24Background: A significant proportion of ischemic strokes are caused by emboli from 25 unstable atherosclerotic carotid artery plaques with inflammation being a key feature of 26 plaque instability and stroke risk. Positron emission tomography (PET) depicting the uptake 27 of 2-deoxy-2-( 18 F)-fluoro-D-glucose ( 18 F-FDG) in carotid artery plaques is a promising 28 technique to quantify plaque inflammation. A consensus on the methodology for plaque 29 localization and quantification of inflammation by 18 F-FDG PET/computed tomography (CT) 30 in atherosclerosis has not been established. High inter-reader agreement is essential if 18 F-31 FDG PET/CT is to be used as a clinical tool for the assessment of unstable plaques and stroke 32 risk. The aim of our study was to assess the inter-reader variability of different methods for 33 quantification of 18 F-FDG uptake in carotid atherosclerotic plaques with a separate CT 34 angiography (CTA) providing anatomical guidance.
35Methods and results: Forty-three patients with carotid artery stenosis ≥70% underwent 18 F-36 FDG PET/CT. Two independent readers separately delineated the plaque in all axial PET 37 slices containing the atherosclerotic plaque and the maximum standardized uptake value 38 (SUV max ) from each slice was measured. Uptake values with and without background 39 correction were calculated. Intraclass correlation coefficients were highest for uncorrected 40 uptake values (0.97-0.98) followed by those background corrected by subtraction (0.89-0.94) 41 and lowest for those background corrected by division (0.74-0.79). There was a significant 42 difference between the two readers definition of plaque extension, but this did not affect the 43 inter-reader agreement of the uptake parameters. 44 Conclusions: Quantification methods without background correction have the highest inter-45 reader agreement for 18 F-FDG PET of carotid artery plaque inflammation. The use of the 46 single highest uptake value (max SUV max ) from the plaque will facilitate the method's clinical 47 49 Ischemic strokes caused by thromboembolism from an unstable atherosclerotic plaque 50 in the carotid artery can be prevented by carotid endarterectomy (CEA) [1-3]. Patients are 51 selected for CEA based on the degree of carotid artery stenosis and presence or absence of 52 cerebral ischemic symptoms. In recent years it has become increasingly clear that the degree 53 of stenosis alone is not the best predictor of stroke risk. This has led to the concept of the 54 'unstable plaque' describing carotid plaques that carry high risk of stroke irrespective of the 55 degree of artery stenosis and increased focus on factors that destabilize the plaque. 56 Inflammation plays a key role in the development of an unstable plaque [4-6].57 Positron emission tomography (PET) imaging of atherosclerosis has been rapidly 58 evolving since the first reports of 2-deoxy-2-( 18 F)-fluoro-D-glucose ( 18 F-FDG) uptake 59 localized to the inflammatory macrophage rich areas in carotid artery plaques [7]. Th...