Abstract / Summary
ABSTRACT Introduction Antipsychotic‐associated heart rate‐corrected QT (QTc) prolongation and sudden cardiac death are uncommon in young people, but risk is concentrated in patients with identifiable clinical vulnerability and during selected drug‐ or exposure‐related situations. We mapped the evidence and developed a risk‐stratified framework for clinical monitoring. Methods This structured narrative review searched PubMed in August 2026 using one comprehensive query and 41 targeted subqueries. After PMID‐based deduplication, 934 unique records underwent title screening, 382 abstract review, and 158 full‐text relevance assessment; 104 database‐derived sources met broad relevance criteria. Backward citation checking and author‐identified sources added 58 articles. Overall, 162 sources were considered and 100 providing direct, non‐redundant support were cited from the original search; three further sources were incorporated during peer review to address reviewer comments, for a final total of 103 cited references. Two authors independently assessed full‐text relevance. Youth evidence was prioritized; adult evidence was used for adult‐only agents or when youth‐specific data were unavailable. Findings were synthesized narratively without formal risk‐of‐bias or certainty assessment. Results Patient‐level factors, particularly electrolyte disturbance, bradycardia, restrictive eating disorder or medical instability, thyroid dysfunction, inherited channelopathy, structural disease, and interacting drugs, were more consistently associated with QTc risk than drug identity for many commonly used agents. Ziprasidone and pimozide had the strongest youth‐specific drug‐related signals. Adult evidence supported heightened caution with sertindole and iloperidone; high‐dose phenothiazines and amisulpride in overdose or renal impairment represented exposure‐ or context‐dependent risks. Clozapine required separate myocarditis‐focused surveillance. The evidence supports structured baseline risk assessment and targeted ECG and electrolyte testing, with repeat monitoring driven by risk factors, treatment changes, and agent‐specific warnings. Conclusion Monitoring should be tiered rather than uniformly scheduled for all patients. The proposed framework distinguishes core clinical risk assessment from targeted cardiac testing and identifies precautionary intervals that require prospective validation.