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February 1, 2017Cardiovascular Drugs and Therapy969 citationsOpen Access

Anthracycline Chemotherapy and Cardiotoxicity

JMJohn McGowanUniversity College LondonRCRobin ChungUniversity College London Hospitals NHS Foundation TrustAMAngshuman MaulikDalhousie University

Key Result

Doxorubicin treatment resulted in a cardiotoxicity incidence of 9% defined as a decrease in LVEF of more than 10% to less than 50% over a median follow-up of 5.2 years.

Key Points

  • Summarize the molecular mechanisms driving anthracycline-induced cardiotoxicity and evaluate established and emerging cardioprotective interventions.
  • Narrative review synthesizing mechanistic and clinical evidence on anthracycline-mediated cardiac damage and preventive strategies.
  • Cardiotoxicity involves direct pathways including reactive oxygen species generation and topoisomerase 2 disruption, alongside indirect cellular injury pathways.
  • Cardioprotective interventions evaluated to date include renin-angiotensin system blockers, beta-blockers, and the iron chelator dexrazoxane.
  • Novel protective approaches under investigation exploit ErbB signaling, pro-survival pathways, and conditioning techniques to reduce long-term cardiac morbidity.

Structured PICO

P
Population
Cancer patients receiving anthracycline chemotherapy
I
Intervention
Anthracycline chemotherapy (e.g., doxorubicin, epirubicin, idarubicin, daunorubicin)
O
Outcome
Cardiotoxicity (clinical decompensation, sub-clinical structural change, biomarker rise, or arrhythmia)safety

Anthracycline chemotherapy is associated with significant dose-dependent cardiotoxicity, highlighting the need for early detection and long-term cardiovascular monitoring in cancer survivors.

Limitations

  • The study is a review article summarizing previous studies rather than presenting new clinical trial data.

Abstract

Anthracycline chemotherapy maintains a prominent role in treating many forms of cancer. Cardiotoxic side effects limit their dosing and improved cancer outcomes expose the cancer survivor to increased cardiovascular morbidity and mortality. The basic mechanisms of cardiotoxicity may involve direct pathways for reactive oxygen species generation and topoisomerase 2 as well as other indirect pathways. Cardioprotective treatments are few and those that have been examined include renin angiotensin system blockade, beta blockers, or the iron chelator dexrazoxane. New treatments exploiting the ErbB or other novel pro-survival pathways, such as conditioning, are on the cardioprotection horizon. Even in the forthcoming era of targeted cancer therapies, the substantial proportion of today's anthracycline-treated cancer patients may become tomorrow's cardiac patient.

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Cite This Study

McGowan et al. (2017) conducted a review in cardiotoxicity due to anthracycline chemotherapy. doxorubicin was evaluated on cardiotoxicity incidence. Doxorubicin treatment resulted in a cardiotoxicity incidence of 9% defined as a decrease in LVEF of more than 10% to less than 50% over a median follow-up of 5.2 years.

synapsesocial.com/papers/696d73620860973dc1fe7ad6https://doi.org/10.1007/s10557-016-6711-0
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Anthracycline-Induced Cardiotoxicity and Exploration of Cardioprotective Drugs2025 · 4 citations
  2. 2Cardioprotection in cancer therapy: novel insights with anthracyclines2019 · 37 citations
  3. 3Anthracycline-induced cardiotoxicity: emerging mechanisms and therapies2025 · 2 citations
  4. 4Anthracycline-induced cardiotoxicity: course, pathophysiology, prevention and management2007 · 312 citations
  5. 5Prevention of Anthracycline-Induced Cardiotoxicity2014 · 682 citations