Dexrazoxane is the only FDA-approved therapy with consistent evidence for reducing anthracycline-induced heart failure and permitting higher cumulative doxorubicin dosing.
Early recognition through biomarkers and imaging, along with cardioprotective strategies like dexrazoxane, are essential to prevent doxorubicin-induced heart failure.
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Doxorubicin remains a cornerstone chemotherapeutic agent in the treatment of both hematologic malignancies and solid tumors. However, its clinical use is limited by dose-dependent cardiotoxicity, which may manifest as asymptomatic left ventricular dysfunction or progress to overt heart failure. Despite the emergence of cardiovascular complications associated with toxicities of novel targeted therapies, doxorubicin-induced cardiotoxicity continues to represent a central challenge in cardio-oncology. This review summarizes current evidence regarding the pathophysiology, dose-related risk thresholds, evolving definition, surveillance strategies, and preventive approaches for doxorubicin-induced cardiotoxicity. Particular emphasis is placed on clinically relevant mechanisms. We discuss strategies for early detection of subclinical myocardial injury, highlighting the roles of cardiac biomarkers such as troponin and natriuretic peptides, echocardiographic assessment including global longitudinal strain, and advanced imaging modalities such as cardiac magnetic resonance imaging. Evidence-based cardioprotective interventions are critically examined. Although neurohormonal blockade and statins have demonstrated variable results across clinical trials, dexrazoxane remains the only United States Food and Drug Administration-approved therapy with consistent evidence supporting its efficacy in reducing anthracycline-associated heart failure (HF) and permitting higher cumulative dosing when clinically necessary. The review also highlights the evolving role of individualized surveillance strategies and cardio-oncology care in mitigating long-term cardiac complications. Early recognition and intervention are key to preserving left ventricular function and allowing continued oncologic treatment without compromising cardiovascular safety. Greater adoption of cardioprotective strategies, particularly dexrazoxane in appropriate patients, has the potential to make anthracycline-induced heart failure a preventable complication of doxorubicin therapy.
Haoyi Zheng (Thu,) reported a other. Dexrazoxane is the only FDA-approved therapy with consistent evidence for reducing anthracycline-induced heart failure and permitting higher cumulative doxorubicin dosing.
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