Skip Navigation LinksHome > September 2013 - Volume 34 - Issue 9 > Delayed time-point 18F-FDG PET CT imaging enhances assessmen...
Nuclear Medicine Communications:
doi: 10.1097/MNM.0b013e3283637512
Original Articles

Delayed time-point 18F-FDG PET CT imaging enhances assessment of atherosclerotic plaque inflammation

Blomberg, Björn A.a,b,e; Akers, Scott R.c; Saboury, Babaka,b; Mehta, Nehal N.d; Cheng, Gangc; Torigian, Drew A.a,b; Lim, Estherc; Del Bello, Catherinec; Werner, Thomas J.b; Alavi, Abassa,b

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Objective: The aim of this study was to determine the ideal circulation time of fluorine-18 fluorodeoxyglucose (18F-FDG) in order to detect and quantify atherosclerotic plaque inflammation with PET computed tomography (CT) imaging.

Methods: Fifteen patients underwent multiple time-point imaging at ∼60, 120, and 180 min after 18F-FDG administration. For each time point, global assessment of aortic and carotid 18F-FDG uptake was determined qualitatively by visual assessment and semiquantitatively by calculation of the mean and maximum standardized uptake values (SUV) and the corresponding target-to-background ratio (TBR).

Results: Delayed imaging achieved significant improvement in visualization of atherosclerotic plaque inflammation [Friedman’s χ2 statistic (d.f.=2, n=15)=24.13, P<0.001, Kendall’s W=0.80]. This observation was confirmed by semiquantitative image analysis. At 1 h, the aortic and carotid SUVmean-calculated TBR was 1.05 [95% confidence interval (CI)=0.98, 1.11] and 0.88 (95% CI=0.81, 0.96), respectively. At 3 h, the TBR significantly increased to 1.57 (95% CI=1.28, 1.86; P=0.001) for the aorta and to 1.61 (95% CI=1.36, 1.87; P<0.001) for the carotid arteries. SUVmax-calculated TBRs showed a similar increase over time.

Conclusion: One- and 2-h 18F-FDG PET CT imaging is suboptimal for global assessment of atherosclerotic plaque inflammation compared with imaging at 3 h. Our data support the utilization of 3-h delayed imaging to obtain optimal data for the detection and quantification of atherosclerotic plaque inflammation in human arteries.

© 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins


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