Ziel/Aim (Micro-)Calcification is an established hallmark of vulnerable atherosclerotic plaque
formation. Given the high sensitivity and specificity of Sodium [18F]Fluoride (Na[18F]F) for vascular calcifications and positive emerging data of vitamin K on vascular
health, the aim of this study is to assess the ability of Na[18F]F to monitor therapy and disease progression in a unitary atherosclerotic mouse
model.
Methodik/Methods C57BL/6 ApoE-/- mice were placed on a western type diet for 12 weeks and then split into 4 groups.
The early stage atherosclerosis group received a chow diet for an additional 12 weeks,
while the advanced atherosclerosis group continued the western type diet. The Menaquinone-7
(MK-7) group received a MK-7-supplementation during the additional 12 weeks, while
the Warfarin, a Warfarin-and-Phylloquinone-supplemented diet. As control, C57BL/6
wild type mice were fed a chow diet for 24 weeks. All mice were scanned with Na[18F]F using a small animal PET/CT and then sacrificed for histological assessment.
Ergebnisse/Results The Warfarin group presented spotty calcifications on CT (average hottest voxel =
390HU) in the proximal aorta. All spots corresponded to dense mineralisations on von
Kossa staining. After the control, the MK-7 group had the lowest Na[18F]F uptake (TBRmax control 0.06 vs. TBRmax MK-7 0.4). The advanced and Warfarin groups presented the highest uptake in the aortic
arch (TBRmax 1.15 and 1.60, respectively) and left ventricle (TBRmax 1.10 and 0.76, respectively). The advanced stage group did not develop spotty calcifications,
however Na[18F]F uptake was still observed, suggesting the presence of micro-calcifications.
Schlussfolgerungen/Conclusions In a newly applied mouse model developing spotty calcifications on CT exclusively
in the proximal aorta ([1]), Na[18F]F can efficiently monitor plaque progression and the beneficial effects of vitamin
K on cardiovascular disease.
