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Vagus nerve stimulator (VNS) malfunction can cause parasympathetic overstimulation, which may lead to significant symptomatic sinus bradycardia as well as atrioventricular nodal block and ventricular asystole.
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VNS can potentially cause noise artifacts leading to abnormal sensing by the wearable cardiac defibrillator (WCD), which may result in inappropriate shocks.
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The effects of high-energy pulses such as external defibrillations on VNS are unknown.
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In case of significant bradyarrhythmias caused by VNS malfunction, application of a magnet over the stimulator to deactivate it should be considered.
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The long-term safety of concurrent use of WCD and VNS is not clear, and frequent follow-ups and device interrogations should be performed, if needed.
Introduction
The use of a vagus nerve stimulator (VNS) is an established therapeutic intervention indicated for the management of medical refractory epilepsy.
It usually is a well-tolerated implant procedure, and device management is not challenging; however, parasympathetic overstimulation and significant cardiac suppression that result in episodes of severe sinus bradycardia, atrioventricular block (AVB), and ventricular asystole (VA) have been reported.
When active, vagal stimulation by VNS is painless. The wearable cardiac defibrillator (WCD) is a bridge external device used for treatment of life-threatening ventricular arrhythmias in a select population of patients who may qualify for an implantable cardioverter-defibrillator (ICD).
To the best of our knowledge, there are no reported cases of a coexisting VNS and WCD that resulted in a malfunction of either device. We report a case of an inappropriate WCD firing in a patient with a VNS that resulted in VNS malfunction, which led to symptomatic bradyarrhythmias and VA.
Case report
The patient was a 53-year-old man with a medical history of drug-refractory epilepsy (levetiracetam 2500 mg twice per day, zonisamide 300 mg twice per day, and lacosamide 200 mg twice per day), which eventually was treated with a SenTiva M1000 VNS (LivaNova Inc., Houston, TX) about 4 years ago (Figure 1). He underwent percutaneous coronary intervention and stenting of the left anterior descending artery for anterior wall myocardial infarction and was discharged with a Zoll® LifeVest® WCD (ZOLL Medical Corporation, Chelmsford, MA) in addition to guideline-directed medical therapy for coronary artery disease and ischemic cardiomyopathy (ejection fraction 25%–30%) with New York Heart Association functional class II symptoms.
Figure 1Anteroposterior chest radiograph showing a left-sided vagus nerve stimulator (black arrowhead) and the wearable cardiac defibrillator pads (white arrows) in close proximity.
Two months later, the patient presented with WCD firing, without preceding chest pain, shortness of breath, palpitations, dizziness, or any syncopal episode(s). The patient was unable to turn off WCD alarms. WCD interrogation revealed artifacts and inappropriate defibrillation due to noise artifact oversensing (Figure 2). No bradyarrhythmias before the inappropriate therapy were noted on WCD interrogation. Interrogation of the VNS revealed an output current of 1.5 mA and signal frequency of 20 Hz.
Figure 2Rhythm strip from wearable cardiac defibrillator interrogation showing normal sinus rhythm (NSR) with significant noise artifacts (A) and inappropriate defibrillation during NSR (B).
On presentation, the patient was hemodynamically stable, with normal sinus rhythm; however, frequent episodes of vagally mediated severe sinus bradycardia, second-degree AVB, complete heart block, and VA that coincided with VNS activation (Figure 3) were witnessed. The patient was symptomatic during the VA episodes, with altered mentation and unresponsiveness. During the AVB episodes, the patient felt pain/discomfort on the left side of the neck (VNS implant site). These episodes persisted even after VNS output was decreased to 1.25 mA. Subsequently, a magnet applied over the VNS for deactivation successfully terminated the bradyarrhythmias including VA, while the patient was monitored in the intensive care unit. No recurrence of bradyarrhythmias including VA was noted, and no breakthrough seizures occurred after deactivation of the VNS for the remainder of the patient’s hospitalization. After discussion of the case with the neurology and cardiology departments, the VNS was turned off completely. The patient was discharged home with the WCD in stable condition, with arrangement to undergo an outpatient ICD implantation evaluation with simultaneous VNS testing to ensure no interference between devices. The patient agreed with the management plan.
Figure 3Rhythm strip showing an episode of severe sinus bradycardia and a transient complete heart block with ventricular asystole that coincided with vagus nerve stimulator activation.
Severe bradyarrhythmias are rare but serious complications that can be experienced with VNS therapy. Severe sinus bradycardia, sinus pauses, second-degree AVB, and complete heart block have been reported.
attempted to assess this theoretical risk by applying a series of high-energy pulses on 3 VNS generators used for autonomic regulatory therapy in heart failure patients. They suggested that VNS may be used safely after exposure to external defibrillation, as all 3 generators passed factory electric testing and their parameters remained unchanged. However, this study was conducted in vitro on 3 generators only. Wittstock et al
reported the case of a patient with VNS who received an external defibrillation during a cardiac arrest resuscitation without malfunction of VNS detected after successful resuscitation. However, the patient died within 24 hours, so no long-term VNS function could be assessed.
Our patient had VNS for many years without any cardiac symptoms, documented bradyarrhythmias, or pain during VNS activation until he received the inappropriate shock from WCD. This likely makes our patient the first documented case of a high-grade AVB and VA due to malfunction of a previous normally functioning VNS after receiving an inappropriate WCD defibrillation.
The impact of the electric pulses delivered by VNS on WCD detection and analysis of different arrhythmias also is unclear. Possible interference between VNS and ICD was previously suggested by a different group of investigators who reported the case of a child with congenital long QT syndrome who had an ICD with an epicardial lead and VNS implanted for a history of ventricular fibrillation and medication-refractory epilepsy, respectively.
Coexistence of vagus nerve stimulation and epicardial implantable cardioverter-defibrillator system, possible interference: a case report and systematic review of the literature.
They reported noise detection on the high-voltage coil channel during VNS activation; however, it was below the sensing threshold, and the patient never received any inappropriate shocks. In our patient, the inappropriate WCD firing was mainly caused by oversensing noise artifacts during periods of normal sinus rhythm (Figure 2). Although VNS interrogation revealed reasonable output current parameters, there was clear clinical evidence of VNS malfunction, including intermittent episodes of neck pain, classic vagally mediated severe sinus bradycardia, and AVB that coincided with VNS activation and never occurred before the inappropriate shock. Also, applying a magnet over the VNS was able to deactivate it and alleviate all the patient’s symptoms. The patient remained free of neck pain and without any bradyarrhythmias after the VNS was turned off completely. This case highlights a potential interference between VNS and WCD that may result in malfunction of one or both devices, leading to serious outcomes.
Conclusion
The safety of WCD in patients with an implantable neuromodulator such as VNS is not clear. We report the case of a patient with VNS who had an inappropriate WCD firing that potentially caused VNS malfunction and high-grade AVB 2 months after wearing the WCD. Additional clinical data are needed to investigate this potential interaction with regard to patient safety.
References
Sirven J.I.
Sperling M.
Naritoku D.
et al.
Vagus nerve stimulation therapy for epilepsy in older adults.
Coexistence of vagus nerve stimulation and epicardial implantable cardioverter-defibrillator system, possible interference: a case report and systematic review of the literature.
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