Electrophysiological characteristics and radiofrequency catheter ablation of accessory pathway connecting the right atrial appendage and the right ventricle
Xiao-gang Guo, MD1; Qi Sun, MD1; Jian Ma, MD1*; Xu Liu, MD1; Gong-bu Zhou, MD1; Jian-du Yang, MD1; Shu Zhang, MD1.
1State
Key Laboratory of Cardiovascular Disease, Arrhythmia Center, Fuwai
Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Short title: AP connecting the RAA and the RV
*Corresponding author: State Key Laboratory of Cardiovascular Disease, Arrhythmia Center, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, 100037 Beijing, China. E-mail: [email protected]. Phone: +8618811213672. Fax: +8601088398435. Disclosures: None
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Abstract BACKGROUND The accessory pathway (AP) connecting the right atrial appendage (RAA) and the right ventricle (RV) is rare. OBJECTIVE We sought to investigate the feature of the AP connecting the RAA and the RV and the efficacy of radiofrequency catheter ablation via the endocardial access. METHODS We retrospectively analyzed 14 consecutive patients with 14 APs connecting the RAA and the RV managed by 15 procedures between January 2003 and December 2014. RESULTS Ten patients presented as preexcitation during sinus rhythm. All APs had retrograde conduction. None had either antegrade or retrograde decremental conduction property. Ablation targeting the sites at the tricuspid annulus failed in all patients. They were successfully managed by ablating the atrial insertion sites with a median of 10.5 (range 5-28) radiofrequency applications. Electrograms at the successful target showed high amplitude atrial electrogram and low amplitude or no ventricular electrogram. The atrial insertion sites were at the floor of the RAA in 10 patients and inside the lower lobe of the RAA in the remaining 4 patients. The shortest distance between the successful target and the tricuspid annulus in the right anterior oblique projection was 19.7±4.0 mm. There were no complications or recurrence during a median follow-up period of 4.3 (range 0.2-11.8) years. CONCLUSION The APs connecting the RAA and the RV had typical conduction properties. The atrial insertion site favored the floor and the lower lobe of the RAA. Ablation targeting the atrial insertion sites was effective and safe, albeit multiple radiofrequency applications were needed. KEYWORDS: accessory pathway; right atrial appendage; radiofrequency catheter ablation; WPW syndrome; right atrial appendage accessory pathway
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Abbreviations and Acronyms AP
=
accessory pathway
AV
=
atrioventricular
AVRT
=
atrioventricular reentrant tachycardia
CS
=
coronary sinus
EAA
=
earliest atrial activation
ECG
=
electrocardiogram
EVA
=
earliest ventricular activation
HBE
=
His bundle electrogram
LAO
=
left anterior oblique
RA
=
right atrium
RAA
=
right atrial appendage
RAO
=
right anterior oblique
RF
=
radiofrequency
RFCA
=
radiofrequency catheter ablation
RV
=
right ventricle
SR
=
sinus rhythm
TA
=
tricuspid annulus
VA
=
ventriculoatrial