Abstract

DRUG-INDUCED CARDIOTOXICITY: MECHANISM AND PREVENTION- A NARRATIVE REVIEW

*Mohammed Fayaz, Anas Khan N., Asish S. S.

ABSTRACT

Background: Advances in pharmacotherapy, particularly in oncology, have markedly improved patient survival; however, drug-induced cardiotoxicity has emerged as a major limitation to long-term treatment success. Cardiotoxic effects range from asymptomatic myocardial dysfunction to heart failure, arrhythmias, ischemia, and inflammatory cardiac conditions, often compromising therapeutic continuity and survival. Objective: This narrative review aims to summarize current evidence on the classification, mechanisms, risk factors, prevention, monitoring, and management of drug-induced cardiotoxicity, with emphasis on anticancer therapies. Methods: A comprehensive narrative review of published literature was conducted, focusing on clinical patterns of cardiotoxicity, underlying molecular mechanisms, implicated drug classes, and contemporary prevention and monitoring strategies within cardio-oncology practice. Results: Cardiotoxicity may present acutely, early, or years after drug exposure and can be reversible or irreversible depending on the agent and mechanism involved. Key pathogenic pathways include oxidative stress, mitochondrial injury, topoisomerase-2β–mediated DNA damage, immune-mediated inflammation, and ion-channel dysfunction. Anthracyclines, targeted therapies, immune checkpoint inhibitors, and several non-oncological drugs are commonly implicated. Risk is amplified by cumulative dose, combination regimens, pre-existing cardiovascular disease, and traditional cardiovascular risk factors. Evidence supports risk-based surveillance using echocardiography, biomarkers, and cardioprotective pharmacotherapy to mitigate adverse outcomes. Conclusion: Drug-induced cardiotoxicity remains a critical challenge in modern therapeutics. A multidisciplinary, risk-stratified cardio-oncology approach emphasizing early detection, prevention, and personalized management is essential to preserve cardiac function while enabling optimal pharmacological treatment.

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