Key result
Carotid FDG-PET uptake strongly correlates with histologic macrophage inflammation in severe stenosis.
Why the study?
Inflammation plays a key role in atherosclerosis, and noninvasive measurement of carotid plaque inflammation in humans using PET was sought to be determined.
Does FDG-PET imaging accurately measure carotid plaque inflammation in patients with severe carotid stenoses?
Observational (n=17)
Does FDG-PET imaging accurately measure carotid plaque inflammation in patients with severe carotid stenoses?
Effect estimate: r = 0.85
p-value: p=< 0.0001
FDG-PET imaging provides a valid, noninvasive measure of carotid plaque inflammation that correlates strongly with histologic macrophage density.
FDG-PET may identify inflamed carotid plaques; leaves open its value for risk stratification or therapy guidance.
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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Tawakol et al. (2006) conducted an observational in Severe carotid stenoses (n=17). FDG-PET imaging was evaluated on Correlation between mean FDG uptake (mean TBR) and mean inflammation (mean percentage CD68 staining) (r = 0.85, p=< 0.0001). In patients with severe carotid stenoses, mean FDG-PET uptake strongly correlated with mean macrophage inflammation in corresponding histologic sections (r = 0.85; p < 0.0001).
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