Fragile X and Fatal Rhythms: Electroconvulsive Therapy-Induced Ventricular Tachycardia

脆性X染色体综合征与致命性心律失常:电休克疗法诱发的室性心动过速

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Abstract

BACKGROUND: 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. CASE SUMMARY: 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. DISCUSSION: 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. TAKE-HOME MESSAGES: 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.

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