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Jenkins, William S; Vesey, Alex T; Vickers, Anna; Neale, Anoushka; Moles, Catriona; Connell, Martin; Joshi, Nikhil Vilas; Lucatelli, Christophe; Fletcher, Alison M; Spratt, James C; Mirsadraee, Saeed; van Beek, Edwin Jr; Rudd, James Hf; Newby, David E; Dweck, Marc R
Heart, 12/2019, Volume: 105, Issue: 24Journal Article
Intraplaque angiogenesis and inflammation are key promoters of atherosclerosis and are mediated by the alpha-V beta-3 (α β ) integrin pathway. We investigated the applicability of the α β -integrin receptor-selective positron emission tomography (PET) radiotracer 18F-fluciclatide in assessing human aortic atherosclerosis. Vascular 18F-fluciclatide binding was evaluated using ex vivo analysis of carotid endarterectomy samples with autoradiography and immunohistochemistry, and in vivo kinetic modelling following radiotracer administration. Forty-six subjects with a spectrum of atherosclerotic disease categorised as stable (n=27) or unstable (n=19; recent myocardial infarction) underwent PET and CT imaging of the thorax after administration of 229 (IQR 217-237) MBq 18F-fluciclatide. Thoracic aortic 18F-fluciclatide uptake was quantified on fused PET-CT images and corrected for blood-pool activity using the maximum tissue-to-background ratio (TBR ). Aortic atherosclerotic burden was quantified by CT wall thickness, plaque volume and calcium scoring. 18F-Fluciclatide uptake co-localised with regions of increased α β integrin expression, and markers of inflammation and angiogenesis. 18F-Fluciclatide vascular uptake was confirmed in vivo using kinetic modelling, and on static imaging correlated with measures of aortic atherosclerotic burden: wall thickness (r=0.57, p=0.001), total plaque volume (r=0.56, p=0.001) and aortic CT calcium score (r=0.37, p=0.01). Patients with recent myocardial infarction had greater aortic 18F-fluciclatide uptake than those with stable disease (TBR 1.29 vs 1.21, p=0.02). In vivo expression of α β integrin in human aortic atheroma is associated with plaque burden and is increased in patients with recent myocardial infarction. Quantification of α β integrin expression with 18F-fluciclatide PET has potential to assess plaque vulnerability and disease activity in atherosclerosis.
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