Considerations on PET/MR imaging of carotid plaque inflammation with 68 Ga-Pentixafor
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Cardiovascular Molecular Imaging Laboratory, Section of Cardiovascular Medicine and Yale Cardiovascular Research Center, Yale University School of Medicine, New Haven, CT ´ de Me ´ decine de Grenoble, UMR UGA Laboratoire Radiopharmaceutiques Biocliniques, Faculte - INSERM U1039, Grenoble, France
Received Aug 12, 2020; accepted Aug 12, 2020 doi:10.1007/s12350-020-02354-3
See related article, https://doi.org/10.10 07/s12350-020-02257-3. The causal factor driving most of cardiovascular disease is atherosclerosis. Atherosclerotic plaque rupture or erosion may lead to thrombosis and ischemia of the downstream vascular territory. Carotid atherosclerotic plaques can cause transient ischemic attacks and ischemic strokes. Such rupture-prone or vulnerable plaques are characterized by their morphology and inflammation.1 While disease presentation has somehow shifted as a consequence of the successful management of risk factors at the population level,2 overwhelming evidence of the major the role of inflammation in the pathogenesis of atherosclerosis and cardiovascular events remains, including the demonstration that pharmacological reduction of inflammation decreases cardiovascular events.3 Chemokines are defined by their ability to induce directed chemotaxis. The C-X-C Motif Chemokine Receptor 4 (CXCR4) is the main receptor for the C-X-C motif chemokine 12 (CXCL12). The receptor and its ligand play a major role in the homing of hematopoietic cells to the bone marrow and control stem cell retention. CXCR4 was also shown to be upregulated in various types of cancers, in association with cancer cell migration and metastasis,4 as well as during inflammation, where CXCR4 drives leucocyte recruitment.5 The exact
Reprint requests: Laurent Riou, Laboratoire Radiopharmaceutiques Biocliniques, Faculte´ de Me´decine de Grenoble, UMR UGA INSERM U1039, Grenoble, France; [email protected] J Nucl Cardiol 1071-3581/$34.00 Copyright Ó 2020 American Society of Nuclear Cardiology.
role of CXCL12/CXCR4 axis in atherosclerosis remains to be fully elucidated, with indications of an atheroprotective role primarily associated with an alternative ligand of CXCR45,6 and independent from leucocyte migration. The prevalent role in cancer prompted the development of CXCR4 positron emission tomography (PET) imaging using a cyclic pentapeptide analog of CXCL12 radiolabeled with gallium-68, 68Ga-pentixafor.7 68Ga-pentixafor has been clinically evaluated for tumor imaging as well as for the imaging of inflammation,8 including in atherosclerosis.9–14 Thus, 68Gapentixafor is among the list of PET radiotracers evaluated for molecular imaging of inflammation in human atherosclerosis, along with tracers targeting the 18 kDa translocator protein, somatostatin receptor, folate receptor, and macrophage metabolism,15 as well as other tracers targeting processes associated with plaque vulnerability such as apoptosis, hypoxia, neovascularization, and microcalcification. PET is indeed the imaging modality of choice for molecular imaging, with hi
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