TY - JOUR
T1 - 18F-NaF PET-MRI for detection of Carotid Atheroma in acute neurovascular syndrome
AU - Kaczynski, Jakub
AU - Sellers , Stephanie
AU - Seidman, Michael A.
AU - Syed, Maaz
AU - Dennis, Martin
AU - Macnaught, Gillian
AU - Jansen, Maurits
AU - Semple, Scott I
AU - Alcaide-Corral, Carlos
AU - Tavares, Adriana A S
AU - MacGillivray, Tom
AU - Debono, Samuel
AU - Forsythe, Rachael
AU - Tambyraja, Andrew
AU - Slomka, Piotr J
AU - Leipsic, Jonathon
AU - Dweck, Marc R
AU - Whiteley, William
AU - Wardlaw, Joanna
AU - van Beek, Edwin J R
AU - Newby, David E
AU - Williams, Michelle C
N1 - Funding Information:
Disclosures of conflicts of interest: J.K. No relevant relationships. S.S. No relevant relationships. M.A.S. No relevant relationships. M.S. No relevant relationships. M.D. No relevant relationships. G.M. No relevant relationships. M.J. No relevant relationships. S.I.S. No relevant relationships. C.A.C. No relevant relationships. A.A.S.T. No relevant relationships. T.M. No relevant relationships. S.D. No relevant relationships. R.F. No relevant relationships. A.T. Educational grants to institution from Medtronic and WL Gore; honoraria for lectures from Shockwave Medical; travel support from Shockwave Medical. P.J.S. Grants from the National Institutes of Health and Siemens Medical Systems; software royalties from Cedars-Sinai Medical Center. J.L. Grant to institution from GE Healthcare; consulting fees from HeartFlow and Circle Cardiovascular Imaging; modest payment for lectures from Philips and GE Healthcare; stock or stock options in HeartFlow and Circle Cardiovascular Imaging. M.R.D. No relevant relationships. W.W. Consulting fees from Bayer; payment for expert testimony as an independent witness to UK courts; participation on data safety monitoring boards for academic trials. J.W. Academic research grants to institution from the Medical Research Council, British Heart Foundation, Stroke Association, Leducq Foundation, EU Horizon 2020 Initiative, Age UK, Alzheimer’s Society, and Alzheimer’s Research UK. E.J.R.v.B. Owner of QCTIS; honoraria for presentations from Roche Diagnostics and AstraZeneca; membership on the advisory board for Aidence and steering committee for AstraZeneca. D.E.N. Educational grant to institution from Siemens Healthineers. M.C.W. Payment for a speaker bureau from Canon Medical Systems; president elect of the British Society of Cardiovascular Imaging/British Society of Cardiac Computer Tomography, member of the board of directors of the Society of Cardiovascular Computed Tomography, and member of the guidelines committee of the European Society of Cardiovascular Radiology.
Funding Information:
J.K., M.S., A.A.S.T., S.D., D.E.N., and M.C.W. are supported by the British Heart Foundation (FS/17/50/33061, FS/18/31/33676, PG/21/10461, FS/19/34/34354, CH/09/002, RG/16/10/32375, RE/18/5/34216, and FS/ICRF/20/26002). A.A.S.T. is a recipient of a Wellcome Trust Technology Development Award (221295/Z/20/Z). J.L. receives support from GE Healthcare. J.W. is supported by the UK Dementia Research Institute, which receives its funding from DRI, funded by the UK Medical Research Council, Alzheimer’s Society, and Alzheimer’s Research UK. D.E.N. is the recipient of a Wellcome Trust Senior Investigator Award (WT103782AIA).
Funding Information:
This study was funded by the British Heart Foundation (FS/17/50/33061) and is part of the British Heart Foundation Centre for Research Excellence at the University of Edinburgh (RE/18/5/34216). The Medical Research Council provided funding for the PET/MRI scanner through the Dementias Platform UK Integrated DEmentiA research environment (IDEA) grant (MR/M024717/1).
Funding Information:
Acknowledgments: We acknowledge the help and support of Edinburgh Clinical Research Facility, Edinburgh Imaging Facility, and the Academic and Clinical Central Office of Research and Development of NHS Lothian, which receive funding from NHS Research Scotland. We also acknowledge financial support from Siemens Healthcare.
Publisher Copyright:
© RSNA, 2022.
PY - 2022/6/7
Y1 - 2022/6/7
N2 - 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.BackgroundMRI 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.PurposeTo evaluate the association between 18F-NaF activity and culprit carotid plaque in acute neurovascular syndrome.Materials and MethodsIn 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.ResultsA 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.ConclusionFluorine 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
AB - 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.BackgroundMRI 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.PurposeTo evaluate the association between 18F-NaF activity and culprit carotid plaque in acute neurovascular syndrome.Materials and MethodsIn 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.ResultsA 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.ConclusionFluorine 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
U2 - 10.1148/radiol.212283
DO - 10.1148/radiol.212283
M3 - Article
SN - 0033-8419
JO - Radiology
JF - Radiology
ER -