Abstract 4372907: A Rare Case of Idiopathic Ventricular Fibrillation Triggered by Short-Coupled PVCs from the Apical Free Wall of the Right Ventricle

Abstract

Introduction: Idiopathic ventricular fibrillation (IVF) refers to VF occurring in the absence of structural heart disease or inherited arrhythmia syndromes such as Brugada, catecholaminergic polymorphic VT, or long/short QT syndromes. In most cases, IVF is triggered by short-coupled premature ventricular complexes (PVCs), typically arising from the Purkinje system or the right ventricular outflow tract (RVOT). However, PVCs originating from the apical free wall of the right ventricle are extremely rare. Background: PVCs from the right ventricular apical free wall represent a dangerous yet uncommon arrhythmogenic substrate. These PVCs may initiate VF via delayed afterdepolarizations (DADs), particularly when coupling intervals are short. Recognizing this atypical origin through surface ECG is essential, especially when invasive mapping is delayed. Characteristic ECG features include a left bundle branch block (LBBB) morphology, superior axis, and late precordial transition—patterns distinct from RVOT or fascicular origins. Case Presentation: A 59-year-old female with a history of idiopathic VF arrest (S/p ICD in 2010), HTN, recurrent ICD shocks despite multiple antiarrhythmics and moderator band ablation 02/24, presented with frequent shocks. Echocardiography revealed a structurally normal heart. Baseline ECG showed sinus rhythm with frequent monomorphic PVCs exhibiting LBBB morphology, superior axis, and late transition (V4–V5), consistent with an apical free wall origin in the right ventricle. PVC coupling interval measured ~280 ms. Telemetry captured polymorphic VT/VF episodes reproducibly triggered by these PVCs. Due to inadequate response and proarrhythmic concerns, flecainide was discontinued and verapamil initiated, resulting in immediate suppression of arrhythmias. The patient underwent successful empiric ablation targeting the apical right ventricular free wall. ICD interrogation at one-month follow-up revealed no recurrent arrhythmic events. Conclusion: This case illustrates a rare but potentially fatal presentation of IVF triggered by short-coupled PVCs from the apical free wall of the right ventricle. The ECG morphology, short coupling interval, and verapamil responsiveness support a DAD-mediated mechanism. Recognition of this unusual origin is crucial, as targeted ablation can be curative. This case expands the spectrum of IVF substrates beyond traditional foci and underscores the importance of ECG-guided localization and early EP collaboration.