Original Research
Correlation Between Arterial FDG Uptake and Biomarkers in Peripheral Artery Disease

https://doi.org/10.1016/j.jcmg.2011.08.019Get rights and content
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Objectives

A prospective, multicenter 18fluorine-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET)/computed tomography (CT) imaging study was performed to estimate the correlations among arterial FDG uptake and atherosclerotic plaque biomarkers in patients with peripheral artery disease.

Background

Inflammation within atherosclerotic plaques is associated with instability of the plaque and future cardiovascular events. Previous studies have shown that 18F-FDG-PET/CT is able to quantify inflammation within carotid artery atherosclerotic plaques, but no studies to date have investigated this correlation in peripheral arteries with immunohistochemical confirmation.

Methods

Thirty patients across 5 study sites underwent 18F-FDG-PET/CT imaging before SilverHawk atherectomy (FoxHollow Technologies, Redwood City, California) for symptomatic common or superficial femoral arterial disease. Vascular FDG uptake (expressed as target-to-background ratio) was measured in the carotid arteries and aorta and femoral arteries, including the region of atherectomy. Immunohistochemistry was performed on the excised atherosclerotic plaque extracts, and cluster of differentiation 68 (CD68) level as a measure of macrophage content was determined. Correlations between target-to-background ratio of excised lesions, as well as entire arterial regions, and CD68 levels were determined. Imaging was performed during the 2 weeks before surgery in all cases.

Results

Twenty-one patients had adequate-quality 18F-FDG-PET/CT peripheral artery images, and 34 plaque specimens were obtained. No significant correlation between lesion target-to-background ratio and CD68 level was observed.

Conclusions

There were no significant correlations between CD68 level (as a measure of macrophage content) and FDG uptake in the peripheral arteries in this multicenter study. Differences in lesion extraction technique, lesion size, the degree of inflammation, and imaging coregistration techniques may have been responsible for the failure to observe the strong correlations with vascular FDG uptake observed in previous studies of the carotid artery and in several animal models of atherosclerosis.

Key Words

atherosclerosis
FDG-PET/CT
inflammation
peripheral artery disease

Abbreviations and Acronyms

CAD
coronary artery disease
CD68
cluster of differentiation 68
CT
computed tomography
18F-FDG
18flourine-fluorodeoxyglucose
PAD
peripheral artery disease
PET
positron emission tomography
TBR
target-to-background ratio

Cited by (0)

This research was funded by the National Institutes of Health/National Heart, Lung and Blood Institute (NIH/NHLBI R01 HL71021, NIH/NHLBI and the Doris Duke Clinical Research Foundation. R01 HL78667, and NIH/NIBIB R01 EB009638 [to Dr. Fayad]) and by unrestricted research grants from Merck Research Laboratories and FoxHollow Technologies. Dr. Myers was supported by the Doris Duke Charitable Foundation and Dr. Rudd by the NIHR Cambridge Biomedical Research Center and an International Fellowship from the British Heart Foundation. Ms. Burke, Ms. Pinto, Mr. Klimas, Mr. Hargreaves, and Dr. Dansky are associated with Merck Research Laboratories. Dr. Hailman and Mr. Bolognese were associated with Merck Research Laboratories during the research study but are currently associated with Novartis Institutes for Biomedical Research Inc. and Cytel Inc., respectively. H. William Strauss, MD, served as Guest Editor for this paper.