We synthesized both T1 and T2 agents to evaluate the ability for each type of probe to visualize inflammation at high resolution in living systems. These probes were utilized for multimodality imaging of vascular plaques in animal models of vascular inflammation to demonstrate the feasibility of using PET screening to guide selection of volumes for high resolution MRI in order to map macrophage distributions in arterial lesions. While no single animal model ideally recreates the human condition, a number of models have shown sufficient parallel to the human disease to justify their use as models for specific disease traits. The difficulty with modeling vulnerable plaques has been that although stenotic lesions can be induced in animal models, they have not been observed to spontaneously rupture as human lesions do. Recent observations of ApoE knockout mice has indicated that in this model, plaques can and do spontaneously rupture. This knockout mouse also has been observed to form lesions similar to the vulnerable human case which are rich in macrophage content. While this model can produce plaques with unstable phenotype, we found it to be inconsistent, producing macrophage-rich plaques in only a fraction of examined animals. Macrophage laden plaques were more reliably produced if a carotid artery was ligated. We used the ApoE ligation model, therefore, as one of the testbeds for our probes. The robustness of the method is demonstrated in that localization of the probe to plaques could be observed in several different animal models of vascular inflammation. We envision that these CT99021 methods could be used as a clinical diagnostic tool wherein PET is used for screening large volumes to identify broad vascular regions that accumulate the macrophage targeted probes. This information is used to guide MR imaging at high resolution to visualize the vessel walls, plaques, and macrophage distribution patterns. Videos are available for this article that demonstrate how the resulting MR data can be presented to provide a type of noninvasive “endoscopy”. Together the information about macrophage density and distribution can be used to estimate plaque probability to rupture and guide patient management decisions. Alone, PET can provide a rough location for macrophage rich plaques and allow some quantitation, but typical plaques are much smaller than the resolution limit of PET, so this method provides only an averaged assessment over all plaques in a given volume, specific information about individual plaque vulnerability is not possible. Human plaques at their largest are a few millimeters thick, up to ten millimeters long and disease is often diffuse throughout vessels. At a resolution of 8–16 mm for whole body scans PET alone is unable to reveal plaque structure but will primarily give general localization. At this resolution it would be difficult to correlate the PET signal with individual stenoses or to determine which regions, specifically, are at risk to rupture. PET is also unable to provide information on exactly degree anywhere in the vascular system.