Abstract 20055: The αvβ3 Integrin Positron Emission Tomography Radiotracer 18F-Fluciclatide is a Marker of Remodeling Following Myocardial Infarction
Introduction: The integrin receptor αvβ3 is upregulated by vascular endothelial cells, macrophages and myofibroblasts during cardiac interstitial remodeling. We evaluated the role for the novel αvβ3 radiotracer 18F-fluciclatide in the non-invasive assessment of repair post-myocardial infarction.
Methods: We performed combined PET/CT and CT-coronary angiography (CTCA) imaging of the heart following intravenous administration of 18F-fluciclatide (230mBq) in 21 patients 12±4 days after acute ST-elevation myocardial infarction, 7 stable patients with occlusion of a major coronary vessel for >6months, and 9 healthy volunteers. ECG-gated PET data was acquired over 30 minutes, 40 minutes after ligand injection. Subjects also underwent Cardiac MRI (CMR) with assessment of late gadolinium enhancement and T1 mapping.
PET data was fused with the CTCA and re-orientated into the left ventricular short-axis plane. The infarct site was identified through co-registration with CMR and delineated using regions of interest and a 16-segment approach. PET values, corrected for blood activity, were expressed as a mean tissue-to-background ratio. Myocardial extracellular volume (ECV) in a 16-segment model was quantified on CMR using T1 mapping pre-and post-gadolinium administration.
Results: 18F-fluciclatide uptake correlated with cardiac ECV (r=0.37(0.29-0.45),p<0.001), and was increased in sites of acute myocardial infarction when compared to regions of remote myocardium (1.32±0.23 vs 0.85±0.17; p<0.001), sites of established infarction in subjects with a chronically occluded coronary vessel (1.32±0.23 vs 0.70±0.14; p<0.001), and when matched with regions in control subjects (0.94±0.23 vs 0.67±0.09; p=0.003).
Conclusions: 18F-Fluciclatide uptake localises to sites of acute myocardial infarction and correlates with extracellular volume on CMR. This holds great potential in the non-invasive quantification of active myocardial remodeling.
Author Disclosures: W.S. Jenkins: None. A. Vesey: None. A. Neale: None. V. Anna: None. C. Moles: None. C. Lucatelli: None. A. Fletcher: None. S. Mirsadee: None. E.J. Van Beek: None. J.H. Rudd: Research Grant; Modest; JHFR is part-supported by the NIHR Cambridge Biomedical Research Centre, the British Heart Foundation and the Wellcome Trust. M.R. Dweck: None. D.E. Newby: None.
- © 2015 by American Heart Association, Inc.