James Rudd

18F-Fluoride and 18F-Fluorodeoxyglucose Positron Emission Tomography After Transient Ischemic Attack or Minor Ischemic StrokeCLINICAL PERSPECTIVE: Case–Control Study

Background— Combined positron emission tomography (PET) and computed tomography (CT) can assess both 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 and Results— We performed 18F-fluoride and 18F-fluorodeoxyglucose PET/CT in 26 patients after recent transient ischemic attack or minor ischemic stroke: 18 patients with culprit carotid stenosis awaiting carotid endarterectomy and 8 controls without culprit carotid atheroma. We compared standardized uptake values in the clinically adjudicated culprit to the contralateral asymptomatic artery, and assessed the relationship between radiotracer uptake and plaque phenotype or predicted cardiovascular risk (ASSIGN score [Assessing Cardiovascular Risk Using SIGN Guidelines to Assign Preventive Treatment]). We also performed micro PET/CT and histological analysis of excised plaque. On histological and micro PET/CT analysis, 18F-fluoride selectively highlighted microcalcification. Carotid 18F-fluoride uptake was increased in clinically adjudicated culprit plaques compared with asymptomatic contralateral plaques (log10standardized uptake valuemean 0.29±0.10 versus 0.23±0.11, P=0.001) and compared with control patients (log10standardized uptake valuemean 0.29±0.10 versus 0.12±0.11, P=0.001). 18F-Fluoride uptake correlated with high-risk plaque features (remodeling 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]). Carotid 18F-fluorodeoxyglucose uptake appeared to be increased in 7 of 16 culprit plaques, but no overall differences in uptake were observed in culprit versus contralateral plaques or control patients. However, 18F-fluorodeoxyglucose did correlate with predicted cardiovascular risk (r=0.53, P=0.019), but not with plaque phenotype. Conclusions— 18F-Fluoride PET/CT highlights culprit and phenotypically high-risk carotid plaque. This has the potential to improve risk stratification and selection of patients who may benefit from intervention.

Cardiac Alpha-V Beta-3 Integrin Expression Following Acute Myocardial Infarction in Humans

The study and MRD, WJ and DEN are supported by the British Heart Foundation (FS/12/84, FS/10/026, CH/09/002, R M/13/2/30158, RE/13/3/30183). DEN is the recipient of a Wellcome Trust Senior Investigator Award (WT103782AIA). JHFR is part-funded by the NIHR Cambridge Biomedical Research Centre. The Wellcome Trust Clinical Research Facility and Clinical Research Imaging Centre are supported by NHS Research Scotland (NRS) through NHS Lothian.

GM-CSF ENHANCES GLYCOLYTIC ACTIVITY IN MACROPHAGES IN VITROAND IMPROVES DETECTION OF ATHEROSCLEROTIC INFLAMMATION IN VIVO

18F-fluorodeoxyglucose (FDG) accumulates in activated macrophages (Mo). Here, we test the hypotheses that GM-CSF, a clinically administered cytokine, augments Mo glycolysis in vitro and enhances imaging of arterial inflammation in vivo. In vitro experiments were conducted in human and murine M

Corrigendum: PET imaging of the neurovascular interface in cerebrovascular disease

This corrects the article DOI: 10.1038/nrneurol.2017.129