Imaging of the Aortic Valve Using Fluorodeoxyglucose Positron Emission Tomography Increased Valvular Fluorodeoxyglucose Uptake in Aortic Stenosis

被引:62
作者
Marincheva-Savcheva, Gergana [1 ,2 ]
Subramanian, Sharath [2 ,3 ]
Qadir, Sadia [2 ,3 ]
Figueroa, Amparo [2 ,3 ]
Truong, Quynh [1 ,2 ,3 ]
Vijayakumar, Jayanthi [2 ,3 ]
Brady, Thomas J. [2 ,3 ]
Hoffmann, Udo [2 ,3 ]
Tawakol, Ahmed [1 ,2 ,3 ]
机构
[1] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA
[2] Massachusetts Gen Hosp, Cardiac MR PET CT Program, Boston, MA 02114 USA
[3] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA
关键词
aortic stenosis; cardiac imaging; FDG-PET; inflammation;
D O I
10.1016/j.jacc.2010.12.046
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objectives 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). Background AS is associated with valvular inflammation. Methods 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. Results 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]). Conclusions 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. (J Am Coll Cardiol 2011;57:2507-15) (C) 2011 by the American College of Cardiology Foundation
引用
收藏
页码:2507 / 2507
页数:1
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