Advances in cancer therapy have improved the outcomes and survival rate of oncology patients. As patient survival is extended, early detection and in-time intervention of therapy-related cardiotoxicity are becoming increasingly important. The cardiotoxicity varies by the type of treatment utilized and the mechanisms of cardiac damage involved. Type 1 cardiotoxicity is caused by the notorious anthracyclines with cumulative dose effects. Anthracyclines such as doxorubicin and epirubicin inhibit topoisomerase II in cardiomyocytes and induce deoxyribonucleic acid double strand breaks and transcription changes.The myocardial damage caused by such type 1 agents is often permanent and irreversible. Patients who are treated with type 1 agents are at an increased risk for significant myocardial dysfunction, subsequent heart failure and death during the followup. Type 2 cardiotoxicity is typically caused by targettherapy agents such as trastuzumab.3 Here, trastuzumab blocks human epidermal growth factor receptor 2 (HER- 2), expressed on cardiomyocytes in addition to tumor cells, leading to the loss of HER-2 – mediated survival pathways. There is no cumulative dose effect and the cardiotoxicity is likely to recover after drug withdrawal.