DOI: 10.1177/10781552261503489 ISSN: 1078-1552

Drug-induced QT prolongation in oncology: A precision-medicine

Abdullah A Assiri

Introduction

Prolongation of the heart-rate–corrected QT interval (QTc) is a defining safety concern in oncology, where patients face an expanding array of repolarization-altering agents superimposed on supportive drugs, electrolyte disturbgances, and organ dysfunction. The anchoring event, torsade de pointes, is uncommon but potentially lethal, and arrhythmic risk must be balanced against the survival benefit of effective cancer therapy.

Methods

The literature was identified through structured searches of PubMed, Scopus, and Web of Science covering the mechanistic, drug-class, pharmacovigilance, pharmacogenomic, risk-prediction, and management aspects of drug-induced QT prolongation in oncology, and was synthesized narratively with an emphasis on precision-medicine dimensions.

Results

QT liability is heterogeneous across tyrosine kinase inhibitors, cyclin-dependent kinase 4/6 inhibitors, antibody-drug conjugates, arsenic trioxide, and supportive agents such as antiemetics, antifungals, opioids, and antibiotics, and is frequently amplified by electrolyte derangement and drug–drug interactions. Genetic susceptibility, real-world pharmacovigilance, and machine-learning risk prediction are emerging but remain underdeveloped in oncology. Pragmatic management rests on baseline and serial Fridericia-corrected electrocardiography, electrolyte optimization, judicious agent selection and dose modification, medication review within a multidisciplinary team, and selection of structured lower-risk alternatives.

Conclusions

Drug-induced QT prolongation in oncology is manageable rather than inevitable. Combining genomic susceptibility, pharmacovigilance, and validated prediction tools offers a route to individualized risk stratification, although prospective oncology-specific evidence and data from under-represented populations remain limited. Early identification and disciplined monitoring allow clinicians to protect the heart without compromising effective cancer treatment.

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