1 18F-fluoride and 18F-fluorodeoxyglucose positron emission tomography after transient ischaemic attack or minor ischaemic stroke

IntroductionCombined positron emission tomography (PET) and computed tomography (CT) has the potential to assess both the anatomy and biology of carotid atherosclerosis. We sought to assess whether 18F-fluoride or 18F-fluorodeoxyglucose can identify culprit and high-risk carotid plaque.MethodsWe per...

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Veröffentlicht in:Heart (British Cardiac Society) 2018-05, Vol.104 (Suppl 5), p.A1
Hauptverfasser: Vesey, Alex T, Jenkins, William SA, Irkle, Agnese, Moss, Alastair, Sng, Greg, Forsythe, Rachael O, Clark, Tim, Roberts, Gemma, Fletcher, Alison, Lucatelli, Christophe, Rudd, James HF, Davenport, Anthony P, Mills, Nicholas L, Al-Shahi Salman, Rustam, Dennis, Martin, Whiteley, William N, van Beek, Edwin JR, Dweck, Marc R, Newby, David E
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Sprache:eng
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Zusammenfassung:IntroductionCombined positron emission tomography (PET) and computed tomography (CT) has the potential to assess both the anatomy and biology of carotid atherosclerosis. We sought to assess whether 18F-fluoride or 18F-fluorodeoxyglucose can identify culprit and high-risk carotid plaque.MethodsWe performed 18F-fluoride and 18F-fluorodeoxygluose PET/CT in 26 patients following recent stroke/transient ischaemic attack: 18 patients with culprit carotid stenosis awaiting carotid endarterectomy and 8 control patients without culprit carotid atheroma. We compared standardised uptake values (SUVs) in the clinically adjudicated culprit to the contralateral asymptomatic artery, and assessed the relationship between radiotracer uptake and plaque phenotype or predicted cardiovascular risk.ResultsCarotid 18F-fluoride uptake was increased in clinically adjudicated culprit plaques compared to the asymptomatic contralateral plaques (log10SUVmean 0.29±0.10 versus 0.23±0.11, p=0.001) and compared to control patients (log10SUVmean 0.29±0.10 versus 0.12±0.11, p=0.001). 18F-Fluoride uptake correlated with high-risk plaque features (remodelling index [r=0.53, p=0.003]; plaque burden [r=0.51, p=0.004]) and predicted cardiovascular risk (r=0.65, p=0.002). Consistent with the binding of necrotic tissue, 18F-fluoride bound avidly to regions of cerebral infarction (SUVmean4.8±1.98 versus SUVmean of 0.07±0.02, infarcted versus non-infarcted cerebrum; p
ISSN:1355-6037
1468-201X
DOI:10.1136/heartjnl-2018-BCVI.1