Key result
Evidence-based monitoring and risk factor correction substantially reduce torsades de pointes from QT-prolonging drugs.
Why the study?
With ubiquitous polypharmacy in ageing populations and oncology, clinicians need a structured understanding of drug-ECG interactions to reduce sudden cardiac death risk.
Systematic Review
Systematic narrative review reveals critical mechanisms and risk factors for drug-induced QT prolongation and arrhythmias, highlighting the need for structured electrocardiographic monitoring.
BACKGROUND: The electrocardiogram (ECG) remains the foremost non-invasive tool for detecting adverse drug effects on cardiac electrophysiology, encompassing QT interval prolongation, torsades de pointes (TdP), atrioventricular (AV) block, and sodium-channel-mediated QRS widening. As polypharmacy becomes ubiquitous - particularly in ageing populations and oncology - clinicians require a structured understanding of drug-ECG interactions to mitigate sudden cardiac death risk. METHODS: A systematic narrative review was conducted using PubMed, Embase, and the Cochrane Library covering January 2006 to April 2026. Priority was given to meta-analyses, systematic reviews, scientific statements, and guidelines addressing drug-induced ECG changes, QTc measurement methodology, TdP risk stratification, and ECG monitoring protocols. Reference lists of key papers were hand-searched. Seventy references meeting quality and relevance criteria are cited. RESULTS: Numerous drug classes - including antiarrhythmics, antibiotics, antipsychotics, antidepressants, antiemetics, and oncology agents - prolong the corrected QT interval primarily through blockade of the cardiac hERG/IKr potassium channel. Modifiable risk factors include hypokalaemia, hypomagnesaemia, bradycardia, and co-prescription of CYP3A4 inhibitors. Female sex, age ≥ 65 years, congenital long QT syndrome carriers, and cardiac failure patients are at disproportionate TdP risk. The validated Tisdale Risk Score enables pre-treatment stratification in hospitalised patients. Drug-specific ECG monitoring protocols with actionable thresholds are summarised. CONCLUSIONS: Drug-induced ECG changes are common, clinically consequential, and often preventable. Evidence-based monitoring protocols, correction of modifiable risk factors, and prompt recognition of ominous ECG patterns substantially reduce adverse outcomes. Prescriber education across all clinical settings is imperative.
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Akman et al. (2026) conducted a systematic review in Drug-induced ECG changes. QT-prolonging drugs was evaluated. Numerous drug classes prolong the QT interval, and evidence-based monitoring protocols alongside correction of modifiable risk factors can substantially reduce adverse outcomes like torsades de pointes.
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