Key result
18F-FDG PET plaque inflammation strongly correlates with MRI-measured lipid-rich necrotic core volume in carotid stenosis.
Why the study?
Pathologic studies suggest unstable plaque morphology and inflammation are associated with cerebrovascular events, but the association of MRI and 18FDG-PET imaging biomarkers in symptomatic carotid stenosis is unclear.
Do 18FDG-PET markers of inflammation correlate with MRI markers of plaque instability in patients with symptomatic carotid stenosis?
Observational (n=25)
Yes
Do 18FDG-PET markers of inflammation correlate with MRI markers of plaque instability in patients with symptomatic carotid stenosis?
Effect estimate: rs = 0.64
p-value: p=<0.001
18FDG-PET markers of inflammation correlate with MRI markers of plaque instability in symptomatic carotid stenosis, supporting the potential of combined imaging to detect vulnerable plaques.
Supports combined PET-MRI for vulnerable plaque detection; hypothesis-generating and leaves open clinical utility in symptomatic carotid stenosis.
Purpose: Pathologic studies suggest that unstable plaque morphology and inflammation are associated with cerebrovascular events. 18F-fluorodeoxyglucose positron emission tomography (18FDG-PET) is a validated technique for non-invasive imaging of inflammation-related plaque metabolism, and MRI can identify morphologic features of plaque instability. The aim of this study was to investigate the association of selected imaging characteristics of plaque vulnerability measured with MRI and PET in patients with symptomatic carotid stenosis. Methods: Patients from the BIOVASC study were selected based on the following inclusion criteria: (1) age ≥ 50 years; (2) recent (<30 days) ischaemic stroke (modified Rankin scale ≤3) or motor/speech/vision TIA; (3) ipsilateral internal carotid artery stenosis (≥5 0% lumen-narrowing); (4) carotid PET/CTA and MRI completed. Semi-automated plaque analysis of MRI images was performed to quantify morphologic features of plaque instability. PET images were co-registered with CTA and inflammation-related metabolism expressed as maximum standardised uptake value (SUVmax). Results: Twenty-five patients met inclusion criteria (72% men, mean age 65 years). MRI-measured plaque volume was greater in men (1,708–1,286 mm3, p = 0.03), patients who qualified with stroke (1,856–1,440 mm3, p = 0.05), and non-statin users (1,325–1,797 mm3, p = 0.03). SUVmax was associated with MRI-measured plaque lipid-rich necrotic core (LRNC) in the corresponding axial slice (rs = 0.64, p < 0.001) and was inversely associated with whole-plaque fibrous cap thickness (rs = −0.4, p = 0.02) and calcium volume (rs = −0.4, p = 0.03). Conclusion: This study demonstrated novel correlations of non-invasive imaging biomarkers of inflammation-related plaque metabolism with morphological MRI markers of plaque instability. If replicated, our findings may support the application of combined MRI and PET to detect vulnerable plaque in future clinical practise and randomised trials.
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Giannotti et al. (2021) conducted an observational in Symptomatic carotid stenosis (n=25). 18F-FDG PET plaque inflammation (SUVmax) was evaluated on Association between SUVmax and MRI-measured plaque lipid-rich necrotic core (LRNC) (rs = 0.64, p=<0.001). In patients with symptomatic carotid stenosis, plaque inflammation measured by 18F-FDG PET SUVmax was significantly associated with MRI-measured lipid-rich necrotic core volume (rs = 0.64, p<0.001).
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