Administration of cytotoxic drugs is accompanied by many serious side effects, with cardiac toxicity as one of the most dangerous. In clinical practice anthracyclines are the best known chemotherapeutic agents linked to cardiotoxicity, however there are a number of other anti-cancer drugs (cyclophosphamide, taxans, trastuzumab, 5-fluorouracil, imunomodulators etc) that may cause cardiac toxicity as well. Basic mechanism through which anthracylines cause cardiac damage is recognized, though many pathogenetic ways of their toxicity still remain to be elucidated. Administration of trastuzumab is also clearly associated with cardiotoxicity, however, depression of left ventricular ejection fraction (LVEF) caused by this agent (unlike anthacyclines) seems to be fully reversible. For monitoring cardiotoxicity we use several methods--biochemical examination, use of X-ray, radionuclides or ultrasound. The most commonly used method to identify patients with heart damage is echocardiography with clinical examination. When a cardiac damage (mostly congestive heart failure with low LVEF) occures, following treatment depends on clinical symptoms and LVEF. These patients are then treated according to common internal medecine recommendations. Several cardioprotective agents have been tested, among these dexarazoxane seems do show significant cardioprotective activity. Also liposomal encapsulation of anthacyclines may reduce heart damage, especially early cardiotoxicity. Cardiotoxicity of cytostatic agents is a very serious side effect of anti-cancer therapy, which may affect survival more than the malignancy itself. Therefore a concentrated effort should be expended to prevent cardiac damage or at least to its early identification and prompt treatment.