After permanent pacemaker implantation the lead electrocardi
After permanent pacemaker implantation, the 12-lead electrocardiogram revealed that the pacing spike appeared at the same time as the P wave and narrow QRS complexes with AV conduction (Fig. 4). This finding demonstrated effective enforcement of the left atrial pacing. The patient had no postoperative complications and was discharged. During the subsequent 12 months, no atrial tachyarrhythmias, including atrial fibrillation, were detected, and the percentage of right ventricular pacing was <1%.
Discussion Atrial tachyarrhythmias after surgical intervention or catheter ablation in patients with structural dna ligase disease are not uncommon because of reentry around a combination of anatomic and surgically created obstacles. However, there are few reports of interatrial electrical dissociation that originates during these procedures [2,3]. In this case, the causes of conduction dissociation between the right and left atria and the left atrial tachycardia may have been attributed to atrial muscle damage. Advanced low electrical activity in the interatrial septum suggested that resection of the atrial tissue and the patch closure performed for the removal of the huge myxoma and cryoablation for the left atrial maze caused the damage. In addition, the appearance of a complete AV block linked to the right atrial activation also implied that the damage affected the anterior regions of the AV node. With regard to the treatment of the complete AV block in this case, if the patient was treated with the standard procedure in which leads are implanted into the right atrium and the right ventricle to perform the DDD mode pacing, right ventricular pacing would have been performed despite the remaining conduction between the left atrium and the ventricles. Because right ventricular pacing creates electrical left ventricular dyssynchrony that results in long-term unfavorable hemodynamic and structural changes, we thought that the use of this procedure was not suitable for this patient. We also considered placing leads in the right and left atria, setting a minimum AV delay in the DDD mode, and pacing the left atrium instead of the right ventricle; however, ventricular pacing would be required when the AV conduction deteriorated. Accordingly, we adopted the DDTA mode because it was possible to sense the right atrial potential and pace the left atrium while simultaneously pacing the ventricles. This approach restored the native AV conduction based on the intrinsic pacemaker activity in the right atrium. The conduction delay in the atrium is known to induce reentry and result in atrial arrhythmias, including atrial fibrillation; therefore, the true intention of the DDTA mode was to prevent atrial fibrillation caused by interatrial conduction disturbances using biatrial pacing . On the other hand, the use of inappropriate trigger pacing has the disadvantage of inducing atrial arrhythmia. However, atrial tachyarrhythmia, including atrial fibrillation, was not documented after pacemaker implantation in our case. We believe that this was due to the following reasons: first, the maze surgery and the mitral isthmus ablation effectively treated the atrial arrhythmias. Second, the mode-switching algorithm that inhibits trigger pacing worked efficiently at the onset of the atrial arrhythmias. Third, the effect of right ventricular pacing on the appearance of atrial arrhythmias decreased because of poor ventriculoatrial conductivity. This case report demonstrates for the first time that the use of a DDTA mode could be a new approach for treating patients with interatrial electrical dissociation and complete conduction blocks from the right atrium to the ventricles.
Conflict of interest
Case report A 49-year-old woman was admitted to our hospital because of palpitations. She had no family history of cardiac arrhythmias or sudden cardiac death. A cardioverter-defibrillator had been implanted 7 years earlier because of nonsustained ventricular tachycardia associated with ARVC/D. This case fulfills the 2 major criteria of ARVC/D : (a) global or regional dysfunction and structural alterations detected by magnetic resonance imaging (MRI) (regional RV akinesia, RV contraction, or RV ejection fraction ≤40%), and (b) arrhythmias (nonsustained ventricular tachycardia of left bundle-branch morphology with a superior axis). The patient\'s chest radiograph showed an increased cardiothoracic ratio of 59% without pulmonary congestion. A 12-lead electrocardiogram (ECG) showed tiny P waves preceded by narrow QRS complexes at a cycle length of 300ms with variable atrioventricular conduction (Fig. 1A). The signal-averaged ECG showed positive late potentials. Transthoracic echocardiography showed a dilated RA and RV and a left ventricular end-diastolic diameter of 52mm with an LV ejection fraction (EF) of 35%. MRI angiography showed an enlarged RV cavity with an RVEF of 6% (Fig. 2). A cardiac biopsy of the RV endocardium showed fibrofatty replacement of the myocardium. During the electrophysiological study, narrow QRS tachycardia was noted. The tachycardia was sustained, although transient termination was observed by pacing from the high RA. A standard mapping and ablation catheter with a 4-mm tip (Navistar; Biosense Webster, Diamond Bar, CA, USA) was introduced into the RA from the right femoral vein. Activation mapping, guided by a CARTO XP system (Biosense Webster), showed that the earliest atrial endocardial activation site of the narrow QRS tachycardia (36ms before the onset of the P wave) was located at the orifice of the RA appendage (RAA) (Fig. 3A) with a cycle length (CL) of 365ms (AT1). The patient was therefore diagnosed with atrial tachycardia (AT) originating from the RAA. Radiofrequency ablation (RFA) (55°C, 25W, 30s per cycle) was delivered, and after the fourth application to the same site, the AT–CL changed to 252ms (AT2). Activation mapping of AT2 showed that the earliest endocardial activation (42ms before the P wave) was localized to the tricuspid annulus (Fig. 3B). RFA at that site transiently terminated the AT. Atrial burst pacing induced a different AT (AT3; CL=430ms), for which activation mapping showed that the earliest endocardial activation (46ms before the P wave) was at the base of the RAA (Fig. 3C). RFA at that site changed the AT–CL to 360ms (AT4). The earliest endocardial activation of AT4 (54ms before the P wave) was located adjacent to AT1, and RFA at that site transiently terminated AT4. The P-wave morphology did not differ among each AT (Fig. 3A–C). In the voltage map during sinus rhythm, a low voltage area was widely observed throughout the RA, except in the RA appendage (Fig. 4). Thereafter, AT was not induced further by atrial extrastimulation or burst atrial pacing. The patient has been free of any atrial or ventricular tachyarrhythmias for 8 months.