Ivabradine as a Cardio-Protective Agent Against Anthracycline-Induced Cardiotoxicity: A Narrative Review

Anthracycline-induced cardiomyopathy (AIC) remains a major limitation in cancer therapy, significantly impacting patient survival and quality of life. Ivabradine, a selective heart rate-lowering agent, has recently attracted attention for its potential cardioprotective effects. This review aims to summarize and critically evaluate the mechanistic, preclinical, and clinical evidence supporting ivabradine's role in preventing or attenuating anthracycline-induced cardiotoxicity.

A comprehensive literature review was conducted using databases including PubMed, Scopus, and Web of Science, focusing on studies investigating the effects of ivabradine on cardiac structure, function, and cellular mechanisms in the context of anthracycline therapy. Both experimental and clinical data were analyzed to identify patterns of cardioprotection and potential translational value.

Preclinical studies demonstrate that ivabradine mitigates anthracycline-induced oxidative stress, inflammation, and mitochondrial dysfunction while preventing cardiomyocyte apoptosis and preserving myocardial performance. Clinical evidence suggests that ivabradine reduces cardiotoxicity, maintains left ventricular ejection fraction, and enhances myocardial efficiency without lowering blood pressure or diminishing chemotherapy efficacy.

Ivabradine shows promising cardioprotective potential against anthracycline-induced cardiotoxicity through multiple cellular and functional mechanisms. However, it is not yet approved for this indication, and large-scale, randomized multicenter trials are required to confirm its efficacy and safety. Integrating ivabradine into precision cardio-oncology may represent a novel strategy to improve outcomes and quality of life in cancer patients receiving anthracycline-based therapy.