The underlying mechanisms of anemia as cause of increased mortality in AMI is largely unidentified. In the previous funding period, we showed that red blood cells (RBC) contribute to the circulating nitric oxide (NO) pool through an active eNOS-dependent signaling pathway. In our experimental models anemia causes RBC dysfunction, eNOS-dependent cardiac and circulatory functional compensation, and increased mortality from AMI. Now, we would like to transfer these experimental findings into clinical studies. The overall hypothesis is that endothelial and RBC dysfunction contributes to the adverse effects of anemia in the acute phase of reperfused AMI.