Key result
Medical therapy linked to a ~0.18 aSUVmax reduction in carotid plaque inflammation after thromboembolic events.
Why the study?
The study investigated timely changes in carotid artery plaque inflammation and morphology after a thromboembolic event using PET/CT and 3D ultrasound imaging.
Does carotid plaque inflammatory activity and morphology change over 3 months following a neurological thromboembolic event?
Cohort (n=14)
Single-blind
No
Does carotid plaque inflammatory activity and morphology change over 3 months following a neurological thromboembolic event?
Mean Difference: -0.18 (95% CI -0.34–-0.02)
Absolute Event Rate: 2.35% vs 2.56%
p-value: p=0.034
A decrease in 2-[18F]FDG-uptake 3 months after a neurological thromboembolic event suggests carotid plaque stabilization over time.
May indicate post-event plaque stabilization with medical therapy; hypothesis-generating for serial FDG-PET monitoring but requires prospective validation.
Background Atherosclerotic plaque vulnerability is comprised by plaque composition driven by inflammatory activity and these features can be depicted with 3D ultrasound and 2-[18F]FDG-PET, respectively. The study investigated timely changes in carotid artery plaque inflammation and morphology after a thromboembolic event with PET/CT and novel ultrasound volumetric grayscale median (GSM) readings. Patients with a single hemisphere-specific neurological symptom and the presence of an ipsilateral carotid artery atherosclerotic plaque were prospectively included to both 2-[18F]FDG PET/CT and 3D ultrasound scans of the plaque immediately after their event and again three months later. On PET/CT images the maximum standardized uptake value (SUVmax) was measured and the volumetric ultrasound acquisitions were analyzed using a semiautomated software measuring GSM values. Results Baseline scans were performed by a mean of 7 days (range 2–14) after the symptom and again after 98 days (range 91–176). For the entire group (n = 14), we found a decrease in average SUVmax from baseline to follow-up of − 0.18 (95% confidence interval: − 0.34 to − 0.02, P = 0.034). GSM did not increase significantly over time (mean change: + 2.21, 95% confidence interval: − 17.02 to 21.44, P = 0.808). Conclusion A decrease in culprit lesion 2-[18F]FDG-uptake 3 months after an event indicates a decrease in inflammatory activity, suggesting that carotid plaque stabilization over time. 3D ultrasound morphological quantitative differences in GSM were not detectable after 3 months.
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Urbak et al. (2021) conducted a cohort in Recent minor ischemic stroke or transient ischemic attack with ipsilateral carotid plaque (n=14). Medical treatment (statin and anti-platelet therapy) post-thromboembolic event vs. Baseline (within-subject comparison) was evaluated on Change in average maximum standardized uptake value (aSUVmax) of carotid plaque on 2-[18F]FDG PET/CT (MD -0.18, 95% CI -0.34 to -0.02, p=0.034). In patients with a recent neurological thromboembolic event, carotid plaque inflammatory activity assessed by 2-[18F]FDG-PET decreased significantly by a mean aSUVmax of 0.18 after 3 months of medical treatment.
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