Cardiovascular Toxicity in Cancer Therapy

Cancer therapies have transformed survival rates but frequently compromise cardiovascular health. Classical cytotoxic agents such as anthracyclines provoke dose-dependent myocardial injury, while targeted treatments—tyrosine kinase inhibitors, immune checkpoint inhibitors and vascular endothelial growth factor antagonists—can induce hypertension, arrhythmias and heart failure. Radiotherapy to thoracic regions further elevates the risk of coronary artery disease, pericarditis and valvular dysfunction. At the molecular level, mechanisms include oxidative stress, mitochondrial dysfunction, dysregulated calcium handling, immune-mediated inflammation and endothelial injury. Clinically, manifestations range from subclinical declines in left ventricular function to fulminant cardiomyopathy, myocarditis or thromboembolic events. The growing population of long-term cancer survivors has emphasised the importance of baseline cardiovascular risk assessment, serial monitoring with biomarkers and imaging, and prophylactic use of renin–angiotensin system inhibitors or β-blockers. Multidisciplinary cardio-oncology programmes are emerging to individualise treatment, balance oncological efficacy against cardiac risk and establish guidelines for prevention and management. Continued investment in mechanistic research and population studies is essential to refine risk stratification, develop targeted cardioprotective strategies and ensure that gains in cancer survival are not offset by cardiovascular morbidity.

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Cardiovascular Toxicity in Cancer Therapy publication trend

The graph below shows the total number of articles in cardiovascular toxicity in cancer therapy across all publications each year (not limited to Nature Index journals).

Technical terms

Anthracycline: A class of cytotoxic antibiotics used in chemotherapy that intercalate DNA and generate reactive oxygen species, often causing dose-dependent myocardial injury.

Tyrosine kinase inhibitor (TKI): A targeted agent that blocks specific tyrosine kinases involved in cell signalling, which can lead to off-target cardiovascular effects.

Oxidative stress: A state of excess reactive oxygen species relative to antioxidant defences, leading to cellular damage and dysfunction.

Ferroptosis: An iron-dependent form of regulated cell death characterised by lipid peroxidation and mitochondrial dysfunction.

Venous thromboembolism (VTE): The formation of blood clots in the venous circulation, encompassing deep vein thrombosis and pulmonary embolism.

References

1. Adverse effects of tyrosine kinase inhibitors in cancer therapy: pathophysiology, mechanisms and clinical management. Signal Transduction and Targeted Therapy (2023).
2. Anthracycline Chemotherapy and Cardiotoxicity. Cardiovascular Drugs and Therapy (2017).
3. Cardiotoxicity associated with CTLA4 and PD1 blocking immunotherapy. Journal for ImmunoTherapy of Cancer (2016).
4. Medium and long-term risks of specific cardiovascular diseases in survivors of 20 adult cancers: a population-based cohort study using multiple linked UK electronic health records databases. The Lancet (2019).
5. Baseline cardiovascular risk assessment in cancer patients scheduled to receive cardiotoxic cancer therapies: a position statement and new risk assessment tools from the Cardio‐Oncology Study Group of the Heart Failure Association of the European Society of Cardiology in collaboration with the International Cardio‐Oncology Society. European Journal of Heart Failure (2020).
6. Enalapril and Carvedilol for Preventing Chemotherapy-Induced Left Ventricular Systolic Dysfunction in Patients With Malignant Hemopathies The OVERCOME Trial (preventiOn of left Ventricular dysfunction with Enalapril and caRvedilol in patients submitted to intensive ChemOtherapy for the treatment of Malignant hEmopathies). Journal of the American College of Cardiology (2013).
7. Early Increases in Multiple Biomarkers Predict Subsequent Cardiotoxicity in Patients With Breast Cancer Treated With Doxorubicin, Taxanes, and Trastuzumab. Journal of the American College of Cardiology (2013).
8. Doxorubicin-induced cardiotoxicity: An update on the molecular mechanism and novel therapeutic strategies for effective management. Biomedicine & Pharmacotherapy (2021).
9. Regulated cell death pathways in doxorubicin-induced cardiotoxicity. Cell Death & Disease (2021).