DEMONSTRATION OF INCREASED AORTIC VALVE INFLAMMATION IN AORTIC STENOSIS USING 18F-FLUORODEOXYGLUCOSE POSITRON EMISSION TOMOGRAPHY

DEMONSTRATION OF INCREASED AORTIC VALVE INFLAMMATION IN AORTIC STENOSIS USING 18F-FLUORODEOXYGLUCOSE POSITRON EMISSION TOMOGRAPHY

A89.E843 JACC March 9, 2010 Volume 55, issue 10A IMAGING AND DIAGNOSTIC TESTING DEMONSTRATION OF INCREASED AORTIC VALVE INFLAMMATION IN AORTIC STENOS...

115KB Sizes 0 Downloads 19 Views

A89.E843 JACC March 9, 2010 Volume 55, issue 10A

IMAGING AND DIAGNOSTIC TESTING DEMONSTRATION OF INCREASED AORTIC VALVE INFLAMMATION IN AORTIC STENOSIS USING 18F-FLUORODEOXYGLUCOSE POSITRON EMISSION TOMOGRAPHY ACC Poster Contributions Georgia World Congress Center, Hall B5 Monday, March 15, 2010, 3:30 p.m.-4:30 p.m.

Session Title: Imaging Inflammation, Neuronal innervation and Metabolism Abstract Category: Nuclear Cardiology/PET Presentation Number: 1205-239 Authors: Gergana N. Marincheva-Savcheva, Sadia Qadir, Thomas J. Brady, Ahmed Tawakol, Massachusetts General hospital, Boston, MA Background: Aortic stenosis (AS) shares many pathophysiological features with atherosclerosis, and is characterized by inflammation. Since fluorodeoxyglucose positron emission tomography (FDG-PET) provides noninvasive imaging of inflammation, we tested the hypothesis that the aortic valve PET signal is increased in AS. Methods: PET-CT data were evaluated in 50 patients (age 72±10 yr, 19 female), 32 with AS and 18 age/gender-matched controls. AS severity was established on ECHO. FDG uptake was measured on aortic valve commissure (while blinded to AS severity). Target-to-background ratio (TBR) was calculated by dividing the commissural and atrial blood activity. Results: TBR was increased in AS patients compared to controls (1.39±0.2 vs. 1.2±0.13, p=0.001, fig 1A). Within AS patients group, there was correlation between TBR and AS severity (p=0.002 for trend). Additionally, TBR was increased in mild and moderate, but not severe AS (fig 1B). Conclusions: We observe increased FDG uptake in mild and moderate, but not severe AS. Our study supports the hypothesis that AS is an inflammatory condition and suggests that inflammation may be reduced in late-stage disease. This may have an important implication in the design of studies assessing the effect of therapeutic agents on modifying progression of AS.