# Aborted Sudden Cardiac Death Due to Acquired QT Prolongation: A Case Report

**Authors:** Georgios Aletras, Maria Bachlitzanaki, Eleni Eleftheriadou, Michael Pitarokoilis, Emmanouil G Foukarakis

PMC · DOI: 10.7759/cureus.78496 · Cureus · 2025-02-04

## TL;DR

A 60-year-old woman nearly died from sudden cardiac arrest caused by drug-induced QT prolongation, highlighting the need for careful medication review and genetic testing in such cases.

## Contribution

The case emphasizes the importance of identifying acquired LQTS and considering genetic predisposition in patients with persistent QT prolongation.

## Key findings

- The patient's cardiac arrest was due to QT prolongation from medications and hypokalemia.
- Discontinuation of QT-prolonging drugs led to QT normalization and clinical stabilization.
- Genetic testing is recommended in cases of persistent QT prolongation after removing contributing factors.

## Abstract

Long QT syndrome (LQTS) is characterized by QT interval prolongation, which significantly increases the risk of malignant arrhythmias and sudden cardiac death, even in the absence of structural heart disease. While LQTS can be congenital, distinguishing it from the acquired form is crucial, though both may coexist in some cases. We present the case of a 60-year-old woman with a history of schizoaffective disorder treated with escitalopram and amisulpride and a recent prescription for ciprofloxacin for a urinary tract infection, who was admitted following a cardiac arrest. The episode was triggered by acquired QT prolongation due to the combined effects of QT-prolonging medications and hypokalemia. The patient was successfully resuscitated, and discontinuation of the offending medications (e.g., escitalopram, amisulpride, and ciprofloxacin) led to clinical stabilization with QT normalization, while other possible causes were ruled out (e.g., ischemia, thyroid disorders, etc.). This case highlights the importance of thorough medication review and early identification of individuals at risk for acquired LQTS to prevent potentially fatal arrhythmias. It also highlights the necessity of considering underlying genetic predisposition, especially in cases where QT prolongation persists despite the discontinuation of the offending agents and/or correction of other contributing factors, making genetic testing advisable in selected patients, as it will guide further management.

## Linked entities

- **Chemicals:** escitalopram (PubChem CID 146570), amisulpride (PubChem CID 2159), ciprofloxacin (PubChem CID 2764)
- **Diseases:** schizoaffective disorder (MONDO:0005487), urinary tract infection (MONDO:0005247), Long QT syndrome (MONDO:0002442), hypokalemia (MONDO:0003019)

## Full-text entities

- **Diseases:** thyroid disorders (MESH:D013959), heart disease (MESH:D006331), ischemia (MESH:D007511), schizoaffective disorder (MESH:D011618), Sudden Cardiac Death (MESH:D016757), cardiac arrest (MESH:D006323), hypokalemia (MESH:D007008), arrhythmias (MESH:D001145), LQTS (MESH:D008133), urinary tract infection (MESH:D014552)
- **Chemicals:** QT-prolonging medications (-), escitalopram (MESH:D000089983), ciprofloxacin (MESH:D002939), amisulpride (MESH:D000077582)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11885193/full.md

## References

14 references — full list in the complete paper: https://tomesphere.com/paper/PMC11885193/full.md

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Source: https://tomesphere.com/paper/PMC11885193