Chemotherapy-induced cardiotoxicity requires early detection with biomarkers and imaging, alongside preventive strategies and personalized cardio-oncology care to balance cancer control with heart health.
This review emphasizes the importance of early detection, preventive interventions, and a multidisciplinary cardio-oncology approach to manage chemotherapy-induced cardiotoxicity.
Introduction: Chemotherapy-Induced Cardiotoxicity (CIC) has become a growing concern in modern oncology. While chemotherapy remains one of the most effective treatments against cancer, its potential to harm the heart often limits its use. The underlying mechanisms involve oxidative stress, mitochondrial dysfunction, and inflammation, all contributing to the gradual weakening of cardiac muscle. As cancer survival improves, the burden of cardiovascular complications is more visible than ever, emphasizing the need for early recognition, prevention, and long-term management. Methods: This review draws upon published literature, recent clinical trials, and translational research to explore current understanding and future directions in CIC. Studies on anthracyclines and HER2 inhibitors were reviewed in depth, along with new data on diagnostic biomarkers, imaging techniques, and evolving therapeutic strategies. Particular attention was given to the role of pharmacogenomics, preventive interventions, and emerging therapies aimed at protecting or restoring cardiac function in patients undergoing chemotherapy. Results: CIC can present as heart failure, arrhythmia, hypertension, myocardial ischemia, or thromboembolism. Factors such as age, obesity, cumulative drug exposure, and genetic predisposition significantly raise the risk. Recent advances have improved early detection—troponins, natriuretic peptides, and echocardiography with Global Longitudinal Strain (GLS) allow for identification before overt symptoms appear. Preventive strategies, including dose adjustments, liposomal formulations, and the cardioprotective agent dexrazoxane, have shown measurable benefits. Established cardiotoxicity can be managed with conventional heart failure medications, antihypertensives, and anticoagulants. Experimental approaches—ranging from mitochondrial stabilizers and histone deacetylase inhibitors to mesenchymal stem cell therapy—show promise in reversing cardiac injury. Discussion: CIC reflects a complex interaction between cancer biology, treatment intensity, and patientspecific vulnerability. A proactive, multidisciplinary approach involving both oncologists and cardiologists is key to balancing cancer control with heart health. Lifestyle measures such as regular exercise and dietary optimization can further strengthen cardiovascular resilience. Advances in genetic testing, molecular imaging, and regenerative therapy are gradually shifting the field toward more personalized cardio-oncology care. Conclusion: Chemotherapy-induced cardiotoxicity continues to challenge clinicians striving for a cure without compromise. The future of cancer care lies in integrating precision medicine with preventive cardiology to minimize cardiac injury while maintaining therapeutic efficacy. Continued research into molecular targets, biomarkers, and cell-based therapies offers genuine hope for improving both survival and quality of life in cancer patients.
Rao et al. (2026) conducted a review in Chemotherapy-Induced Cardiotoxicity. Chemotherapy was evaluated. Chemotherapy-induced cardiotoxicity requires early detection with biomarkers and imaging, alongside preventive strategies and personalized cardio-oncology care to balance cancer control with heart health.