Abstract 15535: A Case of Suspected Menstruation Induced QTc Prolongation Leading to Torsades De Pointes

Estrogen is known to produce changes in cardiac electrophysiology specifically in premenopausal women, increasing the risk of arrhythmias. We report a case of Torsades de Pointes (TdP) in a young premenopausal female. A 25-year-old female with a history of anxiety presented to the emergency room (ED) with several days of vomiting. While in the ED, she had an unwitnessed syncopal event, and was found to be in pulseless ventricular fibrillation (V-Fib) . She required one defibrillation to obtain return of spontaneous circulation (ROSC). Initial work up showed calcium 7.6 mg/dl, phosphorous 1.1 mg/dl, magnesium 2.4 mg/dl, potassium 4.0 mg/dl. Remainder of electrolytes were normal. Toxicology screen was positive for cannabinoids. Post ROSC EKG showed sinus tachycardia at a rate of 103bpm with a prolonged QTc of 531ms. Patient was not on any medications outpatient. On further discussion, patient reported no prior history of syncopal episodes, palpitations, and denied any family history of sudden cardiac death. She did report she was presently on her menses. Shortly after admission, she had recurrent polymorphic ventricular tachycardia which degenerated to TdP. She was loaded with magnesium. Echocardiogram showed an ejection fraction (EF) of 35-39% and global hypokinesis. Diagnostic left heart catheterization was performed revealing clean coronaries. Cardiac MRI revealed EF of 43% without any late gadolinium enhancement. Her QTc remained prolonged even with electrolyte normalization. She underwent successful ICD placement and remained event free during the remainder of the hospital course. She will undergo genetic work up for long QT syndrome. Female sex hormones, specifically estrogen, have been described in literature as pro-arrhythmic given its effects on QT prolongation and ion gated channels. Prior cases of menstruation dependent arrhythmias have speculated that the abrupt reduction in estradiol prior to menstruation is associated with increased cyclic adenosine monophosphate dependent arrhythmogenicity. This case highlights the multifactorial etiology of sudden V-Fib arrest in a young female, and the importance of understanding the role that sex hormones play in the underlying pathogenesis.