Electrophysiology Lab Diagnostic Dilemma: Tunnel Vision

© 2024 HMP Global. All Rights Reserved.

Any views and opinions expressed are those of the author(s) and/or participants and do not necessarily reflect the views, policy, or position of EP Lab Digest or HMP Global, their employees, and affiliates. 

EP LAB DIGEST. 2024;24(1):18-21.

Case Presentation

A 64-year-old male with a past medical history significant for obstructive sleep apnea, symptomatic paroxysmal atrial fibrillation, and atrial flutter (AFL) (Figure 1) underwent pulmonary vein isolation (PVI) and cavotricuspid isthmus (CTI) ablation. However, during follow-up with a 14-day Holter monitor, an abrupt onset arrhythmia was noted at cycle length (CL) range of 480-590 milliseconds (Figure 2). The arrhythmia initiated with spontaneous premature atrial contraction (PAC) and premature ventricular contractions. No discernible p-wave was seen on the single-lead Holter. Most notable, after the run of nonsustained ventricular tachycardia (VT) was a continuation of arrhythmia with no clear atrial activity and a pause (Figure 2). In evaluating the arrhythmia before management in the laboratory, it is important to consider all arrhythmia differential diagnoses.

The differential diagnosis encompasses a range of possibilities, including AFL, atrial tachycardia, and other re-entrant supraventricular tachycardias (SVTs) such as atrioventricular nodal re-entrant tachycardia (AVNRT) or atrioventricular re-entrant tachycardia (AVRT). It is worth noting that the first electrophysiology (EP) study did not reveal evidence of dual AV nodal physiology; on ventricular pacing, atrial activation showed central and decremental ventriculoatrial (VA) conduction, thereby reducing the likelihood of AVRT and typical AVNRT.

Considering the patient’s history of prior ablation and the recurrence of arrhythmia at variable CL, AFL and atrial tachycardia emerge as statistically higher possibilities within the differential diagnosis. However, these findings do not exclude other arrhythmias such as AVRT or AVNRT.

A repeat EP study was performed using a decapolar coronary sinus catheter and ablation catheter, which were placed in the left atrium via transseptal puncture, and high-density mapping catheter in the left atrium. Confirmation of bidirectional conduction block along the CTI was established, and the PVs remained isolated (Figure 3). Given the patient’s documented history, an attempt was made to induce arrhythmia. However, tachycardia initiation with burst atrial pacing proved ineffective in eliciting any arrhythmic response. Subsequently, upon the administration of isoproterenol infusion, a wide complex tachycardia was initiated at a CL of 320 msec (Figure 4).

In the EP laboratory, the evaluation of arrhythmias hinges on the careful analysis of spontaneous occurrences, including initiation, termination, and any inherent variations in arrhythmia CL. Additionally, assessments involve scrutinizing the activation sequence and VA time, as well as the response to specific pacing maneuvers. The following characteristics of the arrhythmia were noted:

1) With septal atrial activation sequence, it should be noted that no right atrial catheter was present at the time (Figure 5). Differential diagnosis for arrhythmia with central activation sequence includes the following if CS is the earliest: atypical AVNRT, AVRT with septal accessory pathway (AP), or atrial tachycardia originating from the parahisian region, triangle of Koch, mitral annulus, right superior pulmonary vein, or the interatrial septum.

2) Spontaneous initiation with minimal alterations in AV time (Figure 5A and 5B).

3) Antecedent changes in atrial CL precede ventricular CL variations (Figure 6).

4) Different VA time post-PAC compared to tachycardia VA time (Figure 6A and 6B).

5) Septal VA time during tachycardia >80 msec.

6) PACs do not result in tachycardia reset (Figure 6).

7) Arrhythmia termination with gradual speed up in the atrium and terminating in the ventricle (Figure 7).

Considering these findings, the possibility of atrial tachycardia is high on the differential, but AVRT using a septal AP or atypical AVNRT was not ruled out. At this point, further confirmation response to ventricular overdrive pacing (VOD) would be helpful; one option was the addition of other catheters for a full EP study including a His catheter and right ventricular catheter. We chose VOD by placing the ablation catheter in the left ventricular base to use as the ventricular pacing catheter (Figure 8). There are several important observations to consider:

1) Atrial advancement did not occur until the 5th paced beat (pacing being done at the base of the LV close to the septum), making presence of a septal AP very unlikely.

2) The response post VOD was VAAV, but the last advanced A was the second A (Figure 9). This essentially ruled out atrial tachycardia as a diagnosis.

3) Spontaneous arrhythmia termination in the atrium further confirmed that the arrhythmia was not atrial tachycardia (Figure 10).

At this point, by process of elimination, the likely arrhythmia was narrowed down to an atypical AVNRT, specifically using a slow-slow circuit. We proceeded with ablation of the slow pathway, successfully terminating the arrhythmia with no further inducibility on isoproterenol (Figure 11).

Discussion

This case underscores the significance of various diagnostic maneuvers and astute observations in the field of EP that can ultimately lead to the correct diagnosis. It serves as a reminder of the necessity to maintain an open-minded approach to all potential scenarios, and emphasizes the importance of comprehensive EP studies. The timeless wisdom of Sherlock Holmes can be applied as well to arrhythmia diagnosis: “When you’ve eliminated the impossible, whatever remains, however improbable, must be the truth.” 

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest, and report no conflicts of interest regarding the content herein.