Gene expression and 18FDG uptake in atherosclerotic carotid plaques

Research output: Contribution to journalJournal articleResearchpeer-review

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Gene expression and 18FDG uptake in atherosclerotic carotid plaques. / Pedersen, Sune Folke; Graebe, Martin; Fisker Hag, Anne Mette; Højgaard, Liselotte; Sillesen, Henrik; Kjaer, Andreas; Pedersen, Sune Folke; Græbe, Martin; Hag, Anne Mette Fisker; Højgaard, Liselotte; Sillesen, Henrik Hegaard; Kjær, Andreas.

In: Nuclear Medicine Communications, Vol. 31, No. 5, 01.05.2010, p. 423-9.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Pedersen, SF, Graebe, M, Fisker Hag, AM, Højgaard, L, Sillesen, H, Kjaer, A, Pedersen, SF, Græbe, M, Hag, AMF, Højgaard, L, Sillesen, HH & Kjær, A 2010, 'Gene expression and 18FDG uptake in atherosclerotic carotid plaques', Nuclear Medicine Communications, vol. 31, no. 5, pp. 423-9. https://doi.org/10.1097/MNM.0b013e32833767e0

APA

Pedersen, S. F., Graebe, M., Fisker Hag, A. M., Højgaard, L., Sillesen, H., Kjaer, A., ... Kjær, A. (2010). Gene expression and 18FDG uptake in atherosclerotic carotid plaques. Nuclear Medicine Communications, 31(5), 423-9. https://doi.org/10.1097/MNM.0b013e32833767e0

Vancouver

Pedersen SF, Graebe M, Fisker Hag AM, Højgaard L, Sillesen H, Kjaer A et al. Gene expression and 18FDG uptake in atherosclerotic carotid plaques. Nuclear Medicine Communications. 2010 May 1;31(5):423-9. https://doi.org/10.1097/MNM.0b013e32833767e0

Author

Pedersen, Sune Folke ; Graebe, Martin ; Fisker Hag, Anne Mette ; Højgaard, Liselotte ; Sillesen, Henrik ; Kjaer, Andreas ; Pedersen, Sune Folke ; Græbe, Martin ; Hag, Anne Mette Fisker ; Højgaard, Liselotte ; Sillesen, Henrik Hegaard ; Kjær, Andreas. / Gene expression and 18FDG uptake in atherosclerotic carotid plaques. In: Nuclear Medicine Communications. 2010 ; Vol. 31, No. 5. pp. 423-9.

Bibtex

@article{e4eb5a40d13711df825b000ea68e967b,
title = "Gene expression and 18FDG uptake in atherosclerotic carotid plaques",
abstract = "PURPOSE: Metabolic assessment of vascular inflammation by 2-[F]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=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=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.",
author = "Pedersen, {Sune Folke} and Martin Graebe and {Fisker Hag}, {Anne Mette} and Liselotte H{\o}jgaard and Henrik Sillesen and Andreas Kjaer and Pedersen, {Sune Folke} and Martin Gr{\ae}be and Hag, {Anne Mette Fisker} and Liselotte H{\o}jgaard and Sillesen, {Henrik Hegaard} and Andreas Kj{\ae}r",
note = "Keywords: Aged; Aged, 80 and over; Atherosclerosis; Biological Markers; Biological Transport; Carotid Stenosis; Female; Fluorodeoxyglucose F18; Gene Expression Profiling; Glycolysis; Humans; Male; Middle Aged; Polymerase Chain Reaction",
year = "2010",
month = "5",
day = "1",
doi = "10.1097/MNM.0b013e32833767e0",
language = "English",
volume = "31",
pages = "423--9",
journal = "Nuclear Medicine Communications",
issn = "0143-3636",
publisher = "Lippincott Williams & Wilkins",
number = "5",

}

RIS

TY - JOUR

T1 - Gene expression and 18FDG uptake in atherosclerotic carotid plaques

AU - Pedersen, Sune Folke

AU - Graebe, Martin

AU - Fisker Hag, Anne Mette

AU - Højgaard, Liselotte

AU - Sillesen, Henrik

AU - Kjaer, Andreas

AU - Pedersen, Sune Folke

AU - Græbe, Martin

AU - Hag, Anne Mette Fisker

AU - Højgaard, Liselotte

AU - Sillesen, Henrik Hegaard

AU - Kjær, Andreas

N1 - Keywords: Aged; Aged, 80 and over; Atherosclerosis; Biological Markers; Biological Transport; Carotid Stenosis; Female; Fluorodeoxyglucose F18; Gene Expression Profiling; Glycolysis; Humans; Male; Middle Aged; Polymerase Chain Reaction

PY - 2010/5/1

Y1 - 2010/5/1

N2 - PURPOSE: Metabolic assessment of vascular inflammation by 2-[F]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=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=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.

AB - PURPOSE: Metabolic assessment of vascular inflammation by 2-[F]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=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=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.

U2 - 10.1097/MNM.0b013e32833767e0

DO - 10.1097/MNM.0b013e32833767e0

M3 - Journal article

VL - 31

SP - 423

EP - 429

JO - Nuclear Medicine Communications

JF - Nuclear Medicine Communications

SN - 0143-3636

IS - 5

ER -

ID: 22361833