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CASE REPORT
Year : 2021 | Volume
: 10
| Issue : 4 | Page : 115-120
A posteroseptal accessory pathway with conflicting predictors to determine the exact location of successful ablation
Farzad Kamali1, Mohammadrafie Khorgami2, Bayan Faridi3, Abbas Soleimani4
1 Department of Cardiac Electrophysiology, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran
2 Cardiac Electrophysiology Research Center, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran
3 School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran
4 Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran
Correspondence Address:
Dr. Abbas Soleimani
Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Vali-Asr Ave, Tehran 1996911101
Iran
Source of Support: None, Conflict of Interest: None
DOI: 10.4103/rcm.rcm_44_21
Radiofrequency ablation of concealed posteroseptal accessory pathway (AP) and differentiating the right posteroseptal from the left is a challenge for electrophysiologists. Considering different electrophysiological characteristics of posteroseptal AP can help to predict the successful ablation site. We report on a 45-year-old man with simultaneous orthodromic reentrant tachycardia and atrioventricular nodal reentrant tachycardia, both of which were successfully ablated in the right posteroseptal area at the site of the slow pathway. The arrhythmia with both right bundle branch block (RBBB) and left bundle branch block (LBBB) aberrant conduction was observed during our study. The ventriculoatrial (VA) interval increased approximately 25 ms when arrhythmia was conducted with LBBB aberrancy, while it did not change during the RBBB aberrancy. This finding is diagnostic for orthodromic reciprocating tachycardia using a left-sided AP rather than right. However, other parameters, such as delta VA interval and sharp/blunt feature in the proximal coronary sinus electrogram, indicated that the AP is located on the right posteroseptal area.
Keywords: Accessory pathway, radiofrequency ablation, reentrant tachycardia
Posteroseptal region has a complex anatomy and accessory pathways (APs) in this area can have different courses; therefor, radiofrequency ablation of posterosepotal APs can be challenging. Despite the complex nature of posterosepotal APs, the success of ablation is high. Common approaches for posteroseptal AP ablation are included: right and left endocardial approaches, endocardial ablation through coronary sinus system and its tributaries, and rarely percutaneous epicardial subxiphoid approach. Various criteria have been proposed to predict the successful site of ablation for posteroseptal APs. These predictive criteria can be contradictory and conflicting.
Case ReportA 45-year-old man was referred for management of palpitation for the last 2 years. Medical therapy with beta-blocker was ineffective at controlling his symptoms. His physical examination and all laboratory work were within normal limits for his age. His surface electrocardiogram was normal without preexcitation [Figure 1]a. An echocardiogram revealed normal left ventricular size and systolic function. An electrophysiologic study was performed to evaluate the cause of palpitation and possible ablation. The baseline AH and HV intervals were 70 and 48 ms, respectively [Figure 1]b. Ventricular overdrive pacing was one of the first tests to perform. Atrial activation in his catheter appeared the earliest site of activation which changed to proximal coronary sinus at a higher rate [Figure 1]c and [Figure 1]d. Ventricular extrastimulus pacing also showed concentric retrograde conduction without decremental properties [Figure 2]a, [Figure 2]b, [Figure 2]c.
Figure 1: (a) The 12-lead electrocardiogram shows normal sinus rhythm with normal PR and QT interval and normal QRS duration, without preexcitation. (b) The baseline intracardiac recording demonstrates normal AH and HV intervals (70 ms and 48 ms, respectively). (c and d) The earliest retrograde atrial activation site during ventricular overdrive pacing changed from His bundle (c) to proximal coronary sinus at higher rate (d)
Figure 2: Ventricular extrastimulation reveals nondecremental retrograde conduction with earliest atrial activation in CS 7–8. The ventriculoatrial intervals and the sequence of atrial activation have no change at premature cycle length of 310 to 260 ms (a-c). (d) Intracardiac tracing during arrhythmia shows a short RP pattern at the CL of 278ms. The HV interval during arrhythmia is 58ms and the earliest atrial activation is in the proximal CS catheter. Intraventricular conduction delay with prolongation of the H–V interval can be one of the reasons for sustaining a reentrant arrhythmia. The proximal coronary sinus electrogram demontrates sharp/blunt electrogram pattern with the delta ventriculoatrial interval (difference between ventriculoatrial interval in His catheter CS 7–8) of 20 ms. Both of these indices indicate the location of the accessory pathway on the right side rather than the leftA short RP arrhythmia was easily and repeatedly induced by a variety of means including spontaneously or following atrial extrastimulation. The HV interval during arrhythmia was 58 ms and the earliest retrograde atrial activation was in the proximal coronary sinus [Figure 2]d.
