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Background: Incessant focal atrial tachycardia (FAT), if untreated, can lead to ventricular dysfunction and heart failure (tachycardia-induced cardiomyopathy). Drug therapy of FAT is often difficult and ineffective. The efficacy of ivabradine has not been systematically evaluated in the treatment of FAT. Methods: The study group consisted of patients with incessant FAT (lasting >24 hours) and structurally normal hearts. Patients with ventricular dysfunction as a consequence of FAT were not excluded. All antiarrhythmic drugs were discontinued at least 5 half-lives before the initiation of ivabradine. Oral ivabradine (adults, 10 mg twice 12 hours apart; pediatric patients: 0.28 mg/kg in 2 divided doses) was initiated in the intensive care unit under continuous electrocardiographic monitoring. A positive response was defined as the termination of tachycardia with the restoration of sinus rhythm or suppression of the tachycardia to <100 beats per minute without termination within 12 hours of initiating ivabradine. Results: Twenty-eight patients (mean age, 34.6±21.5 years; women, 60.7%) were included in the study. The most common symptom was palpitation (85.7%) followed by shortness of breath (25%). The mean atrial rate during tachycardia was 170±21 beats per minute, and the mean left ventricular ejection fraction was 54.7±14.3%. Overall, 18 (64.3%) patients responded within 6 hours of the first dose of ivabradine. Thirteen of 18 ivabradine responders subsequently underwent successful catheter ablation. FAT originating in the atrial appendages was a predictor of ivabradine response compared with those arising from other atrial sites ( P =0.046). Conclusions: Ivabradine-sensitive atrial tachycardia constitutes 64% of incessant FAT in patients without structural heart disease. Incessant FAT originating in the atrial appendages is more likely to respond to ivabradine than that arising from other atrial sites. Our findings implicate the funny current in the pathogenesis of FAT.

Complete atrioventricular (AV) block in association with Takotsubo syndrome (TS) has been well recognized, but the cause and effect relationship has not been elucidated. We describe a 78-year-old female who presented with complete AV block but one week later developed new-onset, diffuse T-wave inversions, QT prolongation, and acceleration of junctional escape rate. Left ventriculogram revealed features typical of TS. One year after permanent pacemaker implantation, complete AV block persisted despite the reversal of wall motion defects implying that conduction abnormality was the trigger of TS rather than its consequence.

Aims Vasovagal syncope (VVS) is a common cardiovascular dysautonomic disorder that significantly impacts health and quality of life (QoL). Yoga has been shown to have a positive influence on cardiovascular autonomics. This study assessed the effectiveness of yoga therapy on the recurrence of VVS and QoL. Methods and results We randomized subjects with recurrent reflex VVS (&gt;3 episodes in the past 1 year) and positive head-up tilt test to guideline-directed therapy (Group 1) or yoga therapy (Group 2). Patients in Group 1 were advised guideline-directed treatment and Group 2 was taught yoga by a certified instructor. The primary endpoint was VVS recurrences and QoL. Between June 2015 and February 2017, 97 highly symptomatic VVS patients were randomized (Group 1: 47 and Group 2: 50). The mean age was 33.1 ± 16.6 years, male:female of 40:57, symptom duration of 17.1 ± 20.7 months, with a mean of 6.4 ± 6.1 syncope episodes. Over a follow-up of 14.3 ± 2.1 months Group 2 had significantly lower syncope burden compared with Group 1 at 3 (0.8 ± 0.9 vs. 1.8 ± 1.4, P &lt; 0.001), 6 (1.0 ± 1.2 vs. 3.4 ± 3.0, P &lt; 0.001), and at 12 months (1.1 ± 0.8 vs. 3.8 ± 3.2, P &lt; 0.001). The Syncope functional score questionnaire was significantly lower in Group 2 compared with Group 1 at 3 (31.4 ± 7.2 vs. 64.1 ± 11.5, P &lt; 0.001), 6 (26.4 ± 6.3 vs. 61.4 ± 10.7, P &lt; 0.001), and 12 months (22.2 ± 4.7 vs. 68.3 ± 11.4, P &lt; 0.001). Conclusion For patients with recurrent VVS, guided yoga therapy is superior to conventional therapy in reducing symptom burden and improving QoL.

AV node reentry, catheter ablation, retrograde conduction, Wenkebach blockA 45-year-old woman was referred for radiofrequency catheter ablation of narrow QRS tachycardia that was terminated with intravenous adenosine. Twelve-lead electrocardiography (ECG) was normal during sinus rhythm. She was taking calcium channel blockers and that was stopped 5 half-lives prior to the procedure. The electrophysiological study showed a normal atrio-Hisian (AH) interval of 104 milliseconds and His-ventricular (HV) interval of 42 milliseconds during sinus rhythm. Retrograde conduction was central and decremental. Anterograde study demonstrated dual atrioventricular (AV) nodal physiology. Atrial pacing protocols easily and reproducibly induced narrow QRS tachycardia. What is the mechanism? CommentaryThe tachycardia represents a slightly irregular supraventricular tachycardia without the requirement for the atrium, ruling out atrial tachycardia and atrioventricular reentry. This leaves only junctional tachycardia (JT), AV nodal reentry, and the much less commonly observed nodoventricular reentry. JT is unlikely by the method of induction and the slight irregularity. The third and seventh cycles of the tachycardia showed prolongation of RR interval as shown in Figures 1 and 2. The intracardiac recordings (Fig. 2) showed 3:2 ventriculoatrial (VA) response for the first 3 beats followed by 4:3 VA response and 3:2 VA response for the last 3 beats. A retrograde VA Wenkebach pattern is noted as evidenced by the progressive prolongation of the VA interval till it stops conducting to atrium. The atrial activation J Cardiovasc Electrophysiol, Vol. 00, pp. 1-2, xxxx 2016. Figure 2. The AH and the His-His (HH) intervals are essentially constant except for the cycle following the retrograde block, during which they are significantly prolonged. Retrograde conduction to atrium resumes after the prolonged AH and HH intervals and it is followed by retrograde HA Wenkebach.The tachycardia represents slow-slow type of AV nodal reentrant tachycardia with retrograde HA Wenkebach and abrupt prolongation of the anterograde AV nodal conduction time after the HA block, as evidenced by the increase in the HH interval, with subsequent resumption of retrograde HA conduction. Prolongation of the anterograde conduction time allowed restoration of retrograde conduction of the subsequent beat, suggesting a dependency and relationship of retrograde conduction on the anterograde AV nodal conduction time by an undefined mechanism. The underlying morphological substrate behind this phenomenon involves 2 anatomical or functional AV nodal or intranodal circuits in the anterograde limb with distinct conduction properties, which is manifested after the retrograde block and a slow conducting AV nodal circuit as the retrograde limb.The patient has undergone a successful slow pathway ablation and neither dual AV node physiology nor tachycardia could be demonstrated after that.