A Wide QRS Complex Tachycardia with Variation of Ventriculoatrial Interval: What is the Mechanism?

TL;DR

This paper discusses the mechanism behind a type of heart rhythm disorder with a wide QRS complex and changing ventriculoatrial interval.

Contribution

The paper highlights how variation in a specific intracardiac interval can aid in diagnosing complex arrhythmias.

Findings

Variation in intracardiac intervals can change tachycardia cycle length.

Such changes can help distinguish between different types of arrhythmias.

Intracardiac interval analysis is a diagnostic tool for wide complex tachycardia.

Abstract

The differential diagnosis for wide complex tachycardia includes all causes of narrow complex tachycardia with bundle branch block, all causes of narrow complex tachycardia with antegrade pre-excitation, ventricular tachycardia, and antidromic and other pre-excited reciprocating tachycardias. The variation in a specific intracardiac interval that causes a subsequent change in the tachycardia cycle length or another intracardiac interval can be diagnostic in these arrhythmias.

Figures

Response to programmed atrial stimulation (A) and the initiation of the left bundle branch block tachycardia (B).

Oscillation in the cycle length and ventriculoatrial intervals. The V–A interval changes preceded and predicted the V–V intervals.

Termination response to a premature atrial beat delivered during atrioventricular nodal refractoriness.

Initiation of the narrow complex tachycardia by a programmed atrial stimulation.

Full text

Case presentation

A 28-year-old woman underwent an electrophysiology study (EPS) because of episodes of palpitations with documented narrow complex tachycardia (NCT) and wide QRS complex tachycardia (WCT) on a 24-h Holter electrocardiogram (ECG). Baseline ECG showed normal sinus rhythm without ventricular pre-excitation. During the EPS, the para-Hisian pacing demonstrated the nodal response. The programmed electrical stimulation from the right atrium (Figure 1) showed a left bundle branch block (LBBB)-shaped WCT. There was an interesting observation in the circuit during ongoing tachycardia (Figure 1B). What diagnostic information can be retrieved from the tracing?

Response to programmed atrial stimulation (A) and the initiation of the left bundle branch block tachycardia (B).

Discussion

Programmed atrial stimulation revealed an antegrade jump with a typical atrioventricular (AV) nodal echo beat with an LBBB-shaped QRS pattern (Figure 1A) and then induction of the LBBB-shaped WCT (Figure 1B). The differential diagnosis for WCT includes all causes of NCT with bundle branch block, all causes of NCT with antegrade pre-excitation, ventricular tachycardia (VT), and antidromic and other pre-excited reciprocating tachycardias.^1–8^ Careful examination of the His bundle activation sequence can lead to the correct diagnosis at first glance in an otherwise highly complex diagnostic challenge.^7^ The lack of a regular H–V interval preceding each QRS complex suggests that activation does not use the orthodromic infranodal conduction system, making aberrant conduction less likely.^9^

The LBBB tachycardia showed a 1:1 A–V relation and negative H–V interval, resulting in only two possibilities for the mechanism: pre-excited tachycardia (with active or passive bystander activation) or VT. The activation of the His bundle is retrograde during tachycardia, but still before ventricular activation. This is only possible in the presence of an extranodal pathway inserted in the fascicle just below the His bundle, most frequently the right bundle. An A–V interval of ≥150 ms during pre-excited tachycardia is also a fast and reliable method for detecting a decremental conducting accessory pathway.^10^ If retrograde activation of the His bundle has been determined and changes in the V–H or H–A intervals predict changes in the atrial cycle length and reset the tachycardia (Figure 2), then antidromic tachycardia, either with an atrioventricular bypass tract or an atriofascicular tract, is present. Changes in the V–H or H–A intervals that cause changes in the A–A interval but do not reset the tachycardia suggest VT as the mechanism of the wide complex rhythm. Therefore, the most striking finding in the present case was that there were oscillations in the cycle length and V–A intervals (Figure 2), which predicted subsequent changes in A–A intervals, implicating the retrograde conduction system in the tachycardia circuit.^4^

Oscillation in the cycle length and ventriculoatrial intervals. The V–A interval changes preceded and predicted the V–V intervals.

The rate changes in antidromic tachycardia in patients with atriofascicular fibers can be based on a shift in ventriculoatrial conduction from one bundle branch to the other by retrograde right bundle branch block.^10^ The ventriculoatrial wobble in Figure 2 was unlikely to be due to variation in retrograde right bundle versus left bundle conduction, as the V–H interval was unchanged. There was a long–short sequence due to a fast pathway block on the first pre-excited beat, with a shortening of the anterograde conduction on the second beat. This likely causes retrograde decrement in the fast pathway (identical atrial activation sequence). Furthermore, the late-coupled premature atrial contraction resulted in tachycardia termination (Figure 3), which suggests the participation of an anterogradely conducting accessory pathway, thus confirming the diagnosis of antidromic reciprocating tachycardia and ruling out pre-excited supraventricular tachycardia, nodofascicular tract, and VT.^7,11,12^ Then, a classical slow–fast atrioventricular nodal re-entrant tachycardia (AVNRT) was induced by programmed atrial stimulation (Figure 4). We made the final diagnosis of dual tachycardia by typical AVNRT with atriofascicular tachycardia.^13^ After ablations at the base of Koch’s triangle for the AV nodal slow pathway and the atriofascicular accessory pathway potential at the lateral tricuspid annulus sequentially, the tachycardias were rendered non-inducible.

Termination response to a premature atrial beat delivered during atrioventricular nodal refractoriness.

Initiation of the narrow complex tachycardia by a programmed atrial stimulation.