Recent epidemiological research indicates that a coexistent anemia among patients with heart failure might worsen their prognosis. However, whether the reduced synthesis of red blood cells is a contributing factor to the development and progression to overt heart failure, or whether it simply is a mere consequence of a dysfunctional heart, remains to be elucidated. Studies in mice with experimentally induced acute myocardial infarction leading to subsequent development of a postinfarction congestive heart failure have shed some light on this problem. Careful analyses of the number and of the functions of various hematopoietic cells residing in either blood or bone marrow point to a possible inhibitory role of cytokines, such tumor necrosis factor α, on hematopoiesis. The present protocols will hopefully encourage further studies of hematopoiesis and immunity in heart failure by using a combination of animal models with state-of-the-art techniques in molecular biology to define and validate possible targets for therapy.