Atrial Tachycardia and Bundle Branch Re-Entry Ventricular Tachycardia With Similar QRS Complex Morphology

Abstract

Background

Wide-QRS-complex tachycardia with QRS complex morphology identical to sinus rhythm has been described in bundle branch re-entry ventricular tachycardia (BBR-VT). However, the coexistence of supraventricular and ventricular tachycardias with identical electrocardiographic (ECG) morphology has not been well described.

Case Summary

A 56-year-old woman exhibited 2 sustained tachycardias with nearly identical right bundle branch block–type QRS complex morphology. One was atrial tachycardia (AT), and the other was malignant reverse-type BBR-VT, confirmed by invasive electrophysiology. Radiofrequency catheter ablation targeting the crista terminalis and coronary sinus eliminated AT, and radiofrequency ablation at the right bundle branch rendered BBR-VT noninducible. Despite similar ECG appearance, mechanisms, prognosis, and management differed significantly.

Discussion

AT and BBR-VT may share common features in ECG QRS complex indistinguishable from sinus rhythm in patients with advanced His-Purkinje conduction disease.

Take-Home Messages

AT and malignant BBR-VT may coexist and produce nearly identical surface ECGs. Surface ECG QRS complex morphology alone may be misleading, and electrophysiologic evaluation is mandatory when wide-QRS-complex tachycardia occurs in patients with septal conduction disease.

Visual Summary

History of Presentation

A 56-year-old woman presented with intermittent palpitations and dizziness. In the emergency department, a wide-QRS-complex tachycardia with preceding ectopic P waves was documented (Figure 1A). She had previously been hospitalized at an outside hospital because of sustained wide-QRS-complex ventricular tachycardia on May 20, 2022 (Figure 1B). Echocardiography showed dyssynchronous motion of the left ventricular (LV) wall without definite regional wall motion abnormality and mild to moderate LV dysfunction (LV ejection fraction of 45%). The cardiac magnetic resonance imaging showed subtle midwall late gadolinium enhancement in the mid-to-basal LV septal wall.

Take-Home Messages

• •Atrial tachycardia and malignant bundle branch re-entry ventricular tachycardia may coexist and produce nearly identical surface ECGs.
• •Surface ECG QRS complex morphology alone may be dangerously misleading and an electrophysiologic evaluation is mandatory when wide-QRS-complex tachycardia occurs in patients with septal conduction disease.

Figure 1.

⁠Baseline Electrocardiogram During Nonsustained and Sustained Tachycardia

(A) 12-lead electrocardiogram obtained in the emergency department shows sinus rhythm with right bundle branch block morphology and initiation of wide-QRS-complex tachycardia. The tachycardia is initiated by an atrial premature beat (asterisk), and the right bundle branch block QRS complex morphology of the tachycardia is identical to that of sinus rhythm after initial, transient aggravation of intraventricular conduction delay in the first 5 beats; and (B) 12-lead electrocardiogram obtained at a referring hospital shows wide-QRS-complex tachycardia with QRS morphology nearly indistinguishable from atrial tachycardia in panel (A). Despite a similar electrocardiogram appearance, beat-by-beat alternation in T-wave morphology (aVL) suggests 2:1 ventriculoatrial conduction block (arrows), which is not compatible with atrial tachycardia.

Differential Diagnosis

Tachycardia 1A was initiated by a preceding P wave, and the first 5 wide QRS complexes of right bundle branch block (RBBB) morphology rapidly changed to QRS complex identical to that of sinus rhythm, strongly suggesting atrial tachycardia (AT) as the mechanism of the tachycardia 1. She also had a history of hospitalization at a different hospital due to wide-QRS-complex tachycardia with similar QRS complex morphology (tachycardia 1B). However, a beat-by-beat alternation in T-wave morphology (aVL) indicates 2:1 retrograde ventriculoatrial conduction block and possible ventricular tachycardia. As the QRS complex of tachycardia 1B is almost identical to the QRS complex of aberrantly conducted AT (tachycardia 1A), the possibility of other mechanisms, including nodoventricular tachycardia, fascicular VT, interfascicular VT, or bundle branch re-entry (BBR) tachycardia, should be considered in the differential diagnosis.

