Rare Heart Rhythm Masqueraded as Supraventricular Tachycardia Until Adenosine Revealed the Truth

A 25-year-old man who had lived with recurrent palpitations for more than four years turned out to have one of cardiology’s great impersonators: a rare ventricular tachycardia arising from the upper septal region of the heart, so close to the conduction system that its electrical signature looked almost identical to a supraventricular tachycardia. The case, published in Frontiers in Cardiovascular Medicine, describes how clinicians untangled the diagnosis and ultimately cured the arrhythmia with two rounds of catheter ablation, the second delivered just 8 millimeters from the His bundle.

The patient had no structural heart disease. Routine laboratory tests were unremarkable, and transthoracic echocardiography showed preserved cardiac function with a left ventricular ejection fraction of 62 percent. His episodes had begun years earlier, occurring once or twice a year and lasting roughly 30 minutes, often accompanied by exertional fatigue or chest discomfort. Over the year before admission, the symptoms worsened and the episodes grew longer. An outside facility had previously suspected supraventricular tachycardia, but the exact rhythm diagnosis remained unclear.

When he was finally captured in rhythm on a 12-lead electrocardiogram, the tracing showed a regular narrow-complex tachycardia at approximately 200 beats per minute with a QRS duration of 116 milliseconds. Lead V1 displayed an rSR′ pattern resembling an atypical right bundle-branch block, the inferior leads showed an rS pattern, and the frontal axis was markedly rightward. In a young patient with a structurally normal heart, a narrow QRS complex usually points to supraventricular tachycardia. Yet the atypical bundle-branch block-like morphology and the extreme right-axis deviation kept other possibilities on the table, including atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, atrial tachycardia, and fascicular ventricular tachycardia.

The first electrophysiological study deepened rather than resolved the confusion. Programmed atrial stimulation produced an approximately 92-millisecond jump in AV nodal conduction along with echo beats, evidence of dual AV nodal physiology. During the tachycardia itself, which had a cycle length of 288 milliseconds, coronary sinus recordings showed a concentric atrial activation sequence with near-simultaneous ventriculoatrial activation. Together with a pseudo-S-wave appearance in lead II, these findings made atrioventricular nodal reentrant tachycardia a plausible working diagnosis, and the team proceeded with a slow-pathway ablation at 30 watts for 180 seconds.

The ablation failed. The tachycardia persisted, unchanged in cycle length, ventricular rate, or surface QRS morphology. That failure prompted a decisive diagnostic maneuver: 6 milligrams of intravenous adenosine, given to transiently suppress AV nodal conduction. The drug did exactly what it was designed to do to the AV node, but the tachycardia marched on, and in doing so it unmasked atrioventricular dissociation, with the ventricular rate clearly exceeding the atrial rate. An atrium beating independently and more slowly than the ventricles is a hallmark of a ventricular mechanism, and this single observation argued strongly against atrioventricular reentrant tachycardia and an atrial-driven rhythm, while making the initially suspected AV nodal reentrant mechanism far less likely.

Subsequent activation mapping identified the earliest Purkinje-related activation in the distal left posterior fascicular region, where a discrete Purkinje potential with a local P–V interval of approximately 34 milliseconds was recorded. Using an irrigated contact-force catheter, the team delivered radiofrequency energy at 30 watts. The tachycardia terminated after just 5 seconds, and three 30-second consolidation lesions followed. After 30 minutes of observation and repeated isoproterenol infusion, no ventricular premature beats or ventricular tachycardia could be induced, and the procedure appeared successful.

It was not. That same night, the tachycardia returned and became incessant, now at approximately 170 beats per minute with a different morphology and, remarkably, a narrower QRS complex, shrinking from 116 to 97 milliseconds. Biphasic 200-joule cardioversion terminated the rhythm for only several seconds before rapid recurrence. Intravenous propafenone, lidocaine, amiodarone, and diltiazem all failed to maintain sinus rhythm; verapamil was unavailable. With the patient symptomatic and hypotensive, the team performed an early repeat electrophysiological study the following day. Ventricular programmed stimulation induced the recurrent tachycardia, designated VT2, with a cycle length of 354 milliseconds. Available His-bundle recordings during VT2 showed an HV interval of just 15 milliseconds, with Purkinje and ventricular activation preceding retrograde His activation.

