ISSN 2996-8215
International Journal of Cardiology | Vol. 16, No. 3, March 2025 | pp. 17–24
DOI: 10.46882/2025/IJC/000191
Review Article
Cardioprotective Strategies and Monitoring Metrics via Strain Echocardiography in Anthracycline-Induced Cardiotoxicity
Emily C. Thorne¹, William H. Edwards²
¹Department of Cardio-Oncology, Royal Marsden Hospital, London, United Kingdom
²Division of Cardiology, Edinburgh Heart Centre, Royal Infirmary of Edinburgh, Edinburgh, United Kingdom
Abstract:
Anthracyclines remain standard, highly effective therapeutic agents for numerous hematological malignancies and solid tumors, yet their long-term clinical utility is limited by dose-dependent cardiotoxicity, which can cause irreversible heart failure. This comprehensive review synthesizes the molecular mechanisms underlying anthracycline-induced cardiotoxicity and provides a structured overview of modern cardioprotective and monitoring strategies. The primary mechanism of anthracycline toxicity involves the generation of reactive oxygen species (ROS) via iron-dependent pathways, coupled with the direct inhibition of topoisomerase II-beta in mature cardiomyocytes, triggering severe mitochondrial damage and cell apoptosis. Clinical screening depends on tracking left ventricular ejection fraction (LVEF); however, modern speckle-tracking echocardiography can identify subclinical injury through variations in global longitudinal strain (GLS). A relative decrease in absolute GLS greater than 15% during active chemotherapy strongly predicts subsequent LVEF reduction, showing a pooled clinical sensitivity of 86.0% and a specificity of 82.0%. Neurohormonal antagonist therapies, particularly beta-blockers (such as carvedilol) and angiotensin-converting enzyme inhibitors (such as enalapril), show efficacy in blocking or attenuating anthracycline-mediated LVEF declines in high-risk patients. Dexrazoxane remains the only approved intracellular iron chelator that directly reduces ROS generation without altering oncological efficacy, providing a hazard ratio of 0.35 (95% CI: 0.22–0.54) for clinical heart failure prevention across historic cohorts. Effectively managing anthracycline cardiotoxicity requires a multidisciplinary cardio-oncology approach emphasizing early subclinical strain detection and prompt neurohormonal initiation.
Keywords: Anthracyclines, Cardiotoxicity, Cardio-oncology, Global longitudinal strain, Dexrazoxane, Heart failure prevention
Received: December 10, 2024; Revised: January 20, 2025; Accepted: February 08, 2025; Published: March 19, 2025