# Fragile X and Fatal Rhythms: Electroconvulsive Therapy–Induced Ventricular Tachycardia

**Authors:** Muhammad Salman Sabri, Nimra Klair, Joshua Wiener, Maria T. Gamero, Drew Johnson

PMC · DOI: 10.1016/j.jaccas.2025.105077 · JACC Case Reports · 2025-08-14

## TL;DR

A man with Fragile X syndrome experienced dangerous heart rhythms during electroconvulsive therapy, highlighting the need for special precautions.

## Contribution

This case highlights the risk of ECT-induced arrhythmias in FXS and suggests strategies like stellate ganglion block for prevention.

## Key findings

- A patient with FXS developed ventricular tachycardia and cardiac arrest during ECT despite standard antiarrhythmic treatment.
- Pretreatment with left stellate ganglion block and intravenous amiodarone was considered to mitigate arrhythmia risk.
- FXS may increase arrhythmia susceptibility due to elevated sympathetic tone and ion channel abnormalities.

## Abstract

Fragile X syndrome (FXS) is associated with autonomic dysfunction and ion channel abnormalities that increase the risk of arrhythmias. Electroconvulsive therapy (ECT), used to treat catatonia in FXS, can trigger a sympathetic surge, potentially inducing ventricular tachycardia.

A 52-year-old man with FXS and catatonia developed recurrent wide complex tachycardia and cardiac arrest during ECT sessions, despite normal electrolytes, no structural heart disease, and a normal baseline electrocardiogram. The patient had recurrent cardiac arrest despite scheduled oral amiodarone 200 mg 3 times a day and premedication with 30 mg of esmolol. Pretreatment with a left stellate ganglion block and intravenous amiodarone infusion was considered before ECT sessions.

FXS may increase susceptibility to arrhythmia owing to elevated sympathetic tone and channelopathies associated with fragile X mental retardation protein. ECT may amplify this risk, requiring proactive strategies.

Patients with FXS may require individualized pre-ECT risk assessment. Antiarrhythmic and sympathetic modulation strategies, including stellate ganglion block, may be essential for arrhythmia prevention in high-risk cases.

## Linked entities

- **Genes:** FMR1 (fragile X messenger ribonucleoprotein 1) [NCBI Gene 2332]
- **Chemicals:** amiodarone (PubChem CID 2157), esmolol (PubChem CID 59768)
- **Diseases:** Fragile X syndrome (MONDO:0010383), catatonia (MONDO:0800105), ventricular tachycardia (MONDO:0005477), cardiac arrest (MONDO:0000745)

## Full-text entities

- **Genes:** FMR1 (fragile X messenger ribonucleoprotein 1) [NCBI Gene 2332] {aka FMRP, FRAXA, POF, POF1}
- **Diseases:** heart disease (MESH:D006331), channelopathies (MESH:D053447), ion channel abnormalities (MESH:C538353), stellate ganglion block (MESH:D045888), arrhythmia (MESH:D001145), cardiac arrest (MESH:D006323), catatonia (MESH:D002389), autonomic dysfunction (MESH:D001342), tachycardia (MESH:D013610), Ventricular Tachycardia (MESH:D017180), FXS (MESH:D005600)
- **Chemicals:** esmolol (MESH:C036604), amiodarone (MESH:D000638)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12789760/full.md

## References

13 references — full list in the complete paper: https://tomesphere.com/paper/PMC12789760/full.md

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Source: https://tomesphere.com/paper/PMC12789760