Occasionally, the arrhythmia showed beat-to-beat variation in the RR interval. The variation in the cycle length (CL) during arrhythmia resulted from changes in antegrade conduction, not in retrograde conduction [Figure 3]. As shown in [Figure 3]a, the preceding VV interval determined AA. These findings ruled out atrial tachycardia as a possible mechanism of arrhythmia. The ventriculoatrial (VA) interval during ventricular overdrive at the same cycle length of arrhythmia is only slightly longer than one during arrhythmia, which favors orthodromic atrioventricular reentrant tachycardia over atrioventricular nodal reentrant tachycardia as the mechanism of the arrhythmia. A “His” synchronous ventricular stimulation consistently advanced the next beat of tachycardia and reset atrial timing [Figure 3]b. The spike to an interval is constant with earlier single ventricular stimulation [Figure 3]c. These findings are consistent with an oral rehydration therapy (ORT).
Figure 3: (a) The intracardiac tracing shows a slight beat-to-beat variation in the RR interval. The variations in the CL of arrhythmia are due to a change in the AV, while the ventriculoatrial intervals are constant. On the other hand, the preceding VV interval determined AA. This finding rules out atrial tachycardia as a possible mechanism of arrhythmia. As shown in b and c, a single ventricular stimulation consistently advanced the next beat of tachycardia and reset atrial timing. Note that the variation in the CL of arrhythmia is due to the change in the AV intervals (94 and 104 ms), while the ventriculoatrial intervals are constant (170 ms). The ventricular pacing morphology is intermediate between native QRS complexes and the pure paced complex. The significance of fusion QRS complex during arrhythmia is similar to His synchronous ventricular stimulation. As demonstrates in d, the spike to an interval (204 ms) is constant with an earlier single ventricular stimulation. These findings are consistent with an oral rehydration therapyThe arrhythmia with both right bundle branch block (RBBB) and left bundle branch block (LBBB) aberrant conduction was observed during our study. Transition of RBBB and LBBB tachycardia to narrow tachycardia after a single ventricular stimulus is shown in [Figure 4]. The cycle length of arrhythmia and VA interval was not changed during the transition of RBBB tachycardia to narrow tachycardia [Figure 4]a. However, the VA interval in LBBB tachycardia is 24 ms longer than without LBBB, indicating that the left-sided AP is an integral part of arrhythmia [Figure 4]b and [Figure 4]c. This finding is diagnostic for orthodromic reciprocating tachycardia using a left-sided AP and excluding AT, AVNRT, and ORT using a right-sided AP.
Figure 4: AS demonstrates in a, the CL of arrhythmia and ventriculoatrial interval is not changed during transition of right bundle branch block arrhythmia to narrow complex arrhythmia. b and c show that the ventriculoatrial interval in LBBB tachycardia is 24 ms (106–82 ms) longer than without left bundle branch block, indicating that the left-sided accessory pathway is an integral part of arrhythmia. (d) Magnification of the intracardiac electrogram during arrhythmia reveals that the proximal CS electrogram has a sharp/blunt pattern indicated that the accessory pathway is located on the right side rather than the leftAdvancement and resetting of arrhythmia that was easily performed by pacing from RV apex indicates that the ventricular pacing site is not far from the ventricular insertion site of the AP. Entrainment from the right ventricle was not possible due to rapid termination of arrhythmia.
Meticulous mapping of right posteroseptal, parahisian, coronary cusps (noncoronary cusp and right coronary cusp), and left posteroseptal areas during arrhythmia revealed the earliest retrograde atrial activation in the proximal coronary sinus.
Arrhythmia termination was unsuccessful through RF application with 4 mm tip irrigated catheter and 25W power in the left posteroseptal (via transseptal approach) and in the proximal coronary sinus.
A typical slow–fast AVNRT was also induced spontaneously by catheter-induced premature atrial complex after antegrade jump, during EP study [Figure 5]a. The timing cycle length of second arrhythmia is not reset by a single ventricular extrastimulation from RV [Figure 5]b.
Figure 5: Typical slow–fast AVNRT with the CL of 368 ms and the ventriculoatrial (HRA) interval of 26 ms is shown in a. The timing cycle of AVNRT is not reset by a single ventricular extrastimulation (b). The ventricular overdrive pacing at the CL of 220 ms before ablation demonstrates one-to-one retrograde conduction (a). However after ablation, there is ventriculoatrial dissociation during ventricular pacing at the same CL, which is in favor of AP ablation or modification (b) change in retrograde conduction from nondecremental to decremental confirms that the AP had been eliminated or modified after ablation at the site of right slow pathway (c and d)Due to the coexistence of typical AVNRT, we also decided to ablate slow pathway. RF application with a 4 mm distal tip nonirrigated catheter for 60 s at the power of 30 W resulted in the appearance of junctional rhythm and complete ablation of slow pathway. Both typical AVNRT and ORT were rendered noninducible even during high-dose infusion of isoproterenol. Ventricular extrasimulation from RV apex, after ablation, showed concentric and decremental conduction. The patient was free of palpitation during 4-month postablation follow-up.
A closed observation at the intracardiac EGM during arrhythmia reveals that the proximal CS EGM has a sharp/blunt pattern and the delta VA interval (defined as the difference in VA interval between the His catheter and one of the electrodes that recorded the earliest atrial activation) of 20 ms [Figure 2]d and [Figure 4]d. Both of these indices indicated that the AP is located on the right rather than the left. However, an increase in VA interval when arrhythmia was conducted with LBBB aberrancy indicates that the AP is located on the left side of the interventricular septum.
DiscussionThis report describes a patient with orthodromic reciprocating tachycardia using a concealed left-sided AP. We proved participation of the left-sided AP in the circuit of arrhythmia by delivering His synchronous ventricular pacing that advanced the subsequent atrial electrogram, and by observing an increase in VA interval (about 25 ms in our case) when arrhythmia was conducted with LBBB aberrancy. The amount of increase in VA interval can also distinguish free wall from septal APs. The increase in VA interval which is equal or <30 ms is in favor of septal location of AP rather than free wall.[1] This AP also had no decremental properties during ventricular pacing. Entrainment of the arrhythmia by RV pacing is not possible for us despite several attempts due to early termination of arrhythmia.
This AP was accidentally eliminated at the site of right slow pathway when we were trying to AVNRT ablation, after failed ablation in the left posteroseptal and proximal coronary sinus. After ablation of SP, there were no recurrence and no inducible both AVNRT and ORT, including intravenous administration of high-dose isoproterenol.
Depending on the successful elimination of arrhythmia at the right slow pathway and its origin from the left side of the interventricular septum, several scenarios are proposed regarding the arrhythmia mechanism and anatomical extension of AP, including:
Anatomic location of slow pathway is within the atrial myocardium. The atrial insertion site of posteroseptal AP may thus be eliminated or modified at the site of right slow pathway[2]An orthodromic reciprocating tachycardia using a posteroseptal AP for the retrograde conduction and a slow pathway as an antegrade limb can be noninducible by slow pathway ablationThe nodoventricular and nodofascicular APs can be inserted into the slow pathway rather than the fast pathway, so successful ablation of these APs can be possible by slow pathway elimination.In our case, the nodoventricular/nodofascicular reentry tachycardia is unlikely due to the absence of VA dissociation and nondecremental properties of this AP. In addition, single ventricular extrastimulation delivered during AVNRT could not cause the arrhythmia to terminate or reset [Figure 5]d. The short AH interval during arrhythmia (94–110 ms) also makes the second hypothesis unlikely.
The change in retrograde conduction from nondecremental to decremental confirms that the AP had been eliminated or modified after ablation at the site of right slow pathway [Figure 5]c and [Figure 5]d.
The posterosuperior process of the left ventricle and inferior wall of the right atrium is adjacent to the posteroseptal region, so the posteroseptal AP can run from the right atrium to the left ventricle.[1],[3] Therefore, another possibility is that the AP is oblique, with the ventricular portion on the left and the atrial portion on the right, that the atrial portion is ablated from the right side.
The amount of change in VA interval during ORT due to ipsilateral bundle branch block can help to determine the location of the AP. If the VA interval is prolonged by <10 ms with BBB, it indicates that the AP is located within the septum. Increasing the VA interval by >35 ms with ipsilateral BBB suggests the free wall location of the AP. But if, like our case, the VA interval between 10 and 30 ms increases with ipsilateral BBB, the ventricular insertion side of AP is more likely to be located in the same direction as the block in the right or left ventricular septum.[1]
The delta VA (defined as the difference in VA interval between the His catheter and one of the electrodes that recorded the earliest atrial activation) <25 ms and a sharp/blunt CS electrogram feature suggest a right-sided endocardial AP location. The sharp near-field signal is caused by CS muscular coat activation and blunt signal is caused by atrial stimulation, which indicates that the AP is located on the right-sided endocardial or an epicardial AP location.[3],[4]
The CS EGM feature and delta VA interval in this case were two predictors of the correct location of the AP in the right posteroseptal, while other parameters indicated that the AP was located on the left.
Various criteria have been proposed to predict the successful location of ablation for posteroseptal APs; therefor, a composite of information collected during the electrophysiological study should be considered before ablation.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
This study was financially supported by Rajaie Cardiovascular Medical and Research Center.
Conflicts of interest
There are no conflicts of interest.
References
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