not-yet-known not-yet-known not-yet-known unknown A 57-year-old woman with frequent palpitations was referred for radiofrequency ablation. The baseline 12-lead electrocardiogram and echocardiography were normal. The baseline atrio-His (AH) and His-ventricular (HV) intervals were 70 and 35 ms, respectively. Dual atrioventricular (AV) nodal physiology was not observed during programmed atrial stimulation. Ventriculoatrial conduction showed a decremental and concentric pattern, with the earliest atrial activation recorded in the His bundle region. There was no evidence of a jump-up phenomenon during programmed ventricular stimulation. Supraventricular tachycardia (SVT) with variable AH and His-atrial (HA) intervals was induced by extra atrial stimulation without any jump-up in the AH interval. The earliest atrial activation during SVT was recorded at the coronary sinus (CS) 7,8 region, corresponding to the CS ostium, which differed from the atrial activation sequence during ventricular pacing. The atrial-atrial (AA) intervals demonstrated variability exceeding 50 ms without any alteration in the atrial activation sequence (Figure 1A). Ventricular entrainment pacing was performed during SVT (Figure 1B). Transient 2:1 AV conduction was observed during SVT (Figure 1C). Based on these findings, what is the mechanism of the variability in the AA, AH, and HA intervals during tachycardia?

A 57-year-old woman with frequent palpitations was referred for radiofrequency ablation. The baseline 12-lead electrocardiogram and echocardiography were normal. The baseline atrio-His (AH) and His-ventricular (HV) intervals were 70 and 35 ms, respectively. Dual atrioventricular (AV) nodal physiology was not observed during programmed atrial stimulation. Ventriculoatrial conduction showed a decremental and concentric pattern, with the earliest atrial activation recorded in the His bundle region. There was no evidence of a jump-up phenomenon during programmed ventricular stimulation. Supraventricular tachycardia (SVT) with variable AH and His-atrial (HA) intervals was induced by extra atrial stimulation without any jump-up in the AH interval. The earliest atrial activation during SVT was recorded at the coronary sinus (CS) 7,8 region, corresponding to the CS ostium, which differed from the atrial activation sequence during ventricular pacing. The atrial-atrial (AA) intervals demonstrated variability exceeding 50 ms without any alteration in the atrial activation sequence (Figure 1A). Ventricular entrainment pacing was performed during SVT (Figure 1B). Transient 2:1 AV conduction was observed during SVT (Figure 1C). Based on these findings, what is the underlying mechanism of the tachycardia?

A 70-year-old man presented with regular wide QRS complex tachycardia (WCT) at a rate of 185 beats/min, characterized by left bundle branch block morphology. WCT termination was achieved through electrical cardioversion. A subsequent 12-lead electrocardiogram revealed sinus rhythm with complete right bundle branch block (CRBBB) morphology. Echocardiography showed normal left ventricular function without structural heart disease. An electrophysiological study was then conducted, followed by catheter ablation. At baseline, the atrio-His and His-ventricular intervals were normal. Fractionated ventricular potentials were observed in the para-Hisian region during sinus rhythm. Neither dual atrioventricular (AV) nodal physiology nor ventriculoatrial conduction was observed during programmed pacing. Clinical WCT was induced by ventricular extra-stimulation with concurrent AV dissociation and no visual His bundle potential, confirming the diagnosis of ventricular tachycardia (VT). Figure 1 illustrates 12-lead electrocardiograms recorded during overdrive pacing from the right ventricular apex (RVA) and right atrial septum during VT. The electroanatomical activation map revealed a distinctive focal breakout pattern with fractionated potentials originating from the para-Hisian region. In the noncoronary cusp (NCC), corresponding to the opposite side of the para-Hisian region, prolonged and fractionated ventricular potentials preceding QRS onset by 56 ms were recorded (Figure 2A). Figure 2B shows the intracardiac electrogram recorded during ventricular overdrive pacing from the NCC during VT. Based on these observations, what is the mechanisms underlying the tachycardia?

Atrial fibrillation (AF) is mainly initiated by arrhythmogenic triggers originating from the pulmonary veins, and ganglion plexus often plays a crucial role in the induction and maintenance of AF. In this report, we describe a case of successful cryoballoon ablation of focal atrial tachycardia originating from the left inferior pulmonary, in which vagal response was observed, and discuss its tachycardia mechanism.

A 72-year-old female with frequent palpitation was referred for radiofrequency ablation. The baseline 12-lead electrocardiogram and echocardiography results were normal. At baseline, the atrio-His (AH) and His-ventricular (HV) intervals were 90 and 41 ms, respectively. Dual atrioventricular (AV) nodal physiology or ventriculoatrial (VA) conduction was not observed during programmed atrial and ventricular stimulation. After isoproterenol infusion, VA conduction became decremental and concentric, with the earliest atrial activation seen at the His bundle (HB) region during ventricular pacing. A supraventricular tachycardia with a long RP interval (SVT) was induced by atrial extra-stimulation, without any jump-up in the AH interval. During the SVT, the AH and HV intervals were 180 and 180 ms, respectively, and the earliest atrial activation was recorded in the HB region (Figure 1A). During the SVT, transient 2:1AV conduction was observed (Figure 1B). Ventricular overdrive pacing at a pacing cycle length (CL) of 360 ms was performed during the SVT with a CL of 390ms (Figures 2A and B). Based on these observations, what is the mechanism of this tachycardia?

A 77-year-old woman with palpitations was referred for a second radiofrequency ablation for persistent atrial tachycardia (AT). She previously underwent pulmonary vein (PV) isolation for paroxysmal atrial fibrillation, linear ablation between the 3’o clock position of the mitral annulus (MA) and left PV from the endocardium, and ablation inside the coronary sinus (CS) for perimitral atrial tachycardia (PMAT) in the first procedure. A baseline 12-lead electrocardiogram in the second procedure showed stable AT with a cycle length (CL) of 250 ms. No PV reconnection was observed. The CS catheter was placed from 3:30 to 5:00 on the MA, and a proximal-to-distal pattern of CS activation during AT was observed. Activation mapping in the left atrial (LA) endocardium using a three-dimensional mapping system (CARTO3, Biosense Webster, Diamond Bar, CA, USA) revealed a sequence of counterclockwise rotations of the MA. Figures 1A and 1B show the intracardiac electrograms during high-output (20 V) and low-output (5 V) atrial entrainment pacing at a pacing CL of 240ms from CS 3,4, which corresponds to the 4’o clock position of the MA. Dose residual conduction occur across the mitral isthmus (MI) endocardium, epicardium, or both? What is the electrophysiological mechanism during high- and low-output entrainment pacing?