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Case PresentationA 46-year-old woman was referred to our institution for evaluation of recurrent narrow QRS complex tachycardia. She complained of frequent episode.s of palpitations that she could easily terminate with Valsalva maneuvers. The tachycardia was terminated by intravenous injection of adenosine when she presented to the emergency department. She continued to have frequent relapses while undergoing sotalol or verapamil treatment.The resting ECG demonstrated normal sinus rhythm, absence of preexcitation. and nonspecific ST .segment abnormalities. During the electrophysioiogic (EP) study, single spontaneous ventricular premature beats repeatedly induced narrow QRS complex tachycardia ( Fig. 1). What is the tachycardia mechanism?Commentary Figure 1, left side, shows the resting ECG in sinus rhythm and the initiation of a narrow complex tachycardia with a cycle length of 310 msec.Several supraventricular tachycardias (SVTs) may be responsible for tbis arrhythmia: (1) orthodromic AV reciprocating tachycardia., (2) AV nodal reentrant tachycardia, and (3) atria! tachycardia.The initiation of an SVT by a single spontaneous ventricular premature beat has been considered to be suggestive of a tachycardia using an accessory pathway. The initiation of SVT by a late coupled ventricular premature depolarization is highly suggestive of SVT using a bypass tract and, if occurs at tbe time of His-bundle refractoriness, is diagnostic ot SVT using u bypass tract.' In that case, ventricular stimulation during sinus rhythm or at long paced cycle lengths usually results in block in the His-Purkinje system and rapid conduction over the bypass tract.Ventricular stimulation can initiate SVT using a concealed bypass tract more readily tban SVT due to AV nodal reentry. Exclusive retrograde conduction over the bypass tract is necessary to initiate SVT, whereas in tbe normal AV system, one of tbree events can occur: (1) block or concealment in the AV node. (2) block in the HisPurkinje system, or (3) block in the bypass tract with retrograde conduction over the normal conduction system to the His bundle, producing a bundle branch reentrant complex that subsequently initiates SVT.Retrograde His-Purkinje system delay during ventricular premature stimulation prevents significant delay or block in the AV nodal region; hence, the induction of common AV nodal reentry seldom is possible with this method.Spontaneous ventricular premature contractions almost never initiate typical AV nodal reentry, and programmed ventricular extrastimuli initiate typical AV nodal reentry in approximately 15% of the patients.2 When typical AV