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J Am Coll Cardiol, 2006; 48:1818-1824, doi:10.1016/j.jacc.2006.05.076
(Published online 16 October 2006). © 2006 by the American College of Cardiology Foundation |
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* Department of Medicine (Cardiac Unit), Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts
Department of Radiology and Nuclear Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts
Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts
Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts
|| Division of Vascular and Endovascular Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts
Manuscript received July 27, 2005; revised manuscript received April 27, 2006, accepted May 2, 2006.
* Reprint requests and correspondence: Dr. Ahmed Tawakol, Cardiac Unit/YAW 5904, Massachusetts General Hospital, Boston, Massachusetts 02114. (Email: atawakol{at}partners.org).
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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