18F-FDG PET and intravascular ultrasonography (IVUS) images compared with histology of atherosclerotic plaques: 18F-FDG accumulates in foamy macrophages | springermedizin.de

Springer Medizin

nach oben

European Journal of Nuclear Medicine and Molecular Imaging

Erschienen in:

01.04.2014 | Original Article

¹⁸F-FDG PET and intravascular ultrasonography (IVUS) images compared with histology of atherosclerotic plaques: ¹⁸F-FDG accumulates in foamy macrophages

verfasst von: Seigo Ishino, Mikako Ogawa, Ikuo Mori, Satoshi Nishimura, Shota Ikeda, Taku Sugita, Tatsuo Oikawa, Takashi Horiguchi, Yasuhiro Magata

Erschienen in: European Journal of Nuclear Medicine and Molecular Imaging | Ausgabe 4/2014

Einloggen, um Zugang zu erhalten

Abstract

Purpose

Intravascular ultrasonography (IVUS) and ¹⁸F-FDG PET have been used to evaluate the efficacy of antiatherosclerosis drugs. These two modalities image different characteristics of atherosclerotic plaques, and a comparison of IVUS and PET images with histology has not been performed. The aim of this study was to align IVUS and PET images using anatomic landmarks in Watanabe heritable hyperlipidaemic (WHHL) rabbits, enabling comparison of their depiction of aortic atherosclerosis. Cellular ¹⁸F-FDG localization was evaluated by ³H-FDG microautoradiography (micro-ARG).

Methods

A total of 19 WHHL rabbits (7 months of age) were divided into three groups: baseline (n = 6), 3 months (n = 4), and 6 months (n = 9). PET, IVUS and histological images of the same aortic segments were analysed. Infiltration by foamy macrophages was scored from 0 to IV using haematoxylin and eosin (H&E) and antimacrophage immunohistochemical staining, and compared with ³H-FDG micro-ARG findings in two additional WHHL rabbits.

Results

IVUS images did not identify foamy macrophage deposition but revealed the area of intimal lesions (r = 0.87). ¹⁸F-FDG PET revealed foamy macrophage distribution in the plaques. The intensity of ¹⁸F-FDG uptake was correlated positively with the degree of foamy macrophage infiltration. Micro-ARG showed identical ³H-FDG accumulation in the foamy macrophages surrounding the lipid core of the plaques.

Conclusion

F-FDG PET localized and quantified the degree of infiltration of foamy macrophages in atherosclerotic lesions. IVUS defined the size of lesions. ¹⁸F-FDG PET is a promising imaging technique for evaluating atherosclerosis and for monitoring changes in the composition of atherosclerotic plaques affecting their stability.

Anzeige

1.

Libby P, Ridker PM, Maseri A. Inflammation and atherosclerosis. Circulation. 2002;105:1135–43.PubMedCrossRef

2.

Fruchart J-C, Nierman MC, Stroes ES, Kastelein JJ, Duriez P. Atherosclerosis: evolving vascular biology and clinical implications. New risk factors for atherosclerosis and patient risk assessment. Circulation. 2004;109:III-15–9.CrossRef

3.

Finn AV, Nakano M, Narula J, Kolodgie FD, Virmani R. Concept of vulnerable/unstable plaque. Arterioscler Thromb Vasc Biol. 2010;30:1282–92.PubMedCrossRef

4.

Perrone FP, Dellegrottaglie S, Rudd JH, Costanzo P, Marciano C, Vassallo E, et al. Molecular imaging of atherosclerosis in translational medicine. Eur J Nucl Med Mol Imaging. 2011;38:969–75.CrossRef

5.

Sastry P, Kaski JC. Atherosclerotic plaque regression – the role of statin therapy. Drugs Today. 2010;46:601–8.PubMedCrossRef

6.

Chiesa G, Mario CD, Colombo L, Vignati L, Marchesi M, Monteggia E, et al. Development of a lipid-rich, soft plaque in rabbit, monitored by histology and intravascular ultrasound. Atherosclerosis. 2001;156:277–87.PubMedCrossRef

7.

Iwata A, Miura S, Imaizumi S, Zhang B, Saku K. Measurement of atherosclerotic plaque volume in hyperlipidemic rabbit aorta by intravascular ultrasound. J Cardiol. 2007;50:229–34.PubMed

8.

Ribbing M, Dorszewski A, Reinecke H, Breithardt G, Kerber S. Time dependent changes of arterial distensibility induced by cholesterol and balloon injury in rabbits: an in vivo intravascular ultrasound study. Int J Cardiovasc Imaging. 2002;18:405–13.PubMedCrossRef

9.

Böse D, von Birgelen C, Erbel R. Intravascular ultrasound for the evaluation of therapies targeting coronary atherosclerosis. J Am Coll Cardiol. 2007;49:925–32.PubMedCrossRef

10.

