ATP activity of actomyosin in dilated cardiomyopathy (DCMP) was studied together with impact on the above activity of tropomyosin-troponin regulatory complexes recovered from the normal myocardium and cardiac muscle of a DCMP patient. Recordable in DCMP was a striking decline (1.5-fold) in ATP activity of actomyosin. But no significant difference was to be seen in sensitivity to Ca2+ ions of actomyosins obtained from the normal myocardium and cardiac muscle of the DCMP patient. The cardial tropomyosin-troponin regulatory complex from the DCMP patient's myocardium was shown to be endowed with somewhat more manifest activity compared to the analogous complex recovered from the normal myocardium.