It is a well known fact that the antitumor agents like the anthracyclines induces a dose-related cardiotoxicity and more to add, the new agents used in the treatement of breast cancer may stimulate these cardiotoxic effects, causing in the end an increased morbidity and mortality rate by cardiovascular diseases. Cardiotoxicity caused by anthracyclines can be divided into 3 types: acute (during administration), early (several days to month following administration) and late (years to decades following exposure to anthracyclines). Mechanisms of this cardiotoxicity are very complex: myocyte damage has been attributed to the production of toxic oxygen free radicals, which cause lipid peroxidation of membranes leading to vacuolation, irreversible damage and myocyte replacement by fibrous tissue. Clinical manifestations of anthracycline cardiotoxicity are variable, depending in part upon the time course of appearence (acute, early or late). A number of risk factors for the development of anthracyclines cardiotoxicity have been identified. The strongest predictor is cumulative dose, age, concomitant administration of other chemotherapeutic agents and underlying heart disease. Approaches to reducing anthracyclines cardiotoxicity involved the use of novel infusion protocols, the development of new anthracycline compounds, the use of adjunctive agents, endomyocardial biopsy and noninvasive monitoring of cardiac function.