• 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • One study reported the role of the Purkinje system


    One study reported the role of the Purkinje system with respect to the relationship between the septum and HCM-related VT. Santangeli et al. reported that patients with HCM also often have His-Purkinje conduction-related septal abnormalities, and bundle branch block often develops as part of the natural history of the disease [4]. Kim et al. reported that reentry within the Purkinje network adjacent to the papillary muscles played an important role in VF stat 3 inhibitor and maintenance in a model using an isolated swine right ventricle [6]. Kuboki et al. and our group have reported cases wherein patients who had HCM showed torsades de pointes or monomorphic VT, the origin of which was suggested to be Purkinje fibers in the left bundle branch [2,7]. The present case report highlights the Purkinje network as the arrhythmogenic substrate even in HCM-related PVCs/NSVT; similar to other Purkinje-related PVCs/VTs, this condition can be cured by using endocardial ablation targeting the presystolic Purkinje potentials.
    Conflict of interest
    Disclosures and finding sources
    Introduction Dual-chamber DDD pacing with triggered atrial pacing (DDTA) is a special mode in which the atria are paced regardless of the atrial electrical potentials. In this mode, a sensed atrial potential triggers the atrial and ventricular pacing after the programmed atrioventricular (AV) delay, while a sensed ventricular potential inhibits the ventricular pacing. Recently, the use of DDTA for biatrial pacing to treat interatrial conduction disturbances and prevent atrial fibrillation was reported [1]. Here we report a case of interatrial and AV conduction block from the right atrium that developed after removal of a left atrial myxoma and was treated efficiently using the DDTA mode.
    Case report A 61-year-old man underwent surgical removal of a myxoma in the left atrium in January 2004. The myxoma (size, 65×55mm) was resected along with part of the atrial septum, which was closed with a pericardial patch (5×1cm). He also underwent a maze surgery in the left atrium using concurrent cryoablation. After that, he was followed up by a cardiovascular surgeon from our hospital. The patient experienced palpitation on exertion in March 2011. Holter electrocardiography results showed an alternating AV block and atrial tachycardia (Fig. 1), and he was referred to and then admitted to our department. On physical examination results were as follows: height, 166cm; weight, 56kg; blood pressure, 90/64mmHg; and pulse rate, irregular at 76/min. Chest radiograph showed a cardiothoracic ratio of 46% and no pleural effusion or congestion. The surface leads V and V1 during the electrophysiological study revealed a complete AV block (Fig. 2). Intracardiac electrocardiograms taken at the same time showed that the right atrium was activated by the sinus node, and that the coronary sinus (CS) was activated by ventriculoatrial conduction of the AV junctional rhythm (Fig. 2). The maximum right ventricular pacing rate with 1:1 ventriculoatrial conduction was 60/min. Electroanatomical mapping of the right atrium demonstrated a wide area of low or no potential in the atrial septum, no potential area in the cavotricuspid isthmus, and disrupted conduction from the right atrium to the left atrium and both the ventricles. Atrial tachycardia was easily induced by high-frequency stimulation of the CS, while left atrial tachycardia at a cycle length of 420ms was conducted to the ventricles in the ratio of 1:1. However, the right atrium was activated by the sinus node. Electroanatomical mapping revealed that the atrial tachycardia was circling the mitral valve. The tachycardia was terminated by linear ablation between the mitral annulus and the left inferior pulmonary vein. The patient later underwent permanent pacemaker implantation to treat the complete AV block. Because of conduction dissociation between the right and left atria, we used the biatrial pacing method. A left ventricular lead (Attain; Medtronic Inc., Minneapolis, MN, USA) typically used for cardiac resynchronization therapy was introduced through the CS and placed into the left atrial branch. This lead was used as a cathode. The stat 3 inhibitor right atrial lead (Capsure; Medtronic Inc.) positioned on the free wall was used as an anode to establish biatrial pacing between the right and left atria. The ventricular lead (J-Line Screwvine, Lifeline Inc., Tokyo, Japan) was implanted into the right ventricular septum. The right and left atrial leads were connected to the atrial port of the pacemaker (REPLY DR; Sorin Inc., Miran, Italy) using a bifurcated connector. In this configuration (Fig. 3), the right atrial electrical potential was tracked between the 2 atrial electrodes and the DDTA mode was used for synchronizing each chamber. The intra-atrial amplitude was 4.1mV, and noise sensing or far field R wave sensing was not detected using the atrial sensitivity setting at 1.0mV. The AV delay was set at 250ms to avoid pacing the right ventricle as much as possible. The mode switching algorithm that can change from a triggered to a non-triggered mode at the atrial arrhythmia onset was also activated.