Abstract
We review the mechanisms of cardiotoxicity of cytotoxic chemotherapies, the substances associated with a particular high risk of cardiac damage, the clinical signs and symptoms of cardiotoxicity with special emphasis on cardiac failure, and the prevention and therapy of possible cardiotoxic effects. Generally, chemotherapy-induced cardiotoxicity is defined as a reduction of the left-ventricular ejection fraction (LVEF) of more than 5 % to less than 55 % with clinical signs of heart failure or as a reduction of the left-ventricular ejection fraction (LVEF) of more than 10 % to less than 55 % without clinical signs of heart failure. The cardiotoxicity of anthracyclines such as doxorubicin results in limitations of the use of this chemotherapeutic class in the treatment of malignant diseases in 5 – 20 % of patients due to asymptomatic impairment of left ventricular function and in 1 – 5 % of patients due to symptomatic heart failure. The common use of trastuzumab, a monoclonal antibody against „human epidermal growth factor receptor 2“ (HER2), has resulted in an incidence of cardiotoxicity – commonly as asymptomatic impairment of left ventricular function or even as symptomatic cardiac failure – in up to 10 % with monotherapy and in up to 30 % in combination with anthracyclines. The prevention of cardiotoxicity, the early detection by echocardiography and measurement of troponin, prompt therapy, and a meticulous cardiological work up of individual risk factors and cardiac comorbidities are essential for the reduction of potentially cardiotoxic effects of cytotoxic chemotherapy.