Investigations and Management

The patient was brought to the electrophysiology laboratory in the fasting and alert state. Under 1.0% lidocaine local anesthesia, the right femoral vein and artery were cannulated percutaneously. A 7-F duodecapolar catheter was placed in the coronary sinus (CS) and the high right atrium (RA). A 5-F multipolar catheter was placed in His-RV. A 7-F DECANAV catheter (Carto, Biosense Webster) was used for mapping in the RA and LV septum. An 8.0-F SL1 sheath was introduced through the right femoral vein to the RA. A 7.5-F Navistar SmartTouch SF irrigation (Biosense-Webster) (D/F curve bidirectional) catheter with a 3.5-mm tip was used for mapping and ablation.

Baseline rhythm was sinus (Figure 2A). Voltage mapping of the RA showed a large scar in the posterior wall of the sinus venosus near the inferior vena cava. Baseline His-ventricular (HV) interval was prolonged at 83 ms. Programmed electrical stimulation induced 2 types of supraventricular tachycardia (Figure 2B) and 1 ventricular tachycardia (Figure 2C). Mapping of the first supraventricular tachycardia revealed a macrore-entry around the mid-to-lower crista terminalis (Figure 2B). The other supraventricular tachycardia was mapped at the ostium of the CS with centrifugal propagation.

Figure 2.

Electrocardiogram QRS Complex of Sinus Rhythm, Atrial Tachycardia, and Ventricular Tachycardia During Electrophysiologic Study

(A) Electrocardiogram obtained during electrophysiologic study shows a sinus rhythm with right bundle branch block QRS complex; (B) programmed electrical stimulation induced 2 types of supraventricular tachycardia, and 1 ventricular tachycardia. Mapping of the supraventricular tachycardia revealed a macrore-entry around the mid-to-lower crista terminalis, and focal atrial tachycardia originating from the coronary sinus; and (C) atrial or ventricular overdrive pacing also induced a wide-QRS-complex tachycardia with similar QRS complex morphology but ventriculoatrial dissociation. The mechanism was bundle branch re-entry ventricular tachycardia. The QRS complexes of the sinus rhythm, atrial tachycardia, and ventricular tachycardia were almost identical.

Radiofrequency (RF) catheter ablation at the lower crista terminalis linearly connecting to the inferior vena cava and focal RF application at the CS ostium eliminated the macroreentrant and focal AT. After these RF lesions, no AT was inducible by programmed electrical stimulation (Figures 3A and 3B).

Figure 3.

Mapping of the Supraventricular Tachycardia

(A) During electrophysiologic study, voltage mapping of the right atrium showed a large scar in the posterior wall of the right atrium (sinus venosus) near the inferior vena cava; activation mapping revealed a clockwise macrore-entry located at the mid-to-low crista terminalis, where radiofrequency lesion through the lower crista terminalis rendered the tachycardia noninducible. (B) After these linear lesions, another supraventricular tachycardia was induced, and the earliest activation was mapped at the ostium of the coronary sinus, which was also eliminated by focal ablation at the tachycardia focus.

However, atrial overdrive pacing induced another RBBB-type, wide-QRS-complex tachycardia with ventriculoatrial dissociation. The morphology of the QRS complex was almost identical to that of the supraventricular tachycardia. Atrial induction of the tachycardia, sharp initial downstroke of the RS complex in V6, 1:1 coupling of the His and ventricular electrograms, and similar (almost identical) QRS complex morphology to AT suggested a bundle branch re-entry ventricular tachycardia (BBR-VT) as the mechanism of tachycardia. Right-sided HV during tachycardia was 145 ms, and left bundle to QRS complex was 45 ms. When overdrive pacing was performed from the DECANAV catheter placed in the LV septal region, entrainment with concealed fusion with a postpacing interval identical to the tachycardia cycle length (320 ms) was demonstrated (Figure 4). Under the diagnosis of reverse type BBR-VT as the mechanism of tachycardia, RF catheter ablation targeting the RBB was performed, and the tachycardia became noninducible. The post-RF HV interval was 82 ms, but surface electrocardiogram (ECG) changed to complete RBBB morphology (QRS complex duration 165 ms compared with 131 ms pre-RF). The patient has remained free of symptoms over the past 3.5 years. However, considering the long HV interval, newly created RBBB, and underlying structural heart disease, she requires careful follow-up for a pacemaker or implantable cardioverter-defibrillator.

Figure 4.

