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Abstract #1197

Chronic Myocardial Infarcts with Iron Deposits Exhibit Lower Rest Perfusion and Elevated Nitric Oxide Synthase Activity

Eric Johnson1,2, Anand Nair2, Ivan Cokic1,2, Hsin-Yung Yang2, Andreas Kumar3, and Rohan Dharmakumar1,2
1UCLA, Los Angeles, CA, United States, 2Cedars Sinai, Los Angeles, CA, United States, 3Northern Ontario School of Medicine, Thunder Bay, ON, Canada

Hemorrhagic myocardial infarction (hMI) patients are predisposed to adverse outcomes in the chronic stage of MI, yet physiological underpinnings contributing to this observation are not well understood. We hypothesized that hMI areas containing iron deposits would negatively impact endothelial function and tested our hypothesis by evaluating perfusion defects in patients and dogs with a history of hMI; with histological staining for iron, endothelial cells and nitric oxide synthase (NOS) in excised myocardial sections of dogs with chronic MI. Hemorrhagic subjects had significantly reduced perfusion and markedly elevated NOS activity.

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