Korean J Radiol.  2015 Oct;16(5):955-966. 10.3348/kjr.2015.16.5.955.

Nuclear Molecular Imaging for Vulnerable Atherosclerotic Plaques

Affiliations
  • 1Department of Nuclear Medicine, Seoul National University Hospital, Seoul 03080, Korea. paengjc@snu.ac.kr
  • 2Department of Nuclear Medicine, National Cancer Center, Goyang 10408, Korea.

Abstract

Atherosclerosis is an inflammatory disease as well as a lipid disorder. Atherosclerotic plaque formed in vessel walls may cause ischemia, and the rupture of vulnerable plaque may result in fatal events, like myocardial infarction or stroke. Because morphological imaging has limitations in diagnosing vulnerable plaque, molecular imaging has been developed, in particular, the use of nuclear imaging probes. Molecular imaging targets various aspects of vulnerable plaque, such as inflammatory cell accumulation, endothelial activation, proteolysis, neoangiogenesis, hypoxia, apoptosis, and calcification. Many preclinical and clinical studies have been conducted with various imaging probes and some of them have exhibited promising results. Despite some limitations in imaging technology, molecular imaging is expected to be used both in the research and clinical fields as imaging instruments become more advanced.

Keyword

Vulnerable plaque; PET; SPECT; Molecular imaging

MeSH Terms

Atherosclerosis/*diagnosis/pathology/radiography
Endothelial Cells/metabolism
Humans
Inflammation/pathology
Lipoproteins, LDL/metabolism
Macrophages/immunology/metabolism
Plaque, Atherosclerotic
Positron-Emission Tomography
Tomography, Emission-Computed, Single-Photon
Lipoproteins, LDL

Figure

  • Fig. 1 Pathogenesis mechanism and molecular imaging targets in vulnerable plaque.

  • Fig. 2 Arterial fluorodeoxyglucose (FDG) uptake related to atherosclerosis. On positron emission tomography (PET) coronal (A), PET/CT fusion coronal (B), and transaxial (C) images of 68-year-old man, focal increased FDG uptake is observed in right brachiocephalic artery (arrows). Increased FDG uptake is often incidentally observed in major arteries during diagnostic workup for cancer. FDG uptake is sometimes very strong, whereas FDG uptake is also observed in other arteries to certain degree (arrowhead).

  • Fig. 3 Variable physiological fluorodeoxyglucose (FDG) uptake in heart. FDG uptake is not suppressed despite standard 6-hour fasting (A), whereas uptake is completely suppressed by same preparation protocol (B).

  • Fig. 4 Translocator protein (TSPO)-targeted imaging in rat model. On transaxial (A) and coronal (B) images of 11C-PBR28 fusion positron emission tomography/CT, increased uptake is observed in whole myocardium. Although TSPO is promising imaging target for inflammation and vulnerable plaque, its role in coronary artery is thought to be limited because of its normal uptake in myocardium.

  • Fig. 5 18F-fluoride positron emission tomography (PET) in atherosclerosis. In patient with unstable angina, increased 18F-fluoride uptake is observed in left main and left anterior descending artery on PET (A), PET/CT fusion (B), and CT (C) images (arrow). Uptake is well-matched with dense calcification on CT. However, 18F-fluoride uptake is also increased in aortic wall (arrowhead), despite lack of definite calcification on CT.


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