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Review
. 2019 Dec 2:5:18.
doi: 10.1186/s40959-019-0054-5. eCollection 2019.

Strategies to prevent anthracycline-induced cardiotoxicity in cancer survivors

Neha Bansal  1 , M Jacob Adams  2 , Sarju Ganatra  3   4 , Steven D Colan  5 , Sanjeev Aggarwal  6 , Rudolf Steiner  7 , Shahnawaz Amdani  8 , Emma R Lipshultz  9   10 , Steven E Lipshultz  11   12   13
Affiliations
Review

Strategies to prevent anthracycline-induced cardiotoxicity in cancer survivors

Neha Bansal et al. Cardiooncology. .

Abstract

Cancer diagnostics and therapies have improved steadily over the last few decades, markedly increasing life expectancy for patients at all ages. However, conventional and newer anti-neoplastic therapies can cause short- and long-term cardiotoxicity. The clinical implications of this cardiotoxicity become more important with the increasing use of cardiotoxic drugs. The implications are especially serious among patients predisposed to adverse cardiac effects, such as youth, the elderly, those with cardiovascular comorbidities, and those receiving additional chemotherapies or thoracic radiation. However, the optimal strategy for preventing and managing chemotherapy-induced cardiotoxicity remains unknown. The routine use of neurohormonal antagonists for cardioprotection is not currently justified, given the marginal benefits and associated adverse events, particularly with long-term use. The only United States Food and Drug Administration and European Medicines Agency approved treatment for preventing anthracycline-related cardiomyopathy is dexrazoxane. We advocate administering dexrazoxane during cancer treatment to limit the cardiotoxic effects of anthracycline chemotherapy.

Keywords: ACE inhibitors; Anthracyclines; Beta-blockers; Cancer; Cardio-oncology; Cardiotoxicity; Pediatrics.

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Conflict of interest statement

Competing interestsRudolf Steiner: Oncology Consultant to Clinigen Group PLC, UK. Steven Lipshultz: Cardiology Consultant to Clinigen Group PLC, UK. Rest of the Authors: None.

Figures

Fig. 1
Fig. 1
Doxorubicin (an anthracycline, A) disrupts the normal catalytic cycle of topoisomerase 2β, causing deoxyribonucleic acid (DNA) double-stranded breaks. Doxorubicin also changes the transcriptome, leading to defective mitochondrial biogenesis and increasing reactive oxygen species (ROS). As a result, cardiomyocytes show myofibrillar disarray and vacuolization. In the inset, dexrazoxane binds to topoisomerase 2β to prevent anthracycline binding. Produced by permission from Vejpongsa P, Yeh ETH. J Am Coll Cardiol 2014;64:938–45
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