Cardiotoxicity in breast cancer patients treated with chemoradiotherapy

With national breast cancer screening programs leading to earlier diagnosis and improved treatments, more women are achieving long-term remission. However, this has resulted in rising rates of cardiotoxicity in breast cancer survivors consequent to their cancer therapies. Anthracyclines, a cornerstone treatment in breast cancer, carry a significant risk of short- and long-term cardiotoxicity through inhibition of topoisomerase II, preventing DNA repair and increasing oxidative stress. This most commonly manifests in the form of left ventricular (LV) systolic dysfunction or heart failure, and in severe cases, death. Many of the other treatments, including taxanes, cyclophosphamide, human epidermal growth factor receptor 2 inhibitors, immunotherapies, hormone therapies, and radiotherapy, also carry a risk of cardiac injury in the form of heart failure, arrhythmias, myocarditis, and pericardial disease. Surveillance has traditionally been performed by monitoring LV ejection fraction by transthoracic echocardiography. However, this has been found to be a late marker of cardiotoxicity, with damage potentially irreversible, and may reflect a missed opportunity for early intervention. Research has focused on identifying cardiac biomarkers and advanced imaging techniques, including strain analysis, to detect subclinical myocardial injury or dysfunction prior to irreversible damage, with LV global longitudinal strain a sensitive marker of subclinical LV systolic dysfunction and superior predictor of future cardiovascular events. Further research is needed to establish standardized guidelines on surveillance and management of this vulnerable patient cohort.

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Publication Details

Journal
Exploration of Targeted Anti-tumor Therapy
Published
2026-09-14
DOI
https://doi.org/10.37349/etat.2026.1002401
Primary Topic
Chemotherapy-induced cardiotoxicity and mitigation
Type
article
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article

Cardiotoxicity in breast cancer patients treated with chemoradiotherapy

Liza Thomas, Peter Emerson
Exploration of Targeted Anti-tumor Therapy
Chemotherapy-induced cardiotoxicity and mitigation
article

Cardiotoxicity in breast cancer patients treated with chemoradiotherapy

Liza Thomas, Peter Emerson
article en

Abstract

With national breast cancer screening programs leading to earlier diagnosis and improved treatments, more women are achieving long-term remission. However, this has resulted in rising rates of cardiotoxicity in breast cancer survivors consequent to their cancer therapies. Anthracyclines, a cornerstone treatment in breast cancer, carry a significant risk of short- and long-term cardiotoxicity through inhibition of topoisomerase II, preventing DNA repair and increasing oxidative stress. This most commonly manifests in the form of left ventricular (LV) systolic dysfunction or heart failure, and in severe cases, death. Many of the other treatments, including taxanes, cyclophosphamide, human epidermal growth factor receptor 2 inhibitors, immunotherapies, hormone therapies, and radiotherapy, also carry a risk of cardiac injury in the form of heart failure, arrhythmias, myocarditis, and pericardial disease. Surveillance has traditionally been performed by monitoring LV ejection fraction by transthoracic echocardiography. However, this has been found to be a late marker of cardiotoxicity, with damage potentially irreversible, and may reflect a missed opportunity for early intervention. Research has focused on identifying cardiac biomarkers and advanced imaging techniques, including strain analysis, to detect subclinical myocardial injury or dysfunction prior to irreversible damage, with LV global longitudinal strain a sensitive marker of subclinical LV systolic dysfunction and superior predictor of future cardiovascular events. Further research is needed to establish standardized guidelines on surveillance and management of this vulnerable patient cohort.

Exploration of Targeted Anti-tumor TherapyVol. 7
Westmead Hospital (AU)
Good health and well-being
Openalex Percentile: Top 11%
Chemotherapy-induced cardiotoxicity and mitigation
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