Therefore, our objectives were to provide evidence that with anaemia (1) there is severe RBC dysfunction with reduced NO bioavailability and impaired cardiac function, (2) there is an increased vascular and cardiac eNOS activation which mediates the adaptation to anaemia, and (3) there is a contribution of both, RBC dysfunction and reduced NO bioavailability to LV dysfunction and fatal outcome in AMI. This evidence concerns the gene NOS3 and anemia (phenotype).