18F-NaF PET-MRI for detection of Carotid Atheroma in acute neurovascular syndrome

Jakub Kaczynski*, Stephanie Sellers , Michael A. Seidman, Maaz Syed, Martin Dennis, Gillian Macnaught, Maurits Jansen, Scott I Semple, Carlos Alcaide-Corral, Adriana A S Tavares, Tom MacGillivray, Samuel Debono, Rachael Forsythe, Andrew Tambyraja, Piotr J Slomka, Jonathon Leipsic, Marc R Dweck, William Whiteley, Joanna Wardlaw, Edwin J R van BeekDavid E Newby, Michelle C Williams

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Fluorine 18–labeled sodium fluoride PET/MRI characteristics were associated with the culprit atherosclerotic plaques in the carotid circulation of study participants with acute neurovascular syndrome; PET/MRI was also usable in the assessment of carotid stenosis, high-risk plaque features, and plaque biologic activity.


MRI and fluorine 18–labeled sodium fluoride (18F-NaF) PET can be used to identify features of plaque instability, rupture, and disease activity, but large studies have not been performed.


To evaluate the association between 18F-NaF activity and culprit carotid plaque in acute neurovascular syndrome.

Materials and Methods

In this prospective observational cohort study (October 2017 to January 2020), participants underwent 18F-NaF PET/MRI. An experienced clinician determined the culprit carotid artery based on symptoms and record review. 18F-NaF uptake was quantified using standardized uptake values and tissue-to-background ratios. Statistical significance was assessed with the Welch, χ2, Wilcoxon, or Fisher test. Multivariable models were used to evaluate the relationship between the imaging markers and the culprit versus nonculprit vessel.


A total of 110 participants were evaluated (mean age, 68 years ± 10 [SD]; 70 men and 40 women). Of the 110, 34 (32%) had prior cerebrovascular disease, and 26 (24%) presented with amaurosis fugax, 54 (49%) with transient ischemic attack, and 30 (27%) with stroke. Compared with nonculprit carotids, culprit carotids had greater stenoses (≥50% stenosis: 30% vs 15% [P = .02]; ≥70% stenosis: 25% vs 4.5% [P < .001]) and had increased prevalence of MRI-derived adverse plaque features, including intraplaque hemorrhage (42% vs 23%; P = .004), necrotic core (36% vs 18%; P = .004), thrombus (7.3% vs 0%; P = .01), ulceration (18% vs 3.6%; P = .001), and higher 18F-NaF uptake (maximum tissue-to-background ratio, 1.38 [IQR, 1.12–1.82] vs 1.26 [IQR, 0.99–1.66], respectively; P = .04). Higher 18F-NaF uptake was positively associated with necrosis, intraplaque hemorrhage, ulceration, and calcification and inversely associated with fibrosis (P = .04 to P < .001). In multivariable analysis, carotid stenosis at or over 70% (odds ratio, 5.72 [95% CI: 2.2, 18]) and MRI-derived adverse plaque characteristics (odds ratio, 2.16 [95% CI: 1.2, 3.9]) were both associated with the culprit versus nonculprit carotid vessel.


Fluorine 18–labeled sodium fluoride PET/MRI characteristics were associated with the culprit carotid vessel in study participants with acute neurovascular syndrome.

Clinical trial registration no. NCT03215550 and NCT03215563

Original languageEnglish
Early online date7 Jun 2022
Publication statusE-pub ahead of print - 7 Jun 2022


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