Aims: Oxidative stress in the myocardium may play an important role in the pathogenesis of heart failure (HF) [1]. The aim of study was to examine the levels of free radicals (superoxide anion (O2-), hydroxyl radical (OH), peroxynitrite (ONOO–)), nitric oxide (NO) and superoxide dismutase (SOD) at the experimental HF, to detect the cardiomyocyte apoptosis and to calculate the apoptotic index (AI). Methods: Wistar 16 male rats were divided at 2 groups. First group consisted from 12 rats, was subjected to post – myocardial infarction HF by 8 hours daily immobilizing rats in supine position [2] during 14 days. Second group was control and consisted from 4 animals. First group was divided at 4 subgroups, each consisting of 3 animals. At the 3rd, 7th, 11th and 14th day of experiment subgroups were subjected to decapitation in turn. Pairs of control animals were decapitated before and at the end of experiment. Experimental work was conducted according to [3;4]. Free-radicals, SOD and NO levels were detected by electron-paramagnetic resonance [5]. Apoptosis was registered by TUNEL method. The analysis of microscopic section was carried out at the microscope with semiachromatic Fluotar lens. AI was calculated in 20 arbitrary chosen vision fields at 400 multiple magnification. AI was calculated as ratio of positive stained cardiomyocyte nucleous to total quantity of cardiomyocytes. All concentrations were presented in nmole/ml. Results: (i) Blood concentrations of free radicals were not only authentically higher of analogous control group levels (O2- 7,86±0,13, OH 2,82±0,16, ONOO– 0,96±0,02), p<0,001, but dynamical growth was registered during 3rd, 7th, 11th, and 14th days of experiment (O2- – 15,73±0,24, 19,93±0,72, 19,39±0,45, 19,56±0,12; OH 5,15±0,29, 6,62±0,51, 7,18±0,86, 6,91±0,10; ONOO– 2,75±0,18, 4,45±0,17, 4,36±0,12, 4,31±0,25), p<0,05. (ii) HF development at 3rd, 7th, 11th, and 14th days of experiment led to authentic decreasing of blood levels of NO (4,28±0,18, 6,44±0,82, 7,42±0,69, 7,44±0,68, p<0,05) and SOD (6,84±0,37, 7,79±0,27, 8,35±0,83, 7,93±0,44, p<0,05), in comparison with analogous dates of control group (NO 35,47±3,14, SOD 15,64±0,29), p<0,05. (iii) TUNEL registered single apoptotic cardiomyocytes in control group microscopic sections. AI was 6,3±3,1%. At experimental group animals the AI variation were from 18% to 61%. At 3rd, 7th, 11th,14th experimental day AI were 21,4 ± 3,5%, 36,2 ± 2,4%, 56,3 ± 3,8%, 47,4 ± 3,6 %, (p < 0,05). Conclusion: Experimental HF led to activation of free-radical system and reduction of NO and SOD levels, which probably promote apoptosis. Quick increasing of apoptotic cardiomyocyte quantity in periinfarct area was registered at first days of experiment and run to maximum at 11th day up. Massive apoptotic damaging led to decreasing of viable cardiomyocytes quantity and quick HF progression.