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Reviews metabolic PET imaging in pulmonary arterial hypertension, demonstrating prognostic value in right ventricular strain while highlighting a lack of specificity for vascular remodeling.
he inaccessibility of the pulmonary vasculature to noninvasive assessment or routine tissue sampling has limited our ability to diagnose pulmonary arterial hypertension (PAH) or assess histopathologic changes with or without therapy. A modality that can measure cellular events contributing to pulmonary vascular remodeling such as vascular cell proliferation, apoptosis, or inflammation could guide its diagnosis and treatment. 4] A noninvasive imaging modality that reflects underlying biological events could reveal important endophenotypes within the spectrum of PAH with distinct prognoses and responses to specific agents. In PAH, positron emission tomography (PET) of the chest using 18 F-fluorodeoxyglucose ( 18 FDG) has been used experimentally to reveal enhanced metabolic activity of the right ventricle (RV) 6 and in the lungs, 7 reflecting the hypertrophic response to pressure overload as well as a shift to a glycolytic metabolism because of relative hypoxemia and metabolic adaption, akin to the Warburg effect seen in cancer biology. The RV 18 FDG PET signal has prognostic significance in PAH, 9,10 tracks therapeutic responses, Although 18 FDG PET detects metabolic adaptations and increased cellular metabolism that may correspond with hyperproliferative phenotypes, neither this nor other currently available imaging modalities can detect vascular remodeling in PAH specifically.
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Yung et al. (2018) studied this question.
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