Intracardiac Electrogram and Entrainment Mapping of Ventricular Tachycardia

Simultaneous surface electrocardiogram and intracardiac electrograms demonstrating 1:1 His-ventricular coupling and prolonged HV interval (145 ms, red asterisk, ABLd) during tachycardia. Ablation catheter was placed at the His bundle recording area, and a DECA was positioned at the left ventricular septum with proximal (DECA 9.10) pole at the high and distal (DECA 1,2 or 3,4) pole at the midseptum. Activation of the left bundle branch from high to midseptal direction (blue asterisk and arrow) preceding ventricular activation suggested a reverse-type bundle branch re-entry. Overdrive pacing from the left septal region (DECA 3,4) at a pacing cycle length of 290 ms yielded a postpacing interval of 326 ms, which was identical to that of tachycardia cycle length (326 ms). ABLd = distal ablation electrode; DECA = decapolar catheter.

Discussion

Traditionally, QRS complex morphology identical to sinus rhythm has been considered strongly suggestive of supraventricular tachycardia with aberrant conduction. However, classical electrophysiologic studies have demonstrated that BBR-VT may present with a surface QRS complex indistinguishable from sinus rhythm in patients with advanced His-Purkinje conduction disease.¹

Despite this established concept, contemporary clinicians are rarely confronted with such a deceptive diagnostic scenario in which 2 distinct tachycardias—one supraventricular and one ventricular—share nearly identical surface ECG morphology within the same patient. Such coexistence represents a diagnostic pitfall because the prognostic and therapeutic implications of these arrhythmias differ fundamentally.

We report a patient who exhibited both AT and malignant reverse-type BBR-VT that were virtually indistinguishable on surface ECG. This case highlights a critical modern ECG pitfall that extends beyond classical diagnostic paradigms and underscores the limitations of morphology-based algorithms.

The most striking feature of this case is that 2 mechanistically distinct tachycardias, AT and BBR-VT, produced nearly identical surface ECG morphologies. Classical studies have established that BBR-VT may exhibit QRS complex morphology identical to sinus rhythm in the presence of septal conduction delay and unidirectional bundle branch block. However, these observations were confined to comparisons between sinus rhythm and ventricular arrhythmias. Our case demonstrates a more clinically challenging phenomenon: a benign supraventricular tachycardia may mimic malignant BBR-VT within the same patient. Under such circumstances, reliance on morphology-based criteria alone may be misleading.

Limitations of Surface ECG Algorithms

Standard ECG algorithms for wide QRS complex tachycardia primarily rely on morphologic criteria and atrioventricular relationships.^2,3 In our patient, conventional criteria failed to distinguish the 2 tachycardias because both exhibited similar RBBB-type morphology, comparable axis, and overlapping cycle length ranges. Although atrioventricular dissociation eventually revealed the ventricular origin of the second tachycardia, this distinction is frequently subtle and easily overlooked during acute clinical encounters. This case underscores that surface ECG morphology alone cannot reliably differentiate supraventricular from ventricular tachycardia in patients with advanced septal conduction disease. In the electrophysiology laboratory, measurement of the HV interval during tachycardia is of great importance for differential diagnosis. BBR-VT is characterized by a longer HV interval compared with that during sinus rhythm. In contrast, HV intervals during fascicular or interfascicular VT are shorter during tachycardia than during sinus rhythm, whereas tachycardia using concealed nodoventricular pathways shows identical HV intervals to sinus rhythm.

Clinical Implications

The coexistence of midseptal scar, prolonged baseline HV interval, and intraventricular conduction delay created the electrophysiologic substrate for macrore-entry within the His-Purkinje system. These same abnormalities permitted AT to conduct with fixed aberrancy, resulting in a surface ECG appearance that closely mirrored that of BBR-VT. Failure to recognize BBR-VT carries potentially catastrophic consequences, including inappropriate pharmacologic therapy and delayed definitive ablation. Conversely, misclassification of AT as ventricular tachycardia may lead to unnecessary implantable cardioverter-defibrillator implantation or inappropriate shocks. Therefore, clinicians must maintain a high index of suspicion when wide-QRS-complex tachycardia occurs in patients with septal conduction disease, even when surface ECG morphology appears benign or unchanged from prior tracings.

Conclusions

AT and BBR-VT may coexist and produce nearly identical surface ECGs. Surface ECG QRS complex morphology alone may be misleading, and an electrophysiologic evaluation is mandatory when wide-QRS-complex tachycardia occurs in patients with septal conduction disease.

Visual Summary.

Electrocardiogram Mimic of Bundle Branch Re-Entry Ventricular Tachycardia

Atrial tachycardia and reverse-type bundle branch re-entry ventricular tachycardia share nearly identical surface electrocardiographic morphology despite completely different mechanisms, prognoses, and therapeutic implications.

Funding Support and Author Disclosures

The authors have reported that they have no relationships relevant to the contents of this paper to disclose.