Abstract #0793

Magnetic susceptibility, R2* and iron evolve during reperfusion injury wound healing

Brianna F. Moon¹, Srikant Kamesh Iyer², Eileen Hwuang¹, Nicholas J. Josselyn², James J. Pilla², Joseph H. Gorman III³, Robert C. Gorman³, Cory Tschabrunn⁴, Samuel J. Keeney³, Estibaliz Castillero⁵, Giovanni Ferrari⁵, Steffen Jockusch⁶, Haochang Shou⁷, Elizabeth M. Higbee-Dempsey⁸, Andrew Tsourkas¹, Victor A. Ferrari⁴, Yuchi Han⁴, Harold I. Litt², and Walter R. Witschey²

¹Bioengineering, University of Pennsylvania, Philadelphia, PA, United States, ²Radiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States, ³Surgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States, ⁴Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States, ⁵Surgery, Columbia University Irving Medical Center, New York City, NY, United States, ⁶Chemistry, Columbia University, New York City, NY, United States, ⁷Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States, ⁸Biochemistry and Molecular Biophysics Graduate Group, Perelman School of medicine, University of Pennsylvania, Philadelphia, PA, United States

There are multiple forms of iron including protein bound and labile iron found in reperfusion injury of acute myocardial infarction (MI). This study investigated iron accumulation, molecular form of iron, and cellular response to reperfusion injury with respect to the duration of wound-healing, in a large animal model. We demonstrate with magnetic susceptibility and R2* imaging biomarkers, there is a significant increase in infarct iron content in acute reperfusion injury that dissipates by 8-week post-MI and validate these findings with histology, iron concentration, and mRNA expression.

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