Objective: A progressive ventricular dysfunction caused by ischemic myocardial injuries remains one of the leading causes of death during the postoperative course in congenital heart disease (CHD). The aim of this study was to investigate the role of oxidative stress in these myocardial injuries. Method: Myocardial injuries and oxidative stress mechanisms were assessed by histopathology and immunohistochemistry and quantified by morphometrical analyses. Results: Myocardial injury was observed in pediatric patients submitted to surgery for CHD with cardiopulmonary bypass, followed by lethal exit. Oxidative stress mechanisms were directly related to these particular types of myocardial injuries. Importantly, 4-hydroxynonenal (4-HNE), a marker of lipid peroxidation, is strongly expressed, especially in irreversible myocardial lesions. Although morphologically similar, myocardial injuries observed in patients who evolved with sepsis in the peri-operatory period exhibited a completely different set of oxidative stress mechanisms. Increased concentrations of nitrotyrosine protein adducts were observed in these patients, suggesting that peroxynitrite-mediated protein nitration may be the predominant oxidative stress mechanism found in these situations. Conclusion: The underlying mechanisms of these lesions seem to be related to the development of ischemia or ischemia/reperfusion followed by oxidative stress mechanisms that vary depending on whether sepsis was present. While the exact mechanism is not fully understood, it has been suggested that endogenous catecholamine release could have a role in this process. Objective: A significant decrease of the mean cardiomyocyte DNA content and increased numbers of diploid cardiomyocytes after ventricular unloading was demonstrated, suggesting a numerical increase of cardiomyocytes. The heart harbours several stem cells populations including c-kit (CD 117) + cells and side population cells (SPC), that might proliferate after unloading and generate diploid cardiomyocytes. It was tested, whether there is an increase of ABCG2+ SPC and CD117+ cells after unloading. Method: In paired myocardial samples (before and after LVAD), the number of cells with immunoexpression of ABCG-2, c-kit/CD 117 and MEF-2 was assessed by immunohistochemistry and morphometrically determined. Results: A significant increase of SPC and cells with coexpression of c-kit and MEF-2 after unloading was observed (p=0.001). A significant positive correlation between both SPC and cells with coexpression of c-kit and MEF-2 expression was observed (p=0.007 and 0.01). No correlation was found between the number of SPC and the mean cardiomyocyte DNA content. Conclusion: SPC are significantly increased in the myocardium after ventricular unloading, suggesting a role of stem cell proliferation during "reverse cardiac remodelling". These cells might proliferate and commit to different cell lineages such as cardiomyocytes or endothelium, and thus ameliorate cardiac function.