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Articles by M. Schwaiger
Total Records ( 2 ) for M. Schwaiger
  I Laitinen , A Saraste , E Weidl , T Poethko , A. W Weber , S. G Nekolla , P Leppanen , S Yla Herttuala , G Holzlwimmer , A Walch , I Esposito , H. J Wester , J Knuuti and M. Schwaiger

Background— 18F-Galacto-RGD is a positron emission tomography (PET) tracer binding to vβ3 integrin that is expressed by macrophages and endothelial cells in atherosclerotic lesions. Therefore, we evaluated 18F-galacto-RGD for imaging vascular inflammation by studying its uptake into atherosclerotic lesions of hypercholesterolemic mice in comparison to deoxyglucose.

Methods and results— Hypercholesterolemic LDLR–/–ApoB100/100 mice on a Western diet and normally fed adult C57BL/6 control mice were injected with 18F-galacto-RGD and 3H-deoxyglucose followed by imaging with a small animal PET/CT scanner. The aorta was dissected 2 hours after tracer injection for biodistribution studies, autoradiography, and histology. Biodistribution of 18F-galacto-RGD was higher in the atherosclerotic than in the normal aorta. Autoradiography demonstrated focal 18F-galacto-RGD uptake in the atherosclerotic plaques when compared with the adjacent normal vessel wall or adventitia. Plaque-to-normal vessel wall ratios were comparable to those of deoxyglucose. Although angiogenesis was not detected, 18F-galacto-RGD uptake was associated with macrophage density and deoxyglucose accumulation in the plaques. Binding to atherosclerotic lesions was efficiently blocked in competition experiments. In vivo imaging visualized 18F-galacto-RGD uptake colocalizing with calcified lesions of the aortic arch as seen in CT angiography.

Conclusions— 18F-Galacto-RGD demonstrates specific uptake in atherosclerotic lesions of mouse aorta. In this model, its uptake was associated with macrophage density. 18F-Galacto-RGD is a potential tracer for noninvasive imaging of inflammation in atherosclerotic lesions.

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