Microvessel Density But Not Neoangiogenesis Is Associated with 18F-FDG Uptake in Human Atherosclerotic Carotid Plaques

Sune Folke Pedersen, Martin Graebe, Anne Mette Fisker Hag, Liselotte Hoejgaard, Henrik Sillesen, Andreas Kjaer

Research output: Contribution to journalJournal articleResearchpeer-review


The vulnerable atherosclerotic lesion exhibits the proliferation of neovessels and inflammation. The imaging modality 2-deoxy-2-[18F]fluoro-d-glucose positron emission tomography (18FDG-PET) is considered for the identification of vulnerable plaques.The purpose of this study was to compare the gene expression of neoangiogenesis and vulnerability-associated genes with 18FDG uptake in patients undergoing carotid endarterectomy.Human atherosclerotic carotid artery plaques from symptomatic patients were used for gene expression analysis by quantitative PCR of vascular endothelial growth factor (VEGF) and integrin αV and integrin β3 subunits, genes essential during neoangiogenesis. We also evaluated the gene expression of CD34, a measure of microvessel density (MVD), as well as CD68, MMP-9, and cathepsin K, genes of major importance in plaque vulnerability. Gene expression analysis was compared with 18FDG-PET.VEGF and integrin αVβ3 gene expression did not correlate with 18FDG uptake, whereas CD34 gene expression exhibited an inverse correlation with 18FDG uptake. Additionally, we established that markers of vulnerability were correlated with 18FDG uptake.Neoangiogenesis is not associated with 18FDG uptake, whereas MVD and markers of vulnerability correlate with 18FDG uptake. The absence of correlation between markers of neoangiogenesis and 18FDG uptake suggests a temporal separation between the process of neoangiogenesis and inflammatory activity.
Original languageEnglish
JournalMolecular Imaging and Biology
Issue number3
Pages (from-to)384-392
Publication statusPublished - 2012
Externally publishedYes


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