Prevention of anthracycline-induced cardiotoxicity: challenges and opportunities

J Am Coll Cardiol. 2014 Sep 2;64(9):938-45. doi: 10.1016/j.jacc.2014.06.1167.


Anthracycline compounds are major culprits in chemotherapy-induced cardiotoxicity, which is the chief limiting factor in delivering optimal chemotherapy to cancer patients. Although extensive efforts have been devoted to identifying strategies to prevent anthracycline-induced cardiotoxicity, there is little consensus regarding the best approach. Recent advances in basic mechanisms of anthracycline-induced cardiotoxicity provided a unified theory to explain the old reactive-oxygen species hypothesis and identified topoisomerase 2β as the primary molecular target for cardioprotection. This review outlines current strategies for primary and secondary prevention of anthracycline-induced cardiotoxicity resulting from newly recognized molecular mechanisms and identifies knowledge gaps requiring further investigation.

Keywords: cancer; cardiomyopathy; cardioprotection; chemotherapy; doxorubicin; heart failure.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Anthracyclines / adverse effects*
  • Antibiotics, Antineoplastic / adverse effects*
  • Clinical Trials as Topic
  • Doxorubicin / therapeutic use
  • Heart Diseases / chemically induced*
  • Heart Diseases / prevention & control*
  • Heart Failure / complications
  • Humans
  • Neoplasms / complications
  • Neoplasms / drug therapy*
  • Reactive Oxygen Species


  • Anthracyclines
  • Antibiotics, Antineoplastic
  • Reactive Oxygen Species
  • Doxorubicin