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

DOI: 10.19102/icrm.2025.16021

ENGIN ALGUL, MD,¹ IDRIZ MEROVCI, MD,² MERYEM KARA, MD,³ ELIF HANDE OZCAN CETIN, MD,³ DUYGU KOCYIGIT BURUNKAYA, MD,³ HAMZA SUNMAN, MD,¹ AHMET KORKMAZ, MD,³ FIRAT OZCAN, MD,³ SERKAN CAY, MD,³ OZCAN OZEKE, MD,³ OZCAN OZDEMIR, MD,¹ DURSUN ARAS, MD,⁴ and SERKAN TOPALOGLU, MD³

¹Department of Cardiology, University of Health Sciences, Ankara Etlik City Hospital, Ankara, Turkey

²Department of Cardiology, University Clinical Center of Kosovo, Prishtina, Kosovo

³Department of Cardiology, University of Health Sciences, Ankara Bilkent City Hospital, Ankara, Turkey

⁴Department of Cardiology, İstanbul Medipol University, İstanbul, Turkey

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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.

KEYWORDS. Atriofascicular pathway, atrioventricular nodal reentrant tachycardia, AVNRT, Mahaim, wide complex tachycardia.

The authors report no conflicts of interest for the published content. No funding information was provided.
Manuscript received March 12, 2024. Final version accepted August 24, 2024.
Address correspondence to: Ozcan Ozeke, MD, Ankara Şehir Hastanesi, Kardiyoloji Klinigi, Bilkent Street, No: 1, Çankaya 06800, Turkey. Email: ozcanozeke@gmail.com.

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?

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

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.

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