Background: Recent observations have provided the evidence of proliferation of cardiomyocytes in the adult failing heart. However, it remains unclear whether terminally differentiated cardiomyocytes in situ reenter the cell cycle or homed bone marrow cells differentiate into new cardiomyocytes coupling with postnatal neovascularization. In this study, we evaluated the presence of mitosis and the stemness among cardiomyocytes in human non-ischemic end-stage heart failure. Methods & Results: Samples from recipient ventricular myocardium were obtained from fifteen idiopathic dilated cardiomyopathy(DCMP) patients undergoing cardiac transplantations. Five normal endomyocardial tissues were used for controls. Immunohistochemical analysis by TUNEL for apoptosis and antibodies against nuclear antigen Ki-67 for cell division, early hematopoietic stem cell marker AC-133 for homed stem cells, and stem cell factor receptor c-kit was performed, and some specimens were subsequently processed for confocal microscopy. Cardiomyocytes demonstrated hypertrophic changes with interstitial fibrosis and prominent immunoreactivity for TUNEL comparing with control myocardium. Immunoreactivity for Ki-67 combined with karyokinesis and cytokinesis for cardiomyocytes was identified, which was highly related with immunoreactivity for c-kit. Whereas c-kit expressed predominantly cardiomyocytes and interstitial cells, AC-133 expressed predominantly in infiltrating mononuclear cells and endothelium-lining cells of the newly formed microvessels. Conclusions: Our study showed that there are notable mitoses of cardiomyocytes in damaged myocardium of human non-ischemic end-stage heart failure. The possibilities that homed hematopoietic stem cells may contribute the proliferating cardiomyocytes and the angiogenic potential are strongly raised, but it is necessary to evaluate whether there are cardiac stem cells in situ.