Microvessel density but not neoangiogenesis is associated with 18F-FDG uptake in human atherosclerotic carotid plaques

The vulnerable atherosclerotic lesion exhibits the proliferation of neovessels and inflammation. The imaging modality 2-deoxy-2-[(18)F]fluoro-D: -glucose positron emission tomography ((18)FDG-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 (18)FDG 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 α(V) and integrin β(3) 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 (18)FDG-PET. VEGF and integrin α(V)β(3) gene expression did not correlate with (18)FDG uptake, whereas CD34 gene expression exhibited an inverse correlation with (18)FDG uptake. Additionally, we established that markers of vulnerability were correlated with (18)FDG uptake.

Neoangiogenesis is not associated with (18)FDG uptake, whereas MVD and markers of vulnerability correlate with (18)FDG uptake. The absence of correlation between markers of neoangiogenesis and (18)FDG uptake suggests a temporal separation between the process of neoangiogenesis and inflammatory activity.