Background: Antiapoptotic and proliferative mechanisms take place at cardiocytes' death in dilatative cardiomyopathy (DCM), ischemic heart disease (IHD) and myocardial remodeling by the mitochondrial pathway. This process is enhanced mainly by Bcl-2 protein. We sought, to estimate Bcl-2 antiapoptotic expression and Ki-67 proliferative activity in cardiomyopathies.
Material/Methods: The study groups included 7 hearts with DCM and 8 hearts with IHD explanted during transplantation. The comparative group consisted of myocardial hypertrophy. The control group were donor fragments. Bcl-2 expression was determined immunohistochemically by NP030 antibody (DAKO), whereas proliferation was detected with M7240 antibody. The reacion was enhanced with Envision-DAB in histologic slides.. The intensity of staining was assessed semiquantitatively.
Results: No Bcl-2 expression was seen in the controls, the strongest reaction was seen in DCM group (mean range 2.71), then in IHD (mean range 1.75) and in the comparative group, myocardial hypertrophy (mean range 0.29). The statistical comparisons showed no differences between control and the comparative group, whereas other comparisons showed statistical significance. The proliferative activity was seen only in endocardial and interstitial fibroblasts in cases with DCM and IHD with no reaction in myocytes in any group. Conclusions: Antiapoptotic Bcl-2 activity plays an important role in cardiocyte preservation, while proliferative activity is resticted to interstitial connective tissue cells as replacement process. Myocardial Bcl-2 expression may serve as a diagnostic tool in differentiation of cardiomyopathies and as an indicator of active myocardial injury.

Keywords: Heart Transplantation