The ultrastructural study of the myocardium of rats received adriamycin for 8-10 weeks revealed the picture of mosaic lesions of cardiomyocytes. Cells with little changes were coincided with apparently changed cardiomyocytes in which hypercontracted or atrophied sarcomeres with distended Z-lines, glycogen disappearance and swollen or hypertrophied mitochondria were seen. Myocardial content of ATP did not change but that of phosphocreatine was decreased by 45 percent. The pump function of the isolated heart was moderately lower that was associated with almost twofold increase in left ventricular diastolic stiffness suggesting a deterioration of its filling. A rise in Ca++ concentration in the perfusate exerted similar positive inotropic effect on hearts of both groups which was associated with a prominent fall of diastolic stiffness. Results suggest that increased diastolic stiffness in adriamycin-treated hearts may be due to both local ATP deficiency in myofibrils or incomplete Ca++ removal from them.