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Session: Poster session II
Session starts: Thursday 24 January, 16:00

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Leah Winkel (Department of Biomedical Engineering, Erasmus Medical Center, Rotterdam)
Harald Groen (Department of Nuclear Medicine, Erasmus Medical Center, Rotterdam)
Bibi van Thiel (Department of Biomedical Engineering, Erasmus Medical Center, Rotterdam)
Ton van der Steen (Department of Biomedical Engineering, Erasmus Medical Center, Rotterdam)
Jolanda Wentzel (Department of Biomedical Engineering, Erasmus Medical Center, Rotterdam)
Marion de Jong (Department of Nuclear Medicine and Department of Radiology, Erasmus Medical Center, Rotterdam)
Kim van der Heiden (Department of Biomedical Engineering, Erasmus Medical Center, Rotterdam)

Abstract:
Atherosclerosis is a lipid driven inflammatory disease of the larger arteries leading to clinical complications such as myocardial infarction or cerebrovascular events. Atherosclerotic plaques are found at specific locations in the arterial tree i.e. near bends and bifurcations, where shear stress is low. Two types of atherosclerotic plaques can develop; vulnerable and stable plaques. Vulnerable plaques have a high risk of rupture, causing acute clinical events. Therefore, the need for non-invasive molecular imaging to distinguish stable from vulnerable atherosclerotic plaques is evident. We have a mouse model in which we can generate both a stable and a vulnerable plaque by placing a tapering cast, which alters shear stress profiles, around the carotid artery of ApoE-/- mice on a high fat diet1. We use this model to test whether we can distinguish vulnerable from stable plaques with non-invasive imaging techniques. In this study, we tested the feasibility of a folate-based radiopharmaceutical; EC0800 (Endocyte Inc.), visualised with high-resolution animal SPECT/CT. This folate tracer binds folate receptors, expressed by activated macrophages. Macrophages play an important role in atherosclerosis and are differentially activated between stable and vulnerable plaques. We intravenously injected our mice with EC0800, radiolabelled to 111Indium via DOTA-benzyl-ethylenediamine-(γ), 24 hours before SPECT/CT imaging. The cast-induced vulnerable and stable plaques showed 111In-EC0800 uptake with a higher uptake in the vulnerable plaque, suggesting EC0800 could function as a vulnerable plaque marker. However, upon histological examination of the plaques we found that the vulnerable plaque was considerably larger in size. We, therefore, determined tracer uptake for plaque volume. Surprisingly, this shows a relatively higher uptake of 111In-EC0800 in stable plaques. We are currently further investigating this. This study could provide a new method to non-invasively distinguish between vulnerable and stable plaques.