AIM: To study efficacy of the myocardial cytoprotector trimethasidine MB and metabolic drug 3-(2,2,2-trimethylhydrasine) propionate dihydrate (3-TMHP) in the treatment of chronic cardiac failure (CCF). MATERIAL AND METHODS: Sixty-five patients with CCF after myocardial infarction (> 6 months) with left ventricular ejection fraction (LV EF) <40% were randomized into 3 groups: group 1 (n=28) received basic therapy plus trimethasidine in a daily dose 70 mg; group 2 (n=25)--basic therapy plus 3-TMHP in a daily dose 1000 mg; control group (n=12) received basic therapy with ACE inhibitors, beta-blockers and diuretics. Before and after 6-month treatment all the patients have undergone stress echocardiography with dobutamine. Perfusion and myocardial metabolism were determined in 34 patients with single photon emission computed tomography of the myocardium (SPECT) with 99m-Tc-technetril and positron-emission tomography of the myocardium (PET) with F-18-fluorodesoxyglucose. RESULTS: Groups 1 and 2 significantly reduced functional class of CCF and prolonged the distance of a 6-min walk. Significant improvement of life quality was observed only in the treatment with trimethasidine. According to PET, treatment with trimethasidine MB and 3-TMHP has an anti-ischemic action manifesting with a significant attenuation of glucose hypermetabolism in the ischemic segment to normal values. However, significant improvement of systolic thickening in hybernated segments by SPECT as well as a significant rise of LV EF were recorded only in the treatment with trimethasidine MB. Stress echocardiography with dobutamine had high specificity (85.7%) but low sensitivity (50.4%) in detection of hybernated myocardium. CONCLUSION: Trimethasidine MB (preductal MB) has advantages over 3-TMHP, so it is preferable in ischemic CHF.