Laura Mechtouff1,2, Monica Sigovan3,4, Philippe Douek3,4,5, Nicolas Costes6, Didier Le Bars6,7, Adeline Mansuy8, Julie Haesebaert9, Alexandre Bani-Sadr10, Jérémie Tordo10, Patrick Feugier11, Antoine Millon11, Stéphane Luong5, Salim Si-Mohamed5, Diane Collet-Benzaquen12, Emmanuelle Canet-Soulas13, Thomas Bochaton13, Claire Crola Da Silva13, Alexandre Paccalet13, David Magne14, Yves Berthezene3,15, Norbert Nighoghossian16,13. 1. Stroke Department, Pierre Wertheimer Hospital, Hospices Civils de Lyon, 59 Boulevard Pinel, 69677, Bron, France. laura.mechtouff@chu-lyon.fr. 2. INSERM U1060, CarMeN Laboratory, University Lyon 1, Lyon, France. laura.mechtouff@chu-lyon.fr. 3. CNRS, UMR 5220, CREATIS, University of Lyon, Lyon, France. 4. INSA-Lyon UCBL, Inserm U1206, UJM-Saint Etienne, Lyon, France. 5. Department of Radiology, Louis Pradel University Hospital, Bron, France. 6. CERMEP - Imagerie du vivant, Lyon, France. 7. ICBMS, University C. Bernard Lyon 1 & Hospices Civils de Lyon, Lyon, France. 8. Cellule Recherche Imagerie, Louis Pradel University Hospital, Bron, France. 9. Clinical Research and Epidemiology Unit, Public Health Department Hospices Civils de Lyon & Université de Lyon, Université Claude Bernard Lyon 1, Université Saint-Étienne, HESPER EA 7425, F-69008 Lyon, 42023, Saint-Etienne, France. 10. Department of Nuclear Medicine, Lyon Sud Hospital, Hospices Civils de Lyon, Lyon, France. 11. Vascular Surgery Department, Edouard Herriot University Hospital & Claude Bernard Lyon 1 University, Lyon, France. 12. Laboratoire d'Anatomie et de Cytologie pathologiques Technipath, Limonest, France. 13. INSERM U1060, CarMeN Laboratory, University Lyon 1, Lyon, France. 14. ICBMS, CNRS, UMR 5246, University Lyon 1, Lyon, France. 15. Neuroradiology Department, Pierre Wertheimer Hospital, Bron, France. 16. Stroke Department, Pierre Wertheimer Hospital, Hospices Civils de Lyon, 59 Boulevard Pinel, 69677, Bron, France.
Abstract
BACKGROUND: Previous studies have suggested the role of microcalcifications in plaque vulnerability. This exploratory study sought to assess the potential of hybrid positron-emission tomography (PET)/magnetic resonance imaging (MRI) using 18F-sodium fluoride (18F-NaF) to check simultaneously 18F-NaF uptake, a marker of microcalcifications, and morphological criteria of vulnerability. METHODS AND RESULTS: We included 12 patients with either recently symptomatic or asymptomatic carotid stenosis. All patients underwent 18F-NaF PET/MRI. 18F-NaF target-to-background ratio (TBR) was measured in culprit and nonculprit (including contralateral plaques of symptomatic patients) plaques as well as in other arterial walls. Morphological criteria of vulnerability were assessed on MRI. Mineral metabolism markers were also collected. 18F-NaF uptake was higher in culprit compared to nonculprit plaques (median TBR 2.6 [2.2-2.8] vs 1.7 [1.3-2.2]; P = 0.03) but was not associated with morphological criteria of vulnerability on MRI. We found a positive correlation between 18F-NaF uptake and calcium plaque volume and ratio but not with circulating tissue-nonspecific alkaline phosphatase (TNAP) activity and inorganic pyrophosphate (PPi) levels. 18F-NaF uptake in the other arterial walls did not differ between symptomatic and asymptomatic patients. CONCLUSIONS: 18F-NaF PET/MRI may be a promising tool for providing additional insights into the plaque vulnerability.
BACKGROUND: Previous studies have suggested the role of microcalcifications in plaque vulnerability. This exploratory study sought to assess the potential of hybrid positron-emission tomography (PET)/magnetic resonance imaging (MRI) using 18F-sodium fluoride (18F-NaF) to check simultaneously 18F-NaF uptake, a marker of microcalcifications, and morphological criteria of vulnerability. METHODS AND RESULTS: We included 12 patients with either recently symptomatic or asymptomatic carotid stenosis. All patients underwent 18F-NaF PET/MRI. 18F-NaF target-to-background ratio (TBR) was measured in culprit and nonculprit (including contralateral plaques of symptomatic patients) plaques as well as in other arterial walls. Morphological criteria of vulnerability were assessed on MRI. Mineral metabolism markers were also collected. 18F-NaF uptake was higher in culprit compared to nonculprit plaques (median TBR 2.6 [2.2-2.8] vs 1.7 [1.3-2.2]; P = 0.03) but was not associated with morphological criteria of vulnerability on MRI. We found a positive correlation between 18F-NaF uptake and calcium plaque volume and ratio but not with circulating tissue-nonspecific alkaline phosphatase (TNAP) activity and inorganic pyrophosphate (PPi) levels. 18F-NaF uptake in the other arterial walls did not differ between symptomatic and asymptomatic patients. CONCLUSIONS: 18F-NaF PET/MRI may be a promising tool for providing additional insights into the plaque vulnerability.
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