In Vivo Mapping of Vascular Inflammation Using the Translocator Protein Tracer (18)F-FEDAA1106.

Noninvasive imaging methods are required to monitor the inflammatory content of atherosclerotic plaques. FEDAA1106 (N-(5-fluoro-2-phenoxyphenyl)-N-(2-(2-fluoroethoxy)-5-methoxybenzyl) acetamide) is a selective ligand for TSPO-18kDa (also known as peripheral benzodiazepine receptor), which is expressed by activated macrophages. We compared F-18-FEDAA1106 and 2-deoxy-2-[F-18]fluoro-D-glucose (F-18-FDG, a marker of glucose metabolism) for positron emission tomographic (PET) imaging of vascular inflammation. This was tested using a murine model in which focal inflammation was induced in the carotid artery via placement of a constrictive cuff. Immunostaining revealed CD68-positive cells (macrophages) at a disturbed flow site located downstream from the cuff. Dynamic PET imaging using F-18-FEDAA1106 or F-18-FDG was registered to anatomic data generated by computed tomographic (CT)/CT angiography. Standardized uptake values were significantly increased at cuffed compared to contralateral arteries using either F-18-FEDAA1106 (p < .01) or FDG (p < .05). However, the F-18-FEDAA1106 signal was significantly higher at the inflamed disturbed flow region compared to the noninflamed uniform flow regions, whereas differences in FDG uptake were less distinct. We conclude that F-18-FEDAA1106 can be used in vivo for detection of vascular inflammation. Moreover, the signal pattern of F-18-FEDAA1106 corresponded with vascular inflammation more specifically than FDG uptake.