Abstract #1009
Dynamic UTE molecular MR imaging targeting pulmonary fibrogenesis in a model of left ventricular dysfunction
Brianna F. Moon1,2, Iris Y. Zhou1,2, Yingying Ning1,2, Sergey Shuvaev1,2, Mariane M. Le Fur1,2, Yin-Ching I. Chen1, Eman A. Akam3, Jonah P. Weigand-Whittier1, Nicholas Rotile1,2, Matthew Drummond4, Avery T. Boice1,2, Samantha E. Zygmont1,2, Rod R. Warburton5, Barry L. Fanburg5, Krishna C. Penumatsa5, and Peter D. Caravan1,2
1Radiology, Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, United States, 2Radiology, Institute for Innovation in Imaging, Massachusetts General Hospital, Charlestown, MA, United States, 3Medicine, Division of Cardiology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, United States, 4Medicine, Division of Pulmonary and Critical Care Medicine, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, United States, 5Pulmonary, Critical Care and Sleep Medicine, Tufts Medical Center, Boston, MA, United States
Synopsis
Group 2 pulmonary hypertension is a complication of chronic left ventricular dysfunction. During the early stages of the disease activity there is an accumulation of extracellular matrix molecules and an increase in allysine content. Molecular MR imaging with an allysine-targeted fibrogenesis probe shows increased lung-to-muscle ΔCNR within the lungs of transverse aortic constriction (TAC)-induced left ventricular dysfunction animal models compared to control animals, which corresponded to increased lung and right ventricle weight, and elevation of fibrogenesis biomarkers (hydroxyproline and allysine).
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