In addition we evaluated the
In addition, we evaluated the left atrium–left ventricle contraction sequence caused by the interatrial conduction delay. When we performed AV sequential pacing using the nominal AV delay setting, left atrial contractions were significantly delayed and were almost simultaneous with the left ventricular contractions under ApVp (Fig. 3b). This setting might cause heart failure in the near future; thus, to avoid using this setting, we had to choose between the long AV delay setting, the safe RR mode, or the AAI mode. An echocardiogram with mitral valve inflow waves confirmed an appropriate left atrium–left ventricle contraction sequence when using any of these 3 settings (Fig. 3b).
Conflict of interest
Acknowledgment This study was supported by the Japan Society for the Promotion of Science (JSPS) through its Funding Program for World-Leading Innovative R&D on Science and Technology (FIRST Program).
Introduction Advanced atrioventricular (AV) block has been reported to occur, albeit rarely, during cavotricuspid isthmus (CTI) ablation of atrial flutter [1,2]. The main mechanism contributing to AV block is direct injury of the AV node via the delivery of radiofrequency (RF) energy, during which the ablation catheter is usually located at a septal site of the CTI near the AV node rather than at the lateral CTI. Here, we describe a unique case, in which a spiky potential appeared at the distal electrode of the ablation catheter immediately after initiating RF delivery at the lateral CTI, and unexpected AV block eventually occurred.
Case report A 69-year-old man with symptomatic paroxysmal atrial fibrillation for 1 year was referred to Nihon University Itabashi Hospital for ablation of AF. He had hypertension, and his baseline electrocardiogram (ECG) revealed left ventricular hypertrophic changes without any conduction block. Coronary sinus (CS) angiography revealed no anatomical abnormalities in the CS. In baseline electrophysiological studies, the Wenckebach AV block order Betaine length was 350ms, and there was no ventriculoatrial conduction during right ventricular pacing. CARTO-guided extended ipsilateral pulmonary vein isolation was performed, and thereafter, typical atrial flutter was induced by rapid atrial pacing from the CS ostium. CTI ablation was performed during CS pacing at a cycle length of 600ms with a deflectable 8-mm tip EPT catheter (EP Technologies Inc., San Jose, CA, USA); each RF application was performed at 60°C and 50W, for 60s. The ablation catheter was positioned at 7:00 on the tricuspid annulus in the left anterior oblique view (Fig. 1A). One second after the first RF application, a spiky potential was noted at the distal electrode 1-2 of the ablation catheter and the Halo catheter, with a time interval of 80–90ms from the local atrial potential. During the ablation, the spiky potential was reproducibly observed, consistently occurring 80–90ms after the local atrial potential. The AH interval was gradually prolonged, and a 2:1 AV block occurred 34s after the ablation (Fig. 1B). Although 1:1 AV conduction was resumed 3s after the termination of RF delivery, it took 30s for the AH interval to recover to baseline. The Wenckebach AV block cycle length was the same as the baseline value. No further RF application was delivered because an additional RF delivery at the same site caused a similar phenomenon.
Discussion In previous studies, advanced AV block during RF application for type 1 atrial flutter raised immediate concerns that the catheter may have been positioned at the septum near the AV node, rather than in the CTI [1,2]. In our case, since the ablation catheter was positioned at a lateral isthmus site according to fluoroscopy, the potential risk of AV node injury by RF delivery at that site was expected to be low. Besides catheter placement, there are 3 other potential mechanisms for AV block during CTI ablation. The first potential mechanism is coronary ischemia. RF delivery at the CTI has been reported to increase the risk of coronary artery damage because the right coronary artery is located in the AV groove just below the CTI [3,4]. However, the possibility of coronary ischemia may be low because neither chest pain nor ST-T changes on the surface ECG were observed during ablation, and there was no evidence of stenoses on coronary angiography. The second potential mechanism is through vagal tone. Sinus bradycardia or AV node block have been reported to occur with excessive vagal tone due to pain during ablation . Recently, a study has also demonstrated that catheter ablation of the left atrial ganglionated plexi can mediate AV node block or sinus bradycardia . In fact, ganglia have been shown to be located in the inferior vena cava-left atrial fat pad, which is not far from the CTI. Therefore, CTI ablation may potentially affect these ganglia, leading to AV block. The absence of AV block during ablation after intravenous atropine supports the mechanism of vagal tone; however, atropine was not administered in the present case. The final potential mechanism involves an anatomical variant of the slow pathway that would place these structures more inferolaterally than normally expected. Transient AH interval prolongation despite RF termination suggested direct thermal injury to the AV node. Even if such an anatomic variant existed, our patient should not have experienced advanced AV block because a shorter AH interval during CS ostial pacing implied that the AV conduction was dependent on the fast pathway. Therefore, RF energy delivered by the slow pathway may have affected the AV node via a specific pathway bridging the slow pathway to the fast pathway and His bundle region, i.e., a lower common pathway. Interestingly, in this case, slow pathway-like spiky potentials were reproducibly observed during ablation from the distal electrodes of the ablation catheter that was placed at the lateral isthmus. Therefore, these spiky potentials may reflect slow pathway potentials as anatomical variants of the rightward extension of the AV node. However, it is also possible that these spiky potentials simply reflect the local atrial electrograms with an intra-atrial conduction delay because the spiky potentials were recorded from the distal electrodes of both the Halo and ablation catheters, and the direction of activation of the spiky potentials was counterclockwise around the tricuspid annulus.