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

BackgroundUpper septal fascicular ventricular tachycardia (VT) is a rare form of idiopathic left ventricular tachycardia arising from the proximal His-Purkinje system. Because near-synchronous ventricular activation can produce a relatively narrow QRS complex, this arrhythmia may closely mimic supraventricular tachycardia (SVT) with aberrant conduction.Case presentationA 25-year-old man without structural heart disease presented with recurrent palpitations for more than 4 years. ECG during tachycardia showed a regular narrow-complex tachycardia at approximately 200 beats/min with atypical right bundle-branch block-like morphology and marked right-axis deviation. Electrophysiological study initially raised suspicion for an AVNRT-like mechanism because programmed atrial stimulation demonstrated dual AV nodal physiology and intracardiac recordings showed an apparent near-simultaneous ventriculoatrial relationship. However, 6 mg intravenous adenosine did not terminate the tachycardia but unmasked atrioventricular dissociation, with the ventricular rate exceeding the atrial rate; together with subsequent Purkinje-system mapping, this supported a ventricular origin. Initial mapping identified an effective target in the distal left posterior fascicular region, where 30-W radiofrequency ablation terminated the tachycardia. The same night, incessant tachycardia recurred with a changed and narrower QRS morphology. Repeat mapping localized the final successful target to the upper septal region approximately 8 mm from the His bundle; 20-W radiofrequency ablation terminated the tachycardia without atrioventricular conduction injury. No symptomatic recurrence was reported during 12-month clinical follow-up.ConclusionA relatively narrow or progressively narrowing QRS complex does not exclude VT. In suspected SVT with atypical features, adenosine-unmasked atrioventricular dissociation should prompt reconsideration of a ventricular mechanism, while invasive electrophysiological assessment and repeat mapping may facilitate accurate diagnosis and safe ablation, particularly when the arrhythmogenic substrate is adjacent to the His bundle.