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(Stroke. 2005;36:2642.)
© 2005 American Heart Association, Inc.

Original Contributions

Identification of Culprit Lesions After Transient Ischemic Attack by Combined ¹⁸F Fluorodeoxyglucose Positron-Emission Tomography and High-Resolution Magnetic Resonance Imaging

John R. Davies, BSc, MRCP; James H.F. Rudd, PhD, MRCP; Tim D. Fryer, PhD; Martin J. Graves, MSc; John C. Clark, DSc; Peter J. Kirkpatrick, MSc, FRCS; Jonathan H. Gillard, MD, FRCR; Elizabeth A. Warburton, DM, MRCP Peter L. Weissberg, MD, FRCP

From the Division of Cardiovascular Medicine (J.R.D., J.H.F.R., P.L.W.), Wolfson Brain Imaging Centre (T.D.F., J.C.C.), and Departments of Radiology (M.J.G., J.H.G.), Neurosurgery (P.J.K.), and Clinical Neurosciences (E.A.W.), University of Cambridge, Addenbrooke’s Hospital, Cambridge, United Kingdom.

Correspondence to John Davies, BSc, MRCP, Division of Cardiovascular Medicine, Level 6, ACCI, Box 110, Addenbrooke’s Hospital, Hills Rd, Cambridge, CB2 2QQ, United Kingdom. E-mail jrd36{at}mole.bio.cam.ac.uk

Background and Purpose— Carotid endarterectomy is currently guided by angiographic appearance on the assumption that the most stenotic lesion visible at angiography is likely to be the lesion from which future embolic events will arise. However, risk of plaque rupture, the most common cause of atherosclerosis-related thromboembolism, is dictated by the composition of the plaque, in particular the degree of inflammation. Angiography may, therefore, be an unreliable method of identifying vulnerable plaques. In this study, plaque inflammation was quantified before endarterectomy using the combination of ¹⁸F fluorodeoxyglucose positron (FDG)-emission tomography (PET) and high-resolution MRI (HRMRI).

Methods— Twelve patients, all of whom had suffered a recent transient ischemic attack, had a severe stenosis in the ipsilateral carotid artery, and were awaiting carotid endarterectomy underwent FDG-PET and HRMRI scanning. A semiquantitative estimate of plaque inflammation was calculated for all of the lesions identified on HRMRI.

Results— In 7 of 12 patients (58%), high FDG uptake was seen in the lesion targeted for endarterectomy. In the remaining 5 patients, FDG uptake in the targeted lesion was low. In these 5 patients, 3 had nonstenotic lesions identified on HRMRI that exhibited a high level of FDG uptake. All 3 of the highly inflamed nonstenotic lesions were located in a vascular territory compatible with the patients’ presenting symptoms.

Conclusions— Our data suggest that angiography may not always identify the culprit lesion. Combined FDG-PET and HRMRI can assess the degree of inflammation in stenotic and nonstenotic plaques and could potentially be used to identify lesions responsible for embolic events.

Key Words: atherosclerosis • carotid endarterectomy • inflammation • MRI • positron emission tomography

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