Nicholls SJ, Borgman M, Nissen SE, Raichlen JS, Ballantyne C, Barter P, et al. Impact of statins on progression of atherosclerosis: rationale and design of SATURN (Study of Coronary Atheroma by InTravascular Ultrasound: effect of Rosuvastatin versus AtorvastatiN). Curr Med Res Opin. 2011;27:1119–29.PubMedCrossRef

11.

Nissen SE, Nicholls SJ, Sipahi I, Libby P, Raichlen JS, Ballantyne CM, et al. Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: the ASTEROID trial. JAMA. 2006;295:1556–65.PubMedCrossRef

12.

Hiro T, Kimura T, Morimoto T, Miyauchi K, Nakagawa Y, Yamagishi M, et al. Effect of intensive statin therapy on regression of coronary atherosclerosis in patients with acute coronary syndrome: a multicenter randomized trial evaluated by volumetric intravascular ultrasound using pitavastatin versus atorvastatin (JAPAN-ACS [Japan assessment of pitavastatin and atorvastatin in acute coronary syndrome] study). J Am Coll Cardiol. 2009;54:293–302.PubMedCrossRef

13.

Ogawa M, Magata Y, Kato T, Hatano K, Ishino S, Mukai T, et al. Application of 18F-FDG PET for monitoring the therapeutic effect of antiinflammatory drugs on stabilization of vulnerable atherosclerotic plaques. J Nucl Med. 2006;47:1845–50.PubMed

14.

Tahara N, Kai H, Ishibashi M, Nakaura H, Kaida H, Baba K, et al. Simvastatin attenuates plaque inflammation: evaluation by fluorodeoxyglucose positron emission tomography. J Am Coll Cardiol. 2006;48:1825–31.PubMedCrossRef

15.

Ogawa M, Ishino S, Mukai T, Asano D, Teramoto N, Watabe H, et al. 18F-FDG accumulation in atherosclerotic plaques: immunohistochemical and PET imaging study. J Nucl Med. 2004;45:1245–50.PubMed

16.

Tawakol A, Migrino RQ, Hoffmann U, Abbara S, Houser S, Gewirtz H, et al. Noninvasive in vivo measurement of vascular inflammation with F-18 fluorodeoxyglucose positron emission tomography. J Nucl Cardiol. 2005;12:294–301.PubMedCrossRef

17.

Rudd JH, Warburton EA, Fryer TD, Jones HA, Clark JC, Antoun N, et al. Imaging atherosclerotic plaque inflammation with [18F]-fluorodeoxyglucose positron emission tomography. Circulation. 2002;105:2708–11.PubMedCrossRef

18.

Davies JR, Izquierdo-Garcia D, Rudd JH, Figg N, Richards HK, Bird JL, et al. FDG-PET can distinguish inflamed from non-inflamed plaque in an animal model of atherosclerosis. Int J Cardiovasc Imaging. 2010;26:41–8.PubMedCrossRef

19.

Nissen SE, Yock P. Intravascular ultrasound: novel pathophysiological insights and current clinical applications. Circulation. 2001;103:604–16.PubMedCrossRef

20.

Shiomi M, Ito T, Shiraishi M, Watanabe Y. Inheritability of atherosclerosis and the role of lipoproteins as risk factors in the development of atherosclerosis in WHHL rabbits: risk factors related to coronary atherosclerosis are different from those related to aortic atherosclerosis. Atherosclerosis. 1992;96:43–52.PubMedCrossRef

21.

Fukumoto Y, Hiro T, Fujii T, Hashimoto G, Fujimura T, Yamada J, et al. Localized elevation of shear stress is related to coronary plaque rupture: a 3-dimensional intravascular ultrasound study with in-vivo color mapping of shear stress distribution. J Am Coll Cardiol. 2008;51:645–50.PubMedCrossRef

22.

Nair A, Kuban BD, Tuzcu EM, Schoenhagen P, Nissen SE, Vince DG. Coronary plaque classification with intravascular ultrasound radiofrequency data analysis. Circulation. 2002;106:2200–6.PubMedCrossRef

Titel: 18F-FDG PET and intravascular ultrasonography (IVUS) images compared with histology of atherosclerotic plaques: 18F-FDG accumulates in foamy macrophages
verfasst von: Seigo Ishino
Mikako Ogawa
Ikuo Mori
Satoshi Nishimura
Shota Ikeda
Taku Sugita
Tatsuo Oikawa
Takashi Horiguchi
Yasuhiro Magata
Publikationsdatum: 01.04.2014
Verlag: Springer Berlin Heidelberg
Erschienen in: European Journal of Nuclear Medicine and Molecular Imaging / Ausgabe 4/2014
Print ISSN: 1619-7070
Elektronische ISSN: 1619-7089
DOI: https://doi.org/10.1007/s00259-013-2635-0