Institutional members access full text with Ovid®

Share this article on:

Gene expression and 18FDG uptake in atherosclerotic carotid plaques

Pedersen, Sune Folkea b; Graebe, Martinc; Fisker Hag, Anne Mettea b; Højgaard, Liselottea b; Sillesen, Henrikc; Kjaer, Andreasa b

Nuclear Medicine Communications: May 2010 - Volume 31 - Issue 5 - p 423-429
doi: 10.1097/MNM.0b013e32833767e0
Original Articles

Purpose Metabolic assessment of vascular inflammation by 2-[18F]fluoro-2-deoxy-D-glucose positron emission tomography (FDG)-PET is a promising new approach for the evaluation of the vulnerability of atherosclerotic plaques. Quantitative real-time PCR allows measurement of gene expression of markers of atherosclerotic plaque vulnerability. These techniques were applied in advanced atherosclerotic disease to relate metabolism and inflammatory activity to the gene expression profile of the vulnerable atherosclerotic plaque.

Methods Seventeen patients with clinical symptoms of cerebral vascular events (<3 months) and an additional ipsilateral internal carotid artery stenosis of greater than 60% were recruited. FDG uptake in the carotids was determined by PET/computed tomography and expressed as mean and maximal standardized uptake values (SUVmean and SUVmax). The atherosclerotic plaques were subsequently recovered by carotid endarterectomy. The gene expression of markers of vulnerability – CD68, IL-18, matrix metalloproteinase 9, cathepsin K, GLUT-1, and hexokinase type II (HK2) – were measured in plaques by quantitative PCR.

Results In a multivariate linear regression model, GLUT-1, CD68, cathepsin K, and HK2 gene expression remained in the final model as predictive variables of FDG accumulation calculated as SUVmean (R 2=0.26, P<0.0001). In addition, a multivariate linear regression model found GLUT-1, CD68, cathepsin K, and HK2 gene expression as independent predictive variables of FDG accumulation calculated as SUVmax (R 2=0.30, P<0.0001).

Conclusion GLUT-1, HK2, CD68, and cathepsin K remained in both multivariate models and thus provided independent information regarding FDG uptake. We suggest that FDG uptake is a composite indicator of macrophage load, overall inflammatory activity and collagenolytic plaque destabilization. Accordingly, FDG-PET could prove to be an important predictor of cerebrovascular events in patients with carotid plaques.

aCluster for Molecular Imaging

bDepartment of Clinical Physiology, Nuclear Medicine and PET,

cDepartment of Vascular Surgery, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark

Correspondence to Sune Folke Pedersen, MSc, Cluster for Molecular Imaging, University of Copenhagen, Blegdamsvej 3, Copenhagen N 2200, Denmark

Tel: +45 35326007; fax: +45 35327555; e-mail:

Received 8 December 2009 Accepted 11 January 2010

© 2010 Lippincott Williams & Wilkins, Inc.