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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