Imaging at the inter-face of inflammation and angiogenesis by 18F-fluciclatide PET
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Peer-reviewed
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Authors
Tarkin, Jason https://orcid.org/0000-0002-9132-120X
Abstract
Mechanisms underlying atherosclerotic plaque rupture are complex and unpredictable by any current imaging test. However, several key pathogenic processes known to increase the likelihood of an acute plaque event can be tracked in vivo using positron emission tomography (PET). In this issue of Heart, Jenkins et al.[1] examine the utility of 18F-fluciclatide, an v3integrin binding PET tracer, for imaging atherosclerosis. This intriguing study adds great momentum in the push to identify novel methods for imaging molecular signatures of high-risk plaques, and raises several important broader considerations for the field.
Description
Keywords
acute myocardial infarction, advanced cardiac imaging, chronic coronary disease, nuclear cardiac imaging, positron emission tomographic (PET) imaging, Atherosclerosis, Humans, Inflammation, Integrin alphaV, Peptides, Polyethylene Glycols, Positron-Emission Tomography
Journal Title
Heart
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Journal ISSN
1355-6037
1468-201X
1468-201X
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Publisher
BMJ Publishing Group
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Sponsorship
Wellcome Trust (211100/Z/18/Z)
J.M.T. is supported by a Wellcome Trust Clinical Research Career Development Fellowship (211100/Z/18/Z) and the National Institute for Health Research (NIHR). J.C.M. acknowledges support from the Imperial NIHR Biomedical Research Centre. Z.A.F is supported by the NIH (P01 HL131478, R01 HL071021, R01 HL128056, R01HL135878, NBIB R01 EB009638) and the American Heart Association (14SFRN20780005).