Nuklearmedizin 2020; 59(02): 132
DOI: 10.1055/s-0040-1708256
Wissenschaftliche Vorträge
Inflammation
© Georg Thieme Verlag KG Stuttgart · New York

Non-invasive identification of inflammation and micro-calcification as markers of atherosclerotic plaque vulnerability

A Florea
1   Uniklinik RWTH Aachen, Klinik für Nuklearmedizin, Aachen
,
A Morgenroth
1   Uniklinik RWTH Aachen, Klinik für Nuklearmedizin, Aachen
,
J Bucerius
2   Maastricht University Medical Centre, Department of Radiology and Nuclear Medicine, Maastricht
,
L Schurgers
3   Maastricht University, Department of Biochemistry, Maastricht
,
FM Mottaghy
1   Uniklinik RWTH Aachen, Klinik für Nuklearmedizin, Aachen
› Institutsangaben
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Publikationsdatum:
08. April 2020 (online)

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Ziel/Aim Inflammation and micro-calcification are established hallmarks of vulnerable plaque formation. Ga-68-Pentixafor and F-18-NaF have been proposed as molecular probes to specifically target the aforementioned processes, however they have mostly been assessed in separate retrospective clinical studies. Here, their ability to correctly identify the distinct mechanism is assessed in an unitary atherosclerotic mouse model via preclinical μPET/CT.

Methodik/Methods ApoE-knockout mice were fed a western type diet for 12 weeks in order to develop an early stage atherosclerosis. To establish a mouse model that develops intimal calcification, the feed of one group (calcification group) was switched to a Warfarin + Vitamin K1 supplemented diet for an additional 12 weeks. Mice on Warfarin develop lethal bleedings, side-effect that can be avoided by adding vitamin K1 to the feed (1). For the inflammation group, the western type diet was maintained up to 24 weeks. For the control, wild type mice on normal diet for 24 weeks were used. All three groups were scanned with both Ga-68-Pentixafor and F-18-NaF μPET/CT in subsequent days. Plaque morphology was assessed via various ex vivo histological, immuno-histological and micro-autoradiography techniques.

Ergebnisse/Results The calcification group has developed spotty calcifications (on μCT) in the proximal aorta, which were confirmed by Alizarin Red stainings. Tracer uptake was correlated with plaques on haematoxylin-eosin and with inflammation markers positive areas or Alizarin Red for Ga-68-Pentixafor and F-18-NaF respectively.

Schlussfolgerungen/Conclusions To our knowledge, this is the first mention of a mouse model that develops only vascular spotty calcifications detectable by μCT. Moreover, Ga-68-Pentixafor is able to specifically target inflamed, COX-2 positive areas, while F-18-NaF correctly targets micro-calcified atherosclerotic plaques.