Repeat electroanatomical mapping localized the earliest Purkinje-related activation to the upper septal region adjacent to the proximal His-Purkinje system, where the local P–V interval was approximately 45 milliseconds. The effective site lay about 8 millimeters from the His recording location, favoring an upper septal fascicular origin rather than an isolated typical left posterior fascicular ventricular tachycardia. Because of the proximity to the His bundle, the team adopted a cautious low-power strategy, monitoring atrioventricular conduction continuously with plans to stop immediately if abnormal junctional rhythm, conduction prolongation, or block appeared. Radiofrequency energy at 20 watts with an irrigation flow of 8 milliliters per minute and a contact force of 5 grams terminated the tachycardia after 5 seconds, again followed by three consolidation lesions. No clinically evident atrioventricular conduction disturbance occurred during or after the procedure, and the post-ablation electrocardiogram showed sinus rhythm without significant conduction abnormality.

The authors caution that the relationship between the initial and recurrent tachycardias remains uncertain. Possible explanations include two distinct but anatomically related fascicular tachycardias, different exits from a common Purkinje-related reentrant circuit, or modification of a single reentrant pathway by the first ablation. Without comprehensive entrainment or resetting data, the precise mechanism cannot be definitively established. Regardless, the shift in QRS morphology and the change in the effective ablation site underscore the value of repeat activation mapping when a tachycardia recurs after an initially successful procedure.

The take-home message is straightforward: a relatively narrow QRS complex does not exclude ventricular tachycardia, particularly when the morphology or axis is atypical. Upper septal fascicular ventricular tachycardia, a rare subtype of idiopathic fascicular ventricular tachycardia, arises near the proximal His-Purkinje network, where rapid propagation through both bundle branches produces near-synchronous ventricular activation and a deceptively narrow QRS. Coincidental dual AV nodal physiology and near-simultaneous ventriculoatrial activation can further tilt the picture toward atrioventricular nodal reentrant tachycardia. When the mechanism is uncertain, persistence of tachycardia with an unchanged ventricular rate despite adenosine-unmasked atrioventricular dissociation should prompt reconsideration of a ventricular origin. The case carries its own limitations: it involves a single patient, incomplete documentation of drug dosing and timing, no systematic ambulatory rhythm monitoring, and incomplete electrophysiological recordings, which preclude definitive characterization of the circuit and full exclusion of asymptomatic recurrence. Still, at 12-month clinical follow-up, no symptomatic recurrence was reported, and the patient’s long ordeal with a rhythm that fooled even the experts had ended.

Subject of Research: A case report of upper septal fascicular ventricular tachycardia mimicking supraventricular tachycardia, diagnosed through adenosine-unmasked atrioventricular dissociation and treated with mapping-guided catheter ablation.

Article Title: Case Report: Upper septal fascicular ventricular tachycardia mimicking supraventricular tachycardia: diagnostic pitfalls and mapping-guided ablation

Article References: Fu, Y., Tang, J., Zhao, Z., Cai, Y., & Chen, Y. (2026). Case Report: Upper septal fascicular ventricular tachycardia mimicking supraventricular tachycardia: diagnostic pitfalls and mapping-guided ablation. Frontiers in Cardiovascular Medicine, 13, Article 1933819. https://doi.org/10.3389/fcvm.2026.1933819

Image Credits: AI Generated

DOI: 10.3389/fcvm.2026.1933819

Keywords: ventricular tachycardia, supraventricular tachycardia, fascicular VT, catheter ablation, adenosine, His-Purkinje system, electrophysiology, AVNRT, case report, atrioventricular dissociation, narrow QRS tachycardia, cardiology