Pharmacologic prevention of anthracycline-induced cardiomyopathy.
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.
Maradia
Kuldeep
K
Department of Cardiology, University of South Florida, Tampa, FL 33618, USA.
Guglin
Maya
M
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D018943:Anthracyclines / Q000009:adverse effects*; D000970:Antineoplastic Agents / Q000009:adverse effects*; D009202:Cardiomyopathies / Q000139:chemically induced* / Q000517:prevention & control*; D004305:Dose-Response Relationship, Drug; D006801:Humans; D007502:Iron Chelating Agents / Q000627:therapeutic use
D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D018943:Anthracyclines; D000970:Antineoplastic Agents; D007502:Iron Chelating Agents