Open Access18F-NaF PET/MRI for Detection of Carotid Atheroma in Acute Neurovascular Syndrome
Author(s) -
Jakub Kaczynski,
Stephanie Sellers,
Michael A. Seidman,
Maaz Syed,
Martin Dennis,
Gillian Mcnaught,
Maurits A. Jansen,
Scott Semple,
Carlos J. Alcaide-Corral,
Adriana Tavares,
Tom MacGillivray,
Samuel Debono,
Rachael Forsythe,
Andrew L. Tambyraja,
Piotr J. Slomka,
Jonathan Leipsic,
Marc R Dweck,
William Whiteley,
Joanna M. Wardlaw,
Edwin Jacques Rudolph van Beek,
David E. Newby,
Michelle C. Williams
Publication year - 2022
Publication title -
radiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.118
H-Index - 295
eISSN - 1527-1315
pISSN - 0033-8419
DOI - 10.1148/radiol.212283
Subject(s) - medicine , culprit , amaurosis fugax , atheroma , stenosis , neurovascular bundle , stroke (engine) , radiology , magnetic resonance imaging , prospective cohort study , cardiology , nuclear medicine , pathology , myocardial infarction , mechanical engineering , engineering
Background MRI and fluorine 18-labeled sodium fluoride ( 18 F-NaF) PET can be used to identify features of plaque instability, rupture, and disease activity, but large studies have not been performed. Purpose To evaluate the association between 18 F-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 18 F-NaF PET/MRI. An experienced clinician determined the culprit carotid artery based on symptoms and record review. 18 F-NaF uptake was quantified using standardized uptake values and tissue-to-background ratios. Statistical significance was assessed with the Welch, χ 2 , Wilcoxon, or Fisher test. Multivariable models were used to evaluate the relationship between the imaging markers and the culprit versus nonculprit vessel. Results 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 18 F-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 18 F-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. Conclusion 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 © RSNA, 2022 Online supplemental material is available for this article.