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1 18F-fluoride and 18F-fluorodeoxyglucose positron emission tomography after transient ischaemic attack or minor ischaemic stroke
  1. Alex T Vesey1,
  2. William SA Jenkins1,
  3. Agnese Irkle2,
  4. Alastair Moss1,
  5. Greg Sng1,
  6. Rachael O Forsythe1,
  7. Tim Clark3,
  8. Gemma Roberts3,
  9. Alison Fletcher3,
  10. Christophe Lucatelli3,
  11. James HF Rudd2,
  12. Anthony P Davenport2,
  13. Nicholas L Mills1,
  14. Rustam Al-Shahi Salman4,
  15. Martin Dennis4,
  16. William N Whiteley4,
  17. Edwin JR van Beek3,
  18. Marc R Dweck1,3,
  19. David E Newby1,3
  1. 1BHF Centre for Cardiovascular Science, University of Edinburgh, UK
  2. 2Division of Experimental Medicine and Immunotherapeutics, University of Cambridge, UK
  3. 3Clinical Research Imaging Centre, University of Edinburgh, UK
  4. 4Centre for Clinical Brain Sciences, University of Edinburgh, UK


Introduction Combined 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.

Methods We 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.

Results Carotid 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<0.001). Carotid 18F-FDG uptake appeared to be increased in 7/16 culprit plaques but no overall differences in uptake were observed in the culprit versus the contralateral plaques or control patients. However, 18F-FDG did correlate with predicted cardiovascular risk (r=0.53, p=0.019) but not with plaque phenotype.

Conclusion 18F-Fluoride PET/CT highlights culprit carotid plaque. This has the potential to improve risk-stratification and the selection of those patients who would benefit from surgical intervention.

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