The Successful Management of a Flecainide-Induced Ventricular Storm

Document Type

Conference Proceeding

Publication Date

10-2025

Publication Title

Chest

Abstract

INTRODUCTION: Flecainide is a first line rhythm control class 1C antidysrhythmic used in atrial fibrillation in patients without left ventricular dysfunction A rare side effect of the medication is inducing ventricular tachycardia (VT) as a result of the medications proarrhythmic nature. There is limited data regarding the treatment for flecainide induced VT. We present a case of a patient with a sustained a monomorphic ventricular tachycardia that was successfully converted into sinus rhythm with amiodarone. CASE PRESENTATION: 68-year-old female with past medical history of COPD, dyslipidemia, GIST, paroxysmal atrial fibrillation on Xarelto and flecainide, GERD who presented for lightheadedness, fatigue, nausea, and vomiting following radiation and sunitinib treatment for her GIST tumor. Patient started taking her flecainide that day prior to admission. On admission, she had presented with atrial fibrillation with rapid ventricular response. The patient initially improved with fluid resuscitation but then developed sustained ventricular tachycardia. The patient's ventricular tachycardia was initially difficult to treatment but ultimately was started on amiodarone with successful conversion of monomorphic ventricular tachycardia to underlying atrioventricular paced rhythm. Patient's flecainide was discontinued following this event DISCUSSION: The proarrhythmic drug of flecainide is known to cause ventricular tachycardia. Around 20 percent of patients treated with the agent flecainide have demonstrated proarrhythmic effects.1 There has been very little literature in understanding how suppression of a flecainide induced ventricular tachycardia can be resolved. In this case, amiodarone was effective in the abortion of the new onset ventricular tachycardia. Amiodarone works by inhibiting inward sodium and inward calcium currents leading to competitive alpha and beta blockade effects.2 This allows for electrical conduction slowing and increased refractoriness of the AV node, which depresses the AV node function and leads to termination of ventricular tachycardia.2 The mechanism by which amiodarone targets flecainide is yet to be understood. Upon review of currently literature, Wynn et al has shown abortion of ventricular tachycardia with lidocaine. However there is limited literature on the resolution of a flecainide induced ventricular tachycardia from amiodarone. CONCLUSIONS: Flecainide has a side effect of being a proarrhythmic drug despite its current treatment of atrial fibrillation. One of the aberrant rhythms that flecainide can cause is ventricular tachycardia. Once ventricular tachycardia occurs various cases have demonstrated lidocaine as an affective measure to abort this tachycardia. However, this case highlights a novel and successful approach of using amiodarone as an effective way to abort ventricular tachycardia caused by flecainide induction.

Volume

168

Issue

4S

First Page

810A

Comments

American College of Chest Physicians CHEST Annual Meeting, October 19-22, 2025, Chicago, IL

Last Page

810A

DOI

10.1016/j.chest.2025.07.479

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