Atypical AVNRT Successfully Treated by Changing Pacemaker Parameters

In this article, the authors provide a case on recurrent supraventricular tachycardias (SVTs) that were successfully treated using a novel concept of device tracking pace prevention of atypical AVNRT.

Understanding the pathophysiology of SVT and working noninvasively around the differential diagnosis could be helpful in treating this arrhythmia. Catheter ablation of SVT is highly effective with a low incidence of adverse events. However, pharmacological management is favored as first-line treatment for SVTs, especially in elderly patients with mild symptoms.

Pacemakers are widely used for patients with sick sinus syndrome; they allow safe titration of rate blocking agents. However, certain patients may still be resistant to escalating doses of rate blocking agents with breakthrough of SVTs.

We report a case of a 96-year-old female with brady-tachy syndrome who recently underwent implantation of a dual chamber pacemaker. The patient was resistant to escalating doses of beta blockers, with frequent episodes of breakthrough tachycardia. After careful analysis of mode of initiation and termination as well as the response to adenosine, we concluded that her arrhythmia was most likely AV nodal dependent and likely to be atypical atrioventricular nodal reentrant tachycardia (AVNRT). We hypothesized that if we were able to track the retrograde P wave or ectopic atrial beats responsible for initiating the tachycardia and track it with a short enough AV delay close to ventricular-atrial (VA) block cycle length (measured noninvasively through the device), we might be able to stop the initiation of the tachycardia. This approach proved effective in conservatively eliminating her tachycardia episodes without the need for catheter ablation or adding other antiarrhythmic medications. 

Case Report

The patient is a 96-year-old female with a past medical history of sick sinus syndrome, recent insertion of a permanent dual chamber pacemaker, Bell’s palsy, mild aortic stenosis, hypertension, and left occipital CVA. She presented to the hospital from her home when the nurse reported an increased pulse. She was found to be tachycardic in the 130s. Her tachycardia was minimally symptomatic. Her medications included amlodipine, aspirin and lisinopril. Her echocardiogram showed biatrial enlargement, mild left ventricular hypertrophy and mild aortic stenosis.

Her EKG on admission (Figure 1A) showed narrow complex (somewhat short R-P) tachycardia consistent with SVT with superior axis (-ve II, III, AVF) of the P wave suggestive of a low origin focus close to AVN.

The patient was given 6 mg adenosine (Figures 2A and 2B), which successfully terminated her tachycardia, only to recur a few seconds later. Her last beat of tachycardia termination with adenosine showed P waves with no QRS complexes, making atrial tachycardia an unlikely diagnosis; the fact that she responded to adenosine also favored an AV nodal dependent mechanism. Her EKG (Figure 1B) showed a premature ventricular contraction (PVC) that was conducted retrograde with an early P wave without affecting R-R interval, suggestive that the reentrant circuit could be contained within a functionally protected region around the AV node.¹ This also favored AVNRT, as AVRT will advance the P wave but more likely advance the R-R cycle. 

We then performed noninvasive program stimulation (NIPS) of the device to assess the VA properties and establish VA block cycle length (Figures 4A-C). The patient indeed exhibited 1:1 retrograde conduction at CL 480 ms; then she started to have retrograde Wenckebach at CL 480 ms, and VA block at CL 420 ms. 

Initial device setup upon interrogation was minimal ventricular pacing mode (MVP) with nominal AV delay (Figures 5A and 5B). We initially changed the parameter to long AV delay (320 ms) and short PVARP in order to track the PACs initiating the tachycardia, and were able to track the PACs or retrograde A wave (intermittently due to long AV delay), but tachycardia continued due to the long sensed AV delay (Figure 6A and 6B). We then thought that if we were able to track retrograde P wave or ectopic atrial beats responsible for initiating the tachycardia and track it with a short enough AV delay close to VA block cycle length, we might prevent the tachycardia from starting. Device parameters were changed to short sensed AV delay and long paced AV delay to allow for tracking of retrograde A wave or PACs and minimize ventricular pacing while the patient was in sinus rhythm, as this may be beneficial.^2-4 These changes allowed the retrograde P wave to be consistently tracked with V pacing for a few beats followed VA block, preventing tachycardia initiation (three different episodes illustrated) (Figures 7A and 7B). The heart trend monitor confirmed no further episodes of tachycardia after final changes (Figures 8A and 8B).

Conclusion

This was a very interesting case that illustrated how a device changing algorithm was helpful in preventing the initiation of atypical AVNRT. The ability to track a retrograde P wave during SVT and tracking them with pacemaker at a short AV delay close enough to VA block cycle length may be a novel idea to prevent certain forms of SVTs. In order to be successful, the P wave has to be late enough (> shortest PVARP programmable, mostly 160 ms in some devices). Also, the VA block cycle length has to be long enough to prevent a faster rate of pacemaker-mediated tachycardia (PMT).

PVARP is an atrial refractory period that occurs after a paced or sensed ventricular event. It prevents the atrial channel from sensing the ventricular pacing pulse, the far-field QRS and retrograde P waves. By programming the device to artificially start a PMT and at the same time activating the PMT intervention so that PMT will not be sustained was successful in preventing initiation of atypical AVNRT.⁵

Setting the upper rate limit to a lower number (e.g., <150 bpm) may also be helpful in preventing faster PMT should the programmed sensed AV delay be too short.

This is the first report that uses complex device parameters to treat recurrent atypical AVNRT. This may be a novel concept to conservatively and noninvasively treat certain forms of SVTs through understanding the pathophysiology and the mechanisms of different arrhythmias as well as integrating this knowledge with device timing to prevent and treat the disease. 

References

1. Otomo K, Okamura H, Noda T, et al. Unique electrophysiologic characteristics of atrioventricular nodal reentrant tachycardia with different ventriculoatrial block patterns: effects of slow pathway ablation and insights into the location of the reentrant circuit. Heart Rhythm. 2006;3(5):544-554.
2. The DAVID Trial Investigators. Dual-chamber pacing or ventricular backup pacing in patients with an implantable defibrillator: the Dual Chamber and VVI Implantable Defibrillator (DAVID) Trial. JAMA. 2002;288:3115-3123.
3. Arya A, Haghjoo M, Emkanjoo Z, Sadr-Ameli MA. Coronary sinus mapping to differentiate left versus right ventricular outflow tract tachycardias. Europace. 2005;7:428-432.
4. Gillis AM, Pürerfellner H, Israel CW, et al. Reducing unnecessary right ventricular pacing with the managed ventricular pacing mode in patients with sinus node disease and AV block. Pacing Clin Electrophysiol. 2006;29:697-705.
5. van Gelder LM, el Gamal MI, Baker R, Sanders RS. Tachycardia-termination algorithm: a valuable feature for interruption of pacemaker-mediated tachycardia. Pacing Clin Electrophysiol. 1984; 7:283-287.