The ability of dexrazoxane (DEX) to protect against anthracycline-induced cardiotoxicity has been evaluated in several European studies using either standard or high-dose regimens. In addition, one randomized trial investigated the value of cardiac radioimmunoscintigraphy with indium-111 antimyosin monoclonal antibodies in the early detection of cardiac damage. The results of these trials demonstrate that DEX is able to ameliorate doxorubicin- and epirubicin-induced cardiotoxicity, even when high single drug doses are used. The cardioprotective effect of DEX has been clearly documented by both clinical and laboratory cardiac evaluation. The use of DEX did not add to the toxicity of the anthracyclines, nor was there clear evidence of an adverse impact of the agent on antitumor activity of the chemotherapeutic regimen. Radioimmunoscintigraphy was very sensitive in detecting anthracycline cardiac damage, but its specificity is low and it cannot be considered a primary test for guiding anthracycline treatment.