Localization of Deoxyglucose and Annexin A5 in Experimental Atheroma Correlates with Macrophage Infiltration but not Lipid Deposition in the Lesion

The aim of this study was to understand the relationship of lipid deposition to the macrophage content, macrophage metabolism, and apoptosis in plaque. We compared the uptake of 2-deoxy-2-fluoro-D-[C-14]glucose ([C-14]FDG) and [Tc-99m]HYNIC-annexin V ([Tc-99m]annexin A5) with the lesion histology in apolipoprotein E knockout (apoE(-/-)) mice. Male apoE(-/-) mice (n = 9) were injected with [C-14]FDG and [Tc-99m]annexin A5. Cryostat sections of aorta samples (n = 49) were used for dual-tracer autoradiography, and regional tracer uptake levels were evaluated. Lesions were identified histologically with Movat's pentachrome (AHA lesion phenotypes), Mac-2 staining (macrophage infiltration) and Oil Red O staining (lipid deposition). The highest uptakes of [C-14]FDG (3.10 +/- 1.50 %ID x kilogram per square millimeter) and [Tc-99m]annexin A5 (0.49 +/- 0.20 %ID x kilogram per square millimeter) were shown in atheromatous lesions (types III and IV). Each tracer uptake showed better correlation with macrophage infiltration than lipid deposition ([C-14]FDG, r = 0.44 vs. r = 0.14; [Tc-99m]annexin A5, r = 0.65 vs. r = 0.48). Both tracers were concentrated in type III and IV atheromatous lesions which corresponded to macrophage infiltration rather than lipid deposition.