Abstract

Idiopathic ventricular tachycardia (VT) with normal heart is not uncommon in our daily practice. However, this VT sometimes cannot be easily differentiated from supraventricular tachycardia with bundle branch block (BBB) if the QRS interval is relatively narrow or the P-QRS relationship is consistent [1]. Here, we present a unique case with wide QRS tachycardia and two consistent P wave morphologies. A 38-year-old man complained of occasional palpitations and came to our hospital. Twelve-lead electrocardiography (ECG) during the palpitations revealed a wide QRS tachycardia with two different P wave morphologies. Transthoracic echocardiography revealed no structural heart disease. During the cardiac electrophysiology study, incremental pacing from the right ventricular apex induced a sustained tachycardia with right BBB pattern, which was identical to the clinically documented tachycardia. The idiopathic left VT was diagnosed in this case by atrioventricular dissociation and the short His–ventricular interval, which was revealed in the intracardiac His lead recordings (Fig. 1). The two different P-wave morphologies from the surface ECG recordings were comparable to the two different atrial activation sequences in the intracardiac recordings. The first type of atrial activation pattern was retrograde concentric ventriculoatrial (VA) conduction with the earliest atrial activation at the proximal coronary sinus, which created a negative polarity of P wave in lead II of ECG. The second type of atrial activation pattern was conducted from the right atrium to the coronary sinus, which was considered to be a normal sinus impulse and created a positive polarity of P wave in lead II of ECG (Fig. 1). Recordings of the surface and intracardiac electrocardiography during tachycardia. Atrioventricular dissociation and short His–ventricular interval were demonstrated in the intracardiac His recordings. a The first atrial activation pattern was retrograde concentric ventriculoatrial conduction with a negative polarity of P wave in lead II. b The other atrial activation pattern was antegrade from the high right atrium to the coronary sinus with a positive polarity of P wave in lead II. A = atrial potential; CS D = distal pairs of the coronary sinus electrogram; CS M = middle pairs of the coronary sinus electrogram; CS P = proximal pairs of the coronary sinus electrogram; H = His bundle potential; HIS = His bundle electrogram; HRA = high right atrium electrogram; RV = right ventricular apex electrogram; V = ventricular potential. The VT mapping and ablation was performed by 4-mm tip ablation catheter during VT attack. The site of catheter ablation was located at the distal septum of the left ventricle, where the characteristic double diastolic potentials were recorded, as in previous studies. The tachycardia was terminated after one pulse of ablation. No further tachycardia could be induced after ablation. Sustained monomorphic VT in patients with normal heart has been identified as being more prevalent in Asian populations [2]. However, >26% of idiopathic left VT coexists with another supraventricular tachycardia [3]. From a review of the related literature, most coexisting supraventricular tachycardia that is associated with idiopathic left VT is atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, atrial flutter, and nonsustained atrial flutter–fibrillation [4]. From surface ECG in our case, the initial tentative differential diagnosis of tachycardia might include: (1) VT with frequent atrial premature complex; (2) multifocal atrial tachycardia with aberrant conduction; and (3) VT with sinus P wave and retrograde VA conduction P wave. After analyzing the intracardiac electrogram, we found that normal sinus antegrade atrial activation and retrograde VA conduction activation created two different P-wave morphologies during the idiopathic left VT in this patient. In conclusion, we present a unique case of idiopathic left VT with two different P-wave morphologies, which were created by normal sinus antegrade atrial activation and retrograde VA conduction activation.

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