MULTI-SPECTRAL IMAGING OF ATHEROSCLEROSIS

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Scans will be performed at energies ranging between 80 - 140 kVp. These are ApoE -/- mice specimens---the standard mouse model used in the study atherosclerosis. The development of atherosclerosis in humans involve formation of calcifications and accumulation of inflammatory cells, such as macrophages, at sites of plaque. A major challenge in the diagnosis of vulnerable from non-vulnerable plaque is to identify the extent of inflammation and calcification. The goal of this project is to investigate the feasibility of multi-spectral imaging for differentiating iodine-loaded macrophages from calcifications in atherosclerotic plaques. Preliminary studies will be performed in specimens of mice models of atherosclerosis (ApoE mice). The specific aims are: 1. Imaging of control mice specimens at different energy settings. We will try to answer the following questions: a) how does calcification signal (HU) vary as a function of kVp; b) how does iodine signal vary as a function of kVp; c) can we differentiate iodine signal from calcification signal ? 2. Imaging of iodine-loaded ApoE mice: ApoE mice will be injected with liposomal-iodine. The animals will be sacrificed at later time points (all of the live animal studies will be performed in Houston under approval animal protocol). The mice specimens will then undergo multi-spectral micro-CT imaging. We will try to answer the following questions: a) Can we separate iodine signal from calcium signal within the plaque; b) Can we quantify iodine signal and correlate it with the number of macrophages present in the plaque ? The ability to differentiate iodine signal from calcium signal could have facilitate development of contrast agents for differentiating stable from'rupture-prone' atherosclerotic plaques. This would have huge implications in the screening of patients who are at late stage of the disease.