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Abstract #3018

18F-FDG PET/MRI Allows Early Detection of Foam Cell Formation and Fat Deposition in Hemorrhagic Myocardial Infarctions

Ivan Cokic1, Jane Sykes2, John Butler2, Michael S Kovacs2, Hsin-Jung Yang2, Damini Dey1, Frank S Prato2, and Rohan Dharmakumar1

1Cedars-Sinai Medical Center, Los Angeles, CA, United States, 2Lawson Health Research Institute, London, ON, Canada

Inability of macrophages (MΦ) to switch from pro-inflammatory (M1, glycolytic) to anti-inflammatory (M2, oxidative) phenotype can lead to increased glucose transporter 1 (GLUT1)-mediated glucose metabolism, decreased fatty acid (FA) beta oxidation, increased intracellular lipid accumulation, and MΦ-to-foam cell transformation. Recent studies in the field of chronic venous leg ulcers have shown that iron-overloaded MΦ fail to switch from M1 to M2 phenotype. In this study we hypothesized that inability of iron-overloaded MΦ to switch from M1 to M2 phenotype underlies fatty degeneration of hemorrhagic myocardial infarction via MΦ lipid accumulation and their transformation into foam cells.

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