Morbidity and mortality resulting from cardiotoxic complications of anticancer therapy is still unacceptably high. Despite advances in the understanding of the pathomechanisms of cardiotoxicity, in prevention and detection of these complications, progressive ventricular dysfunction in cancer survivors represents a great therapeutic problem. Ventricular dysfunction is a life-threatening complication particularly in patients treated with anthracycline cytostatics. Anthracycline-induced loss of myocytes leads to an inadequate ventricular hypertrophy, which produces a rise in left ventricular (LV) afterload and deterioration of ventricular contractility culminating in heart failure. Efficacy of angiotensin-converting enzyme (ACE) inhibitors for the treatment of asymptomatic and symptomatic LV dysfunction in various clinical settings has been confirmed in a number of controlled, randomized trials. Until now, there are only few published data supporting the use of ACE inhibitors to treat patients with ventricular dysfunction-induced by anthracyclines. Cardioprotection with ACE inhibitors in children and adolescents treated with anthracyclines in contrast to ACE inhibition in adults after anthracycline therapy is a controversial topic. Evidence from the recent follow up study indicates a progressive deterioration of left ventricular wall thinning in childhood cancer survivors treated with enalapril. The ongoing large controlled, double blind, randomized trials will provide an important information concerning the efficacy of ACE inhibitors to prevent progression of ventricular dysfunction in paediatric oncologic patients.

        Key words: anthracyclines – late cardiotoxicity – ventricular dysfunction – heart failure – ACE inhibitors