CORRESPONDENCE: LETTER TO THE EDITOR
Reply
Hisashi Kai, MD, PhD*,
Nobuhiro Tahara, MD, PhD,
Masatoshi Ishibashi, PD, PhD and
Tsutomu Imaizumi, PD, PhD
* Department of Internal Medicine, Division of Cardiovascular Medicine, Cardiovascular Research Institute, Kurume University School of Medicine, 67 Asahi-Machi, Kurume 830-0011, Japan (Email: naikai{at}med.kurume-u.ac.jp).
We thank Drs. Rudd, Machac, and Fayad for having interest in our recent study (1). There is a growing body of evidence that fluorodeoxyglucose positron emission tomography (FDG-PET) imaging has a great potential for noninvasively detecting and quantifying plaque inflammation in humans. Anecdotal studies have reported increased FDG uptake in the regions of the aorta and large arteries in patients who had undergone FDG-PET imaging for cancer diagnosis and staging (2,3). Recently, we and others have validated FDG uptake in the arterial wall (i.e., plaques) by coregistering FDG-PET imaging with structural imaging, such as computed tomography and magnetic resonance imaging (1,4–7). More importantly, histological examination of the endarterectomized specimen obtained from the FDG uptake-documented carotid arteries has provided solid evidence that the vascular FDG uptake is associated with macrophage accumulation, namely plaque inflammation, not only in symptomatic but also asymptomatic carotid plaques, irrespective of the severity of the luminal stenosis (5–7). In addition, our recent study has revealed that FDG-PET imaging is a practical tool to monitor the effectiveness of anti-inflammation therapy for atherosclerotic diseases (1).
Because of limited time available for PET imaging for patients in our institution, PET imaging was performed 1 h after FDG injection. We agree that longer time may provide clearer PET imaging. Standardized uptake value (SUV) of the juglar vein (blood uptake) was low and almost constant in our study. Thus, we did not normalize SUV of the plaque by blood SUV. However, we agree that normalization may give more accurate identification of inflamed plaques. The dose of FDG administered, the duration between FDG injection and PET image acquisition, and the method of quantification of FDG uptake should be standardized before this modality is widely applied for clinical practice, especially for plaque inflammation imaging. The use of a combined PET/computed tomographic scanner will improve the accuracy of the anatomical diagnosis of plaque FDG uptake. Also, more macrophage-specific PET tracer is desirable to image plaques in metabolically active tissues such as the heart and brain.
Considering the future direction, it would be interesting to study 1) the prevalence of inflammation of the documented plaques, 2) risk factors contributing to plaque inflammation, and 3) whether more powerful statins would show greater reduction in plaque inflammation or whether other potentially anti-inflammatory drugs, such as angiotensin receptor blockers, would decrease FDG uptake in inflamed plaques. A prospective study with a large number of patients is warranted to elucidate whether vascular FDG uptake can be a predictor of cardiovascular events. Finally, the comments made by Rudd et al. will be very helpful in making FDG-PET imaging clinically more useful in future studies.
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1. Tahara N, Kai H, Ishibashi M, et al. Simvastatin attenuates plaque inflammation: evaluation by fluorodeoxyglucose positron emission tomography J Am Coll Cardiol 2006;48:1825-1831.[Abstract/Free Full Text]2. Mochizuki Y, Fujii H, Yasuda S, et al. FDG accumulation in aortic walls Clin Nucl Med 2001;26:68-69.[CrossRef][Web of Science][Medline] 3. Yun M, Jang S, Cucchiara A, Newberg AB, Alavi A. 18F FDG uptake in the large arteries: a correlation study with the atherogenic risk factors Semin Nucl Med 2002;32:70-76.[CrossRef][Web of Science][Medline] 4. Tatsumi M, Cohade C, Nakamoto Y, Wahl RL. Fluorodeoxyglucose uptake in the aortic wall at PET/CT: possible finding for active atherosclerosis Radiology 2003;229:831-837.[Abstract/Free Full Text] 5. Rudd J, Warburton EA, Fryer TD, et al. Imaging atherosclerotic plaque inflammation with [18F]-fluorodeoxyglucose positron emission tomography Circulation 2002;105:2708-2711.[Abstract/Free Full Text] 6. Davies JR, Rudd JH, Fryer TD, et al. Identification of culprit lesions after transient ischemic attack by combined 18F-fluorodeoxyglucose positron-emission tomography and high-resolution magnetic resonance imaging Stroke 2005;36:2642-2647.[Abstract/Free Full Text] 7. Tawakol A, Migrino RQ, Bashian GG, et al. In vivo 18F-fluorodeoxyglucose positron emission tomography imaging provides a noninvasive measure of carotid plaque inflammation in patients J Am Coll Cardiol 2006;48:1818-1824.[Abstract/Free Full Text]
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