Imaging of the Aortic Valve Using Fluorodeoxyglucose Positron Emission Tomography

Because fluorodeoxyglucose positron emission tomography (FDG-PET) imaging provides a noninvasive index of inflammation, we sought to assess whether FDG uptake in the aortic valve (AV) is increased in aortic stenosis (AS). AS is associated with valvular inflammation. FDG-PET/computed tomography data...

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Published inJournal of the American College of Cardiology Vol. 57; no. 25; pp. 2507 - 2515
Main Authors Marincheva-Savcheva, Gergana, Subramanian, Sharath, Qadir, Sadia, Figueroa, Amparo, Truong, Quynh, Vijayakumar, Jayanthi, Brady, Thomas J., Hoffmann, Udo, Tawakol, Ahmed
Format Journal Article
LanguageEnglish
Published Elsevier Inc 21.06.2011
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ISSN0735-1097
1558-3597
DOI10.1016/j.jacc.2010.12.046

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Summary:Because fluorodeoxyglucose positron emission tomography (FDG-PET) imaging provides a noninvasive index of inflammation, we sought to assess whether FDG uptake in the aortic valve (AV) is increased in aortic stenosis (AS). AS is associated with valvular inflammation. FDG-PET/computed tomography data were retrospectively evaluated in 84 patients (age 73 ± 9 years, 45% female), 42 patients with AS, and 42 age-matched controls. FDG uptake was determined within the AV while blinded to AS severity. Target-to-background ratio (TBR) was calculated as valvular/blood activity. Stenosis severity was established on echocardiography, and presence of AV calcification was independently assessed on computed tomography. The aortic valve PET signal (TBR) was increased in AS compared with controls (median 1.53 [interquartile range (IQR): 1.42 to 1.76] vs. 1.34 [IQR: 1.20 to 1.55]; p < 0.001). Further, compared with controls, TBR was increased in mild (median 1.50 [IQR: 1.36 to 1.75]; p = 0.01) and moderate (median 1.70 [IQR: 1.52 to 1.94]; p < 0.001), but not in severe AS (median 1.49 [IQR: 1.40 to 1.54]; p = 0.08). When subjects were categorized according to AV calcification, valvular FDG uptake was increased in mildly (median 1.50 [IQR: 1.36 to 1.79]; p < 0.01) and moderately (median 1.67 [IQR: 1.50 to 1.85]; p < 0.001), but not severely calcified valves (median 1.51 [IQR: 1.38 to 1.54]; p = 0.15), compared with noncalcified valves (median 1.35 [IQR: 1.20 to 1.52]). This study supports the hypothesis that AS is an inflammatory condition and suggests that inflammation may be reduced in late-stage disease. This may have important implications in the design of studies assessing the effect of therapeutic agents in modifying progression of AS.
ISSN:0735-1097
1558-3597
DOI:10.1016/j.jacc.2010.12.046