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.
