Introduction: The morphological and immunohistochemical analysis of subendocardial bioptates in patients suffering from inflammatory (ICM) and dilated cardiomyopathy (DCM). Methods: Within the study there were included 138 patients with circulatory insufficiency functional class (FC) I-IV NYHA: 71 patients with DCM – (average age 35.6 ±1.3): 63 men (88.8%) and 8 women (11.2%); 67 patients with ICM (average age 38.5 ± 1.4): 57 men (85.1%) and 10 women (14.9%). The acuity degree of ICM estimated by the number of inflammatory interstitial cells, their qualitative composition, the distribution degree and the gravity of the changing cardiomyocytes as well as the presence of necroted miofibres led to a division of patients with ICM within four groups. The degenerative changes were highlighted with the immunohistochemical and electronic microscope in serial paraffined sections by ISEL method, using a commercial set of reactives Apoptag-Kit (ONCOR, USA & France). Results: In the first three groups of patients with ICM there was no cell apoptotic degeneration, the apoptosis of cardiomyocytes only being highlighted in the fourth group. The morphological analysis of subendocardial bioptates in DCM revealed in all cases cardiomyocytes with signs of apoptotic degeneration. In cell nuclei the chromatin was distributed irregularly and mostly disposed on margins. The investigation at optical microscope also confirmed the presence of singular cells with a vesicle content, which is characteristic for apoptosis. The immunohistochemical method of research of apoptosis highlighted the presence of immunoreactive nuclei in all myocardial bioptates of patients with DCM and ICM in the fourth group. The apoptotic index was 2.19 ± 0.82%. Conclusions: The complex immunohistochemical and morphological research of subendocardial intravital bioptates has shown that in inflammatory cardiomyopathy, what is characteristic is the death of cardiomyocytes through necrosis and the apoptosis is observed only at patients with residual infl ammatory phenomena. This is the main mechanism of death of cells at patients with DCM.