Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2010 Dec;12(6):404-10.
doi: 10.1007/s11906-010-0146-y.

Mechanisms of anthracycline cardiotoxicity and strategies to decrease cardiac damage

Affiliations

Mechanisms of anthracycline cardiotoxicity and strategies to decrease cardiac damage

Carrie Anna Geisberg et al. Curr Hypertens Rep. 2010 Dec.

Abstract

Anthracyclines are common chemotherapeutic agents used to treat many different types of cancer. Unfortunately, the use of anthracyclines is limited by their cardiotoxic effects, which may become manifest as late as 20 years from initial exposure. Studies in cells and animals suggest that the mechanism of anthracycline-induced cardiotoxicity (AIC) is multifactorial. Anthracyclines induce multiple forms of cellular injury by free radical production. In addition, anthracyclines alter nucleic acid biology by intercalation into DNA and modulate intracellular signaling, leading to cell death and the disruption of homeostatic processes such as sarcomere maintenance. In an effort to decrease AIC, many strategies have been tested, but no specific therapies are universally acknowledged to prevent or treat anthracycline-induced cardiac dysfunction. Newer imaging modalities and cardiac biomarkers may be useful in improving early detection of cardiac injury and dysfunction. As long as there is no cardiac-specific therapy for AIC, evidence suggests that high-risk patients will benefit from prophylactic treatment with neurohormonal blockade by angiotensin-converting enzyme inhibitors and beta-adrenergic receptor blockers.

PubMed Disclaimer

Conflict of interest statement

Disclosure

Dr. Sawyer has received payments (part of licensing fees paid by Zensun) related to his role as a coinventor of recombinant neuregulin for the treatment of heart failure. He is currently receiving grant support from Acorda Therapeutics related to the development of recombinant neuregulin. No other potential conflicts of interest relevant to this article were reported.

References

    1. Shankar SM, Marina N, Hudson MM, et al. Monitoring for cardiovascular disease in survivors of childhood cancer: report from the Cardiovascular Disease Task Force of the Children’s Oncology Group. Pediatrics. 2008;121:e387–e396. - PubMed
    1. Steinherz LJ, Steinherz PG, Tan CT, et al. Cardiac toxicity 4 to 20 years after completing anthracycline therapy. JAMA. 1991;266:1672–1677. - PubMed
    1. Cardinale D, Colombo A, Lamantia G, et al. Anthracycline-induced cardiomyopathy: clinical relevance and response to pharmacologic therapy. J Am Coll Cardiol. 2010;55:213–220. In a prospective clinical trial, 201 patients with AIC were treated with enalapril and carvedilol promptly after diagnosis of LV ejection fraction of 45% or less. Complete recovery of the ejection fraction occurred in 85 patients (42%). The percentage of responders decreased when the time from chemotherapy to diagnosis of reduced ejection fraction was greater than 4 months. - PubMed
    1. Lipshultz SE, Alvarez JA, Scully RE. Anthracycline associated cardiotoxicity in survivors of childhood cancer. Heart. 2008;94:525–533. A review of results from the Childhood Cancer Survivor Study (CCSS) discussing increased cumulative incidence of chronic health conditions 30 years after treatment. The review highlights proposed pathophysiology that occurs during late-onset cardiotoxicity after childhood exposure and recommendations for monitoring and treatment. - PubMed
    1. Shan K, Lincoff AM, Young JB. Anthracycline-induced cardiotoxicity. Ann Intern Med. 1996;125:47–58. - PubMed

Publication types

MeSH terms