The mechanism of cardiomyopathy development and the factors of compensation used by the organism are still largely unclear. The purpose of the review is to compare compensatory factors in acute and chronic development of cardiomyopathy due to impaired metabolism of cardiomyocytes. Compensatory mechanisms in natural cardiac loads and the results of laboratory's work with the involvement of other authors are reviewed in the article. Acute cardiomyopathy model was presented as cardiomyocytes damage by isoproterenol followed by multiple myocardial necrosis while the model of slow development — by prolonged administration of doxorubicin. Myocardial contractility had similar features in both models despite different injury: 1) diastolic dysfunction occurred at lower doses of the drugs, higher doses were followed by systolic dysfunction; 2) peripheral resistance decreased that facilitated cardiac output; 3) myocardial elasticity increased that facilitates development of pressure; 4) myocardial relaxation retardation prolonging the active state of myofibrils. Thus, factors facilitating the development of pressure are mobilized in the myocardium on the background or reduced peripheral resistance. These factors are more pronounced in systolic dysfunction and decompensation with left ventricular dilatation occurs earlier. Prevention of further development of cardiomyopathy at the stage of diastolic dysfunction is an actual objective of modern cardiology.