Purpose: 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-[(14)C]glucose ([(14)C]FDG) and [(99m)Tc]HYNIC-annexin V ([(99m)Tc]annexin A5) with the lesion histology in apolipoprotein E knockout (apoE(-/-)) mice.
Procedures: Male apoE(-/-) mice (n = 9) were injected with [(14)C]FDG and [(99m)Tc]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).
Results: The highest uptakes of [(14)C]FDG (3.10 ± 1.50 %ID × kilogram per square millimeter) and [(99m)Tc]annexin A5 (0.49 ± 0.20 %ID × 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 ([(14)C]FDG, r = 0.44 vs. r = 0.14; [(99m)Tc]annexin A5, r = 0.65 vs. r = 0.48).
Conclusions: Both tracers were concentrated in type III and IV atheromatous lesions which corresponded to macrophage infiltration rather than lipid deposition.