In Vivo 18F-Fluorodeoxyglucose Positron Emission Tomography Imaging Provides a Noninvasive Measure of Carotid Plaque Inflammation in Patients

Ahmed Tawakol, Raymond Q. Migrino, Gregory G. Bashian, Shahinaz Bedri, David Vermylen, Ricardo C. Cury, Denise Yates, Glenn M. LaMuraglia, Karen Furie, Stuart Houser, Henry Gewirtz, James E. Muller, Thomas J. Brady, Alan J. Fischman

Research output: Contribution to journalArticle

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Abstract

Objectives: Given the importance of inflammation in atherosclerosis, we sought to determine if atherosclerotic plaque inflammation could be measured noninvasively in humans using positron emission tomography (PET). Background: Earlier PET studies using fluorodeoxyglucose (FDG) demonstrated increased FDG uptake in atherosclerotic plaques. Here we tested the ability of FDG-PET to measure carotid plaque inflammation in patients who subsequently underwent carotid endarterectomy (CEA). Methods: Seventeen patients with severe carotid stenoses underwent FDG-PET imaging 3 h after FDG administration (13 to 25 mCi), after which carotid plaque FDG uptake was determined as the ratio of plaque to blood activity (target to background ratio, TBR). Less than 1 month after imaging, subjects underwent CEA, after which carotid specimens were processed to identify macrophages (staining with anti-CD68 antibodies). Results: There was a significant correlation between the PET signal from the carotid plaques and the macrophage staining from the corresponding histologic sections (r = 0.70; p < 0.0001). When mean FDG uptake (mean TBR) was compared with mean inflammation (mean percentage CD68 staining) for each of the 17 patients, the correlation was even stronger (r = 0.85; p < 0.0001). Fluorodeoxyglucose uptake did not correlate with plaque area, plaque thickness, or area of smooth muscle cell staining. Conclusions: We established that FDG-PET imaging can be used to assess the severity of inflammation in carotid plaques in patients. If subsequent natural history studies link increased FDG-PET activity in carotid arteries with clinical events, this noninvasive measure could be used to identify a subset of patients with carotid atherosclerosis in need of intensified medical therapy or carotid artery intervention to prevent stroke.

Original languageEnglish
Pages (from-to)1818-1824
Number of pages7
JournalJournal of the American College of Cardiology
Volume48
Issue number9
DOIs
Publication statusPublished - 7 Nov 2006
Externally publishedYes

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Fluorodeoxyglucose F18
Positron-Emission Tomography
Inflammation
Staining and Labeling
Carotid Endarterectomy
Atherosclerotic Plaques
Carotid Arteries
Macrophages
Carotid Artery Diseases
Carotid Stenosis
Natural History
Smooth Muscle Myocytes
Anti-Idiotypic Antibodies
Atherosclerosis
Stroke

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

In Vivo 18F-Fluorodeoxyglucose Positron Emission Tomography Imaging Provides a Noninvasive Measure of Carotid Plaque Inflammation in Patients. / Tawakol, Ahmed; Migrino, Raymond Q.; Bashian, Gregory G.; Bedri, Shahinaz; Vermylen, David; Cury, Ricardo C.; Yates, Denise; LaMuraglia, Glenn M.; Furie, Karen; Houser, Stuart; Gewirtz, Henry; Muller, James E.; Brady, Thomas J.; Fischman, Alan J.

In: Journal of the American College of Cardiology, Vol. 48, No. 9, 07.11.2006, p. 1818-1824.

Research output: Contribution to journalArticle

Tawakol, A, Migrino, RQ, Bashian, GG, Bedri, S, Vermylen, D, Cury, RC, Yates, D, LaMuraglia, GM, Furie, K, Houser, S, Gewirtz, H, Muller, JE, Brady, TJ & Fischman, AJ 2006, 'In Vivo 18F-Fluorodeoxyglucose Positron Emission Tomography Imaging Provides a Noninvasive Measure of Carotid Plaque Inflammation in Patients', Journal of the American College of Cardiology, vol. 48, no. 9, pp. 1818-1824. https://doi.org/10.1016/j.jacc.2006.05.076
Tawakol, Ahmed ; Migrino, Raymond Q. ; Bashian, Gregory G. ; Bedri, Shahinaz ; Vermylen, David ; Cury, Ricardo C. ; Yates, Denise ; LaMuraglia, Glenn M. ; Furie, Karen ; Houser, Stuart ; Gewirtz, Henry ; Muller, James E. ; Brady, Thomas J. ; Fischman, Alan J. / In Vivo 18F-Fluorodeoxyglucose Positron Emission Tomography Imaging Provides a Noninvasive Measure of Carotid Plaque Inflammation in Patients. In: Journal of the American College of Cardiology. 2006 ; Vol. 48, No. 9. pp. 1818-1824.
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abstract = "Objectives: Given the importance of inflammation in atherosclerosis, we sought to determine if atherosclerotic plaque inflammation could be measured noninvasively in humans using positron emission tomography (PET). Background: Earlier PET studies using fluorodeoxyglucose (FDG) demonstrated increased FDG uptake in atherosclerotic plaques. Here we tested the ability of FDG-PET to measure carotid plaque inflammation in patients who subsequently underwent carotid endarterectomy (CEA). Methods: Seventeen patients with severe carotid stenoses underwent FDG-PET imaging 3 h after FDG administration (13 to 25 mCi), after which carotid plaque FDG uptake was determined as the ratio of plaque to blood activity (target to background ratio, TBR). Less than 1 month after imaging, subjects underwent CEA, after which carotid specimens were processed to identify macrophages (staining with anti-CD68 antibodies). Results: There was a significant correlation between the PET signal from the carotid plaques and the macrophage staining from the corresponding histologic sections (r = 0.70; p < 0.0001). When mean FDG uptake (mean TBR) was compared with mean inflammation (mean percentage CD68 staining) for each of the 17 patients, the correlation was even stronger (r = 0.85; p < 0.0001). Fluorodeoxyglucose uptake did not correlate with plaque area, plaque thickness, or area of smooth muscle cell staining. Conclusions: We established that FDG-PET imaging can be used to assess the severity of inflammation in carotid plaques in patients. If subsequent natural history studies link increased FDG-PET activity in carotid arteries with clinical events, this noninvasive measure could be used to identify a subset of patients with carotid atherosclerosis in need of intensified medical therapy or carotid artery intervention to prevent stroke.",
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T1 - In Vivo 18F-Fluorodeoxyglucose Positron Emission Tomography Imaging Provides a Noninvasive Measure of Carotid Plaque Inflammation in Patients

