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Anthracyclines are highly effective anticancer drugs. However, a major factor limiting their use in humans is a cumulative, dose-related cardiotoxicity which can result in a permanent loss of cardiomyocytes, which ultimately leads to asymptomatic and symptomatic heart failure. Experiences with various approaches to reduce the cardiotoxicity of anthracyclines without jeopardizing their antineoplastic effects have been reported in the oncology literature. This article reviews the etiology and natural history of anthracycline-induced cardiotoxicity and provides options available for limiting and/or preventing cardiotoxicity.

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