Case Study

Recurrent Ventricular Fibrillation Induced by Atrial Tachycardia in a Patient with Hypertrophic Cardiomyopathy

Adam Oesterle, MD, and Edward P. Gerstenfeld, MD
Division of Cardiology, Section of Cardiac Electrophysiology,
University of California, San Francisco
San Francisco, California

Adam Oesterle, MD, and Edward P. Gerstenfeld, MD
Division of Cardiology, Section of Cardiac Electrophysiology,
University of California, San Francisco
San Francisco, California


Tracings from implantable cardioverter-defibrillators (ICDs) have shown that atrial tachycardia (AT) and atrial fibrillation (AFib) can precede ventricular tachycardia (VT) and ventricular fibrillation (VF).1 Dual-chamber ICDs have shown paroxysmal AT or AFib preceding VT/VF 8.9% of the time.2 Termination of both atrial and ventricular arrhythmias with ICD therapy resulted in longer time to the next VT/VF episode than if the atrial arrhythmias persisted, suggesting a link between atrial arrhythmias and VT/VF.2 AFib ablation in patients with an ICD has been shown to reduce both appropriate and inappropriate ICD therapies.3 Clinically, VT that can be induced from the atrium typically involves the conduction system, either the left and right bundle branches (RBB) or the Purkinje fascicles.4,5 The mechanism for the induction of VT/VF that is not related to the conduction system by AT or AFib is not entirely clear.

We present a case of a supraventricular tachycardia (SVT)-induced VF in a patient with hypertrophic cardiomyopathy (HCM).

Case Description

The patient is a 23-year-old female with HCM (mean gradient 12 mmHg) who had a subcutaneous ICD (S-ICD System, Boston Scientific) implanted in 2015 after a VF arrest. She had multiple episodes of syncope and VF, with appropriate shocks that were induced by a narrow complex tachycardia (Figure 1). An implantable loop recorder was placed and demonstrated that some of the narrow complex tachycardia episodes that degenerated into VF were preceded by sinus tachycardia at times of walking or other physical activity. An EP study showed inducible non-sustained atrial flutter and the patient underwent a cavotricuspid isthmus (CTI) ablation 18 months before presentation, followed by pulmonary vein isolation cryoablation 12 months before presentation at another institution. She was initially treated with metoprolol and digoxin, and the digoxin was subsequently discontinued. A cardiac magnetic resonance imaging (MRI) scan (Figure 2) demonstrated asymmetric left ventricular hypertrophy, a septal thickness of 30 mm, and late gadolinium enhancement (LGE) in the mid septum. She continued to have episodes of VF and appropriate ICD shocks, and presented to our institution in 2019 for repeat EP study and possible ablation.

Quadripolar catheters were placed in the right atrium (RA) and right ventricle (RV), a duodecapolar catheter was placed across the His bundle and RBB, and a decapolar catheter was advanced to the coronary sinus (CS). There was no VA conduction or evidence of dual AV node physiology at baseline. A narrow complex tachycardia with a left posterior fascicular (LPF) block aberrancy with a cycle length (CL) of 345-365 ms and distal to proximal CS activation was induced with ventricular burst pacing at 700 ms on 2 mcg/min of isoproterenol (Figure 3A); this degenerated into VF and required a 360-joule external shock for restoration of sinus rhythm (Figure 3B).

The tachycardia was re-initiated, and ventricular overdrive pacing demonstrated VA dissociation with the A-A driving the H-H interval. The atrial-His (A-H) bundle interval during right atrial pacing at the tachycardia cycle length was 131 ms, and the A-H in SVT was 116 ms (difference 15 ms); the tachycardia spontaneously terminated with a V, PACs demonstrated VA unlinking on the return beat, and adenosine reproducibly terminated the tachycardia. Therefore, the tachycardia was diagnosed as a likely triggered AT.6 There was an episode of a wide complex tachycardia, which occurred during AT with a RBBB/LPF morphology that spontaneously narrowed; it was unclear if this was a dual tachycardia or AT with aberration (Figure 3C).

A 3D activation map of the RA was performed with the CARTO System and THERMOCOOL SMARTTOUCH Catheter (Biosense Webster, Inc., a Johnson & Johnson company). The tachycardia was diffusely early on the RA septum, and a double transseptal puncture was performed with an NRG Transseptal Needle (Baylis Medical) under intracardiac ultrasound guidance after the administration of heparin. A SL1 and deflectable Agilis sheath (Abbott) were advanced to the left atrium (LA). Activation mapping of the LA was performed with a PENTARAY catheter (Biosense Webster, Inc., a Johnson & Johnson company).

The pulmonary veins remained isolated from the previous cryoablation and the earliest A was mapped to 10:30 on the mitral annulus (Figure 4A). The tachycardia terminated immediately with a single ablation lesion at 30-35 watts (Figure 4B). After ablation, atrial and ventricular burst pacing and programmed extrastimulation (double ventricular extrastimuli to refractoriness) on and off isoproterenol demonstrated no inducible supraventricular or ventricular arrhythmia. With atrial burst pacing at 260 ms, an identical RBBB/LPF aberration was seen, confirming that the wide complex tachycardia seen during AT was SVT with aberrancy, and not dual tachycardia. The CTI remained blocked from the previous ablation.

At two-month follow-up in clinic, the patient had no further tachycardia or ICD shocks on interrogation.


We present a case of a focal triggered LA AT from 10:30 on the mitral annulus that degenerated into VF and resulted in multiple appropriate ICD shocks in a patient with HCM. Aside from pre-excited Wolff-Parkinson-White and catecholaminergic polymorphic VT, SVT- or AFib-induced VT/VF is reported only in studies examining ICD therapies, and the electrophysiologic mechanism has not been elucidated in human or animal studies.2,7,8 AFib has not been associated with increased risk of appropriate ICD shocks or sudden death events in outcome studies of HCM patients.9

However, a study of ICD interventions of ventricular arrhythmias in patients with HCM demonstrated that over 50% of the episodes of VT or VF occurred during moderate or physical activity.10 Sinus tachycardia or rapid AFib preceded 38% of all treated episodes, 44% of the VF episodes, and 75% of the ventricular flutter episodes.10 While the mechanism of sinus tachycardia, SVT, or rapid AFib degenerating to VF is not known, it may be related to abnormal adrenergic tone, increased outflow tract obstruction, long-short stimulation in the setting of rapid AFib or AT with Wenckebach conduction, changes in cardiac output related to decreased diastolic filling time, or transient myocardial ischemia due to supply-demand mismatch. The increased ventricular arrhythmia incidence seen in HCM is related both to the physiologic changes noted above and increased myocardial fibrosis seen in the disease.11

Given the septal LGE seen on the MRI, a septal VT was considered to be a likely etiology of the VF arrests prior to the EP study. However, once the sustained AT was induced and degenerated to VF, attention turned to mapping and ablation of the AT. It is important to be aware that SVT can induce VF, even in patients who have an increased incidence of both VT and VF, in order to eliminate the arrhythmia. Atrial and ventricular programmed extrastimulation after ablation, both on and off isoproterenol, demonstrated no inducible VT or VF; therefore, the mitral annular AT was considered to be the mechanism of the VF arrests.


We present a case of an HCM patient with recurrent ICD shocks and VF arrests that were induced by an AT, which was mapped and ablated at 10:30 on the mitral annulus with no further inducible or clinical ventricular arrhythmias. This case highlights the importance of considering SVT in the potential mechanisms of VF. 

Disclosure: The authors have no conflicts of interest to report regarding the content herein.   

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