Author + information
- James H.F. Rudd, MD, PhD, MRCP⁎ (, )
- Josef Machac, MD and
- Zahi A. Fayad, PhD, FAHA, FACC
- ↵⁎Imaging Science Laboratory, Room BM24, Mount Sinai Hospital, One Gustave L. Levy Place, New York, New York 10029
We read with great interest the study by Tahara et al. (1) published recently in the Journaland concerned with tracking statin-induced inflammation reduction in atherosclerotic plaques using fluorodeoxyglucose positron emission tomography (FDG-PET).
Although this study highlights the very real potential of FDG-PET imaging of atherosclerosis for the detection and monitoring of plaque inflammation, we would like to comment on several aspects of the study’s methodology that may have impacted the results seen by the investigators.
First, we believe that the time between injection of FDG and PET image acquisition was too short at 1 h. Previous studies have shown that a circulation time for FDG in excess of 2 h gives a much higher target (plaque)-to-background (blood) ratio (2–4). A high target-to-blood ratio is crucial to ensuring proper region-of-interest placement and thus accurate quantification of plaque FDG uptake.
Second, especially given their choice of early imaging time point, the researchers should have attempted to correct the plaque FDG uptake for blood activity. This is typically achieved by measurement of the mean of several blood values from a large vein. This value is then divided into the plaque standardized uptake value to yield a tissue-to-blood ratio of FDG uptake. This is the method adopted in previous studies, and in the elegant study by Tawakol et al. (2) which appears in the same issue of the Journal.Although Tahara et al. (1) defend their decision not to do this, we do not believe the reasons they give justify the absence of a correction. The investigators suggest that the patchy uptake of vascular FDG and the nonvisualization of veins means that the blood-pool signal is likely insignificant. More likely is the fact that atherosclerosis is a diffuse condition, taking up FDG variably along the length of the vessel. Additionally, we believe that blood-pool activity would still be significant at such an early imaging time point, with a standardized uptake value well above other background structures.
Additionally, we suggest the use of a combined PET/computed tomography scanner may have made accurate anatomical coregistration easier. This will be particularly important when extending this kind of study into the aorta and other vascular beds.
Finally, we contend that the investigators might have chosen a more potent anti-inflammatory drug than low-dose simvastatin for testing their hypothesis that FDG-PET imaging could track inflammatory change within plaque. Although their study yielded positive results, the magnitude of the effect would surely have been greater with a higher dose of a more powerful statin, and this might have answered some of the questions with which the researchers were left at the end of their study, such as why the FDG reduction induced by statin treatment correlated more closely with the high-density lipoprotein increase than with low-density lipoprotein decrease.
Tahara et al. (1) should be congratulated on completing such an exciting piece of work, but we suggest that for future studies in this area a longer FDG circulation time with appropriate blood activity correction should be used. If these ideas had been adopted by the investigators in their current study, we believe they would have shown an even greater positive impact of the statin on plaque inflammation as assessed by FDG-PET.
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