AU - Tawakol, Ahmed

AU - Migrino, Raymond Q.

AU - Bashian, Gregory G.

AU - Bedri, Shahinaz

AU - Vermylen, David

AU - Cury, Ricardo C.

AU - Yates, Denise

AU - LaMuraglia, Glenn M.

AU - Furie, Karen

AU - Houser, Stuart

AU - Gewirtz, Henry

AU - Muller, James E.

AU - Brady, Thomas J.

AU - Fischman, Alan J.

PY - 2006/11/7

Y1 - 2006/11/7

N2 - Objectives: Given the importance of inflammation in atherosclerosis, we sought to determine if atherosclerotic plaque inflammation could be measured noninvasively in humans using positron emission tomography (PET). Background: Earlier PET studies using fluorodeoxyglucose (FDG) demonstrated increased FDG uptake in atherosclerotic plaques. Here we tested the ability of FDG-PET to measure carotid plaque inflammation in patients who subsequently underwent carotid endarterectomy (CEA). Methods: Seventeen patients with severe carotid stenoses underwent FDG-PET imaging 3 h after FDG administration (13 to 25 mCi), after which carotid plaque FDG uptake was determined as the ratio of plaque to blood activity (target to background ratio, TBR). Less than 1 month after imaging, subjects underwent CEA, after which carotid specimens were processed to identify macrophages (staining with anti-CD68 antibodies). Results: There was a significant correlation between the PET signal from the carotid plaques and the macrophage staining from the corresponding histologic sections (r = 0.70; p < 0.0001). When mean FDG uptake (mean TBR) was compared with mean inflammation (mean percentage CD68 staining) for each of the 17 patients, the correlation was even stronger (r = 0.85; p < 0.0001). Fluorodeoxyglucose uptake did not correlate with plaque area, plaque thickness, or area of smooth muscle cell staining. Conclusions: We established that FDG-PET imaging can be used to assess the severity of inflammation in carotid plaques in patients. If subsequent natural history studies link increased FDG-PET activity in carotid arteries with clinical events, this noninvasive measure could be used to identify a subset of patients with carotid atherosclerosis in need of intensified medical therapy or carotid artery intervention to prevent stroke.

AB - Objectives: Given the importance of inflammation in atherosclerosis, we sought to determine if atherosclerotic plaque inflammation could be measured noninvasively in humans using positron emission tomography (PET). Background: Earlier PET studies using fluorodeoxyglucose (FDG) demonstrated increased FDG uptake in atherosclerotic plaques. Here we tested the ability of FDG-PET to measure carotid plaque inflammation in patients who subsequently underwent carotid endarterectomy (CEA). Methods: Seventeen patients with severe carotid stenoses underwent FDG-PET imaging 3 h after FDG administration (13 to 25 mCi), after which carotid plaque FDG uptake was determined as the ratio of plaque to blood activity (target to background ratio, TBR). Less than 1 month after imaging, subjects underwent CEA, after which carotid specimens were processed to identify macrophages (staining with anti-CD68 antibodies). Results: There was a significant correlation between the PET signal from the carotid plaques and the macrophage staining from the corresponding histologic sections (r = 0.70; p < 0.0001). When mean FDG uptake (mean TBR) was compared with mean inflammation (mean percentage CD68 staining) for each of the 17 patients, the correlation was even stronger (r = 0.85; p < 0.0001). Fluorodeoxyglucose uptake did not correlate with plaque area, plaque thickness, or area of smooth muscle cell staining. Conclusions: We established that FDG-PET imaging can be used to assess the severity of inflammation in carotid plaques in patients. If subsequent natural history studies link increased FDG-PET activity in carotid arteries with clinical events, this noninvasive measure could be used to identify a subset of patients with carotid atherosclerosis in need of intensified medical therapy or carotid artery intervention to prevent stroke.

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