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  • br Discussion In previous studies advanced AV block

    2019-04-28


    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 [5]. Recently, a study has also demonstrated that catheter ablation of the left atrial ganglionated plexi can mediate AV node block or sinus bradycardia [5]. 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 purchase apexbio calculator 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.
    Conflict of interest
    Case presentation A 64-year-old female presented to the emergency room with persistent dizziness that began early that morning. She had a 30-year history of palpitations and known electrocardiogram (ECG) abnormalities. Her pulse was irregular at 130–270min−1 and blood pressure was 90/40mmHg. There were no other abnormalities on physical examination. A chest X-ray was normal and without cardiomegaly. Echocardiography revealed normal left ventricular contraction without structural abnormalities. Blood chemistry evaluation, including electrolytes and cardiac enzymes, was within normal limits. Twelve-lead ECG showed irregular wide QRS tachycardia of various configurations (Fig. 1).
    Commentary The patient\'s ECG shows wide QRS tachycardia with a rate from 150 to 300beats/min. The RR intervals are irregularly irregular and no P wave preceding QRS was confirmed. The QRS complex has beat–beat variations in morphology. At this point, some of the arrhythmias that should be considered are: (1) irregular ventricular tachycardia (such as torsades des pointes or polymorphic ventricular tachycardia); (2) atrial fibrillation (AF) with bundle branch block; (3) AF in Wolff–Parkinson–White (WPW) syndrome (pseudo-ventricular tachycardia). The QRS complex shows right axis deviation during tachycardia with no progressive change in cardiac axis, thus polymorphic ventricular tachycardia and torsades des pointes associated with QT prolongation are excluded. Polymorphic ventricular tachycardia associated electrolyte abnormality and myocardial ischemia could not be totally excluded by this ECG, however laboratory examination did not indicate myocardial ischemia or an electrolyte abnormality. The representative arrhythmia of the patient\'s irregular heart rate is AF, which is the most common cardiac arrhythmia. When the ventricular rate is slow, AF can be easily diagnosed. However if the ventricular rate is rapid, AF is difficult to appreciate because QRS complexes are clustered together and fibrillatory waves become more difficult to evaluate. The QRS complexes during AF with bundle branch block usually do not have beat–beat variation, and both an Rr′ pattern in lead V1 and Ratrioventricular (AV) node and accessory pathways.