 18F-FDG uptake [standardized uptake value (SUV)] max and plaque-to-background ratio) was highly reproducible in carotid, iliac, and femoral arteries. These findings suggested that 18F-FDG PET allows the quantitative evaluation of inflammatory cells in plaques, particularly macrophages, which may enable the selective imaging of vulnerable atherosclerotic plaques.
Tahara et al.  and Ogawa et al.  recently investigated the application of 18F-FDG PET to monitor the therapeutic effects of lipid-lowering therapy and antioxidant therapy on atherosclerosis, and found it useful. Tahara et al.  randomly allocated 43 patients with arterial 18F-FDG accumulation to groups treated with simvastatin and dietary therapy alone and performed 18F-FDG PET after 3 months, and observed significant reductions of low-density lipoprotein (LDL)-
cholesterol and 18F-FDG accumulation in the simvastatin treatment group. Ogawa et al.  treated rabbits exhibiting spontaneous atherosclerosis with an antioxida-tive agent, probucol, and performed 18F-FDG PET before and 1, 3, and 6 months after the initiation of treatment. They found that 18F-FDG accumulation in the arterial wall slowly increased in the control group, but decreased with the reduction of inflammatory reaction in the treatment group, and the accumulation in the arterial wall was undetectable 6 months after the initiation of treatment. These findings indicate the potential of 18FDG PET to evaluate the therapeutic effects of statins and probucol on atherosclerosis, based on the reduction of inflammatory reactions in aortic tissues.
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