Why the study?
Pre-clinical studies suggest a relationship between lipid rich necrotic core, intraplaque hemorrhage, and inflammation, but this had not been previously explored quantitatively in patients.
Is it feasible to assess the relationship between lipid-rich necrotic core, intraplaque hemorrhage, and inflammation using PET/MRI in patients with high-grade carotid stenosis?
Is it feasible to assess the relationship between lipid-rich necrotic core, intraplaque hemorrhage, and inflammation using PET/MRI in patients with high-grade carotid stenosis?
This pilot study demonstrates the feasibility of using PET/MRI to quantitatively analyze the relationship between lipid-rich necrotic cores, intraplaque hemorrhage, and plaque inflammation, though no significant correlations were found in this small cohort.
Feasibility of PET/MRI shown for carotid plaque assessment; leaves open links between inflammation and necrotic core or hemorrhage.
Inflammation inside Atherosclerotic plaques represents a major pathophysiological process driving plaques towards rupture. Pre-clinical studies suggest a relationship between lipid rich necrotic core, intraplaque hemorrhage and inflammation, not previously explored in patients. Therefore, we designed a pilot study to investigate the feasibility of assessing the relationship between these plaque features in a quantitative manner using PET/MRI. In 12 patients with high-grade carotid stenosis the extent of lipid rich necrotic core and intraplaque hemorrhage was quantified from fat and R2* maps acquired with a previously validated 4-point Dixon MRI sequence in a stand-alone MRI. PET/MRI was used to measure 18 F-FDG uptake. T1-weighted images from both scanners were used for registration of the quantitative Dixon data with the PET images. The plaques were heterogenous with respect to their volumes and composition. The mean values for the group were as follows: fat fraction (FF) 0.17% (± 0.07), R2* 47.6 s −1 (± 10.9) and target-to-blood pool ratio (TBR) 1.49 (± 0.48). At group level the correlation between TBR and FF mean was − 0.406, p 0.19 and for TBR and R2* mean 0.259, p 0.42. The lack of correlation persisted when analysed on a patient-by-patient basis but the study was not powered to draw definitive conclusions. We show the feasibility of analysing the quantitative relationship between lipid rich necrotic cores, intraplaque haemorrhage and plaque inflammation. The 18 F-FDG uptake for most patients was low. This may reflect the biological complexity of the plaques and technical aspects inherent to 18 F-FDG measurements. Trial registration: ISRCTN, ISRCTN30673005. Registered 05 January 2021, retrospectively registered.
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Good et al. (2021) studied this question.
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