Pacemaker Syndrome in a Patient with Heart Block after Accessory Pathway Ablation

Subbiah Rajauru, MD and Abraham G. Kocheril, MD, FACC, FACP, FHRS Christie Clinic, Provena Covenant Medical Center, and University of Illinois College of Medicine at Urbana-Champaign Champaign, Illinois
Subbiah Rajauru, MD and Abraham G. Kocheril, MD, FACC, FACP, FHRS Christie Clinic, Provena Covenant Medical Center, and University of Illinois College of Medicine at Urbana-Champaign Champaign, Illinois

Pacemakers are in common use nowadays for a variety of reasons. These devices have been very successful in the treatment of various bradyarrhythmias and have even proven lifesaving in patients with Stokes–Adams Syndrome. However, normal pacemaker function can produce some unusual responses in patients with accessory pathways. In this article we present a case illustrating one such interaction at our institution.

Case Presentation

A 53-year-old Caucasian male presented to the emergency department with symptoms of dizziness and palpitations. He also reported occasional near syncope. He had undergone catheter ablation for Wolff–Parkinson-White syndrome more than a decade ago. However, the exact details could not be obtained from the patient or the other health facility.

During evaluation, the patient was found to be in normal sinus rhythm with a pre-excited QRS complex. However, conduction over the accessory pathway would cease intermittently, resulting in complete heart block. This suggested that the only anterograde conduction from atrium to ventricle was over the accessory pathway, and that AV nodal function was absent (Figure 1). Since the details of the original ablation were not known, a dual chamber pacemaker was implanted as a precaution against complete heart block, as the anterograde conduction over the accessory pathway was not reliable.

He did well for over two years, and then presented to his primary physician’s office complaining of symptoms of palpitations. Workup was unremarkable. His symptoms got worse, so about three years after the original pacemaker implant, we elected to do an electrophysiology (EP) study to look for any inducible atrial or ventricular arrhythmias that could explain his symptoms.

EP study was done with catheters positioned in the His bundle position, coronary sinus, and RV apex. Initial evaluation showed the underlying rhythm was normal sinus rhythm with complete heart block at the level of the AV node. The RV was paced 100% of the time after an appropriate AV delay (Figure 2).

With each paced ventricular beat there was retrograde conduction over the accessory pathway, resulting in atrial depolarization. This phenomenon was also demonstrated by pacing directly from the RV catheter (Figures 3 and 4).

Using the EnSite mapping system (St. Jude Medical, Inc., St. Paul, MN), the accessory pathway was mapped to the antero-superior tricuspid annulus (12 o’ clock position on LAO view) (Figure 4), and was successfully ablated with resolution of retrograde conduction (Figure 5). The patient’s symptoms of palpitations and fatigue subsequently resolved.

Discussion

Manifest accessory pathways can typically conduct both anterograde and retrograde. In this patient, who had prior ablation for Wolff-Parkinson-White syndrome, we found complete loss of anterograde conduction but preserved retrograde conduction. AV node function was probably lost during the previous ablation of his septal accessory pathway; when anterograde accessory pathway conduction eventually failed, he required a permanent pacemaker. Persistent retrograde conduction caused atrial depolarization just after each ventricular beat, which created symptoms commonly associated with pacemaker syndrome, despite the initial appearance of A-V synchrony. Interestingly, the retrograde conduction was not detected in his pacemaker follow-ups, possibly due to the rapid accessory pathway conduction, causing the atrial depolarization to fall in the ventricular and post-ventricular atrial refractory periods; atrial depolarization was also occurring prior to each ventricular paced beat. This clinical issue required a formal EP study and catheter ablation for resolution.

Conclusion

This case illustrates an interaction between normal pacemaker function and accessory pathway conduction. Symptoms of palpitations and fatigue resulted from retrograde atrial depolarization with each ventricular paced beat, producing two atrial beats around each ventricular depolarization. EP study readily revealed the cause, and catheter ablation of the remainder of the accessory pathway relieved the patient’s symptoms.