Aortic Valve 18F-Fluoride Positron Emission Tomography
Author(s) -
Ian C Chang,
Panithaya Chareonthaitawee
Publication year - 2016
Publication title -
circulation cardiovascular imaging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.584
H-Index - 99
eISSN - 1942-0080
pISSN - 1941-9651
DOI - 10.1161/circimaging.116.005574
Subject(s) - positron emission tomography , fluoride , medicine , tomography , nuclear medicine , radiology , chemistry , inorganic chemistry
Calcific aortic valve disease (CAVD) is the most common valvular disease in the developed world.1,2 The disease prevalence is projected to reach 4.5 billion worldwide in 2030, underscoring its significance as a worldwide public health burden. Valve replacement is the only established therapy, but despite recent advances, both surgical and transcatheter approaches still have substantial morbidity and mortality and remain reserved for those with significant hemodynamic complications from severe aortic stenosis.2,3 For ineligible patients, no proven medical therapy exists to prevent, reverse, or delay the progression of CAVD. The ability to identify individuals who are at risk for CAVD progression and to provide disease-modifying treatment would substantially transform the field.See Article by Pawade et al The study by Pawade et al4 in this issue of Circulation: Cardiovascular Imaging exemplifies the ongoing efforts to use multimodality imaging not only for the diagnosis and management of CAVD but also for greater understanding of the underlying cellular mechanisms and pathogenesis of the disease, which are potential pharmacological targets for CAVD.5,6 These efforts have their basis in evidence that CAVD is not only a degenerative condition but also the result of complex and tightly regulated processes of inflammation and calcification.1,7,8 The pathophysiology begins with an early initiation phase, which resembles atherosclerosis, and is characterized by valvular lipid deposition, injury, and inflammation. Because activated macrophages produce pro-osteogenic factors, a transition to the propagation phase occurs, whereby valvular interstitial myofibroblasts become osteoblast-like cells. The propagation phase is also characterized by severe proinflammatory conditions, which further enhance inflammation and microcalcifications, contributing to greater calcium deposition and leaflet stiffening. In the later stages, calcification seems to be irreversible and unresponsive to medical therapy, in contrast to the early stages when both inflammation …
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