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(Circulation. 2002;105:2708.)
© 2002 American Heart Association, Inc.
Brief Rapid Communication |
From the Division of Cardiovascular Medicine (J.H.F.R., H.A.J., P.L.W.), Division of Stroke Medicine (E.A.W.), Wolfson Brain Imaging Centre (T.D.F., J.C.C., J.D.P.), Department of Radiology (N.A.), Clinical Pharmacology Unit (P.J., A.P.D.), Division of Neurosurgery (P.J.K.), and Centre for Applied Medical Statistics (B.N.A), University of Cambridge, Addenbrookes Hospital, Cambridge, UK.
Correspondence to Professor Peter L Weissberg, Box 110, Level 6, ACCI, Addenbrookes Hospital, Hills Road, Cambridge CB2 2QQ, UK. E-mail plw{at}mole.bio.cam.ac.uk
Background Atherosclerotic plaque rupture is usually a consequence of inflammatory cell activity within the plaque. Current imaging techniques provide anatomic data but no indication of plaque inflammation. The glucose analogue [18F]-fluorodeoxyglucose (18FDG) can be used to image inflammatory cell activity non-invasively by PET. In this study we tested whether 18FDG-PET imaging can identify inflammation within carotid artery atherosclerotic plaques.
Methods and Results Eight patients with symptomatic carotid atherosclerosis were imaged using 18FDG-PET and co-registered CT. Symptomatic carotid plaques were visible in 18FDG-PET images acquired 3 hours post-18FDG injection. The estimated net 18FDG accumulation rate (plaque/integral plasma) in symptomatic lesions was 27% higher than in contralateral asymptomatic lesions. There was no measurable 18FDG uptake into normal carotid arteries. Autoradiography of excised plaques confirmed accumulation of deoxyglucose in macrophage-rich areas of the plaque.
Conclusions This study demonstrates that atherosclerotic plaque inflammation can be imaged with 18FDG-PET, and that symptomatic, unstable plaques accumulate more 18FDG than asymptomatic lesions.
Key Words: atherosclerosis imaging nuclear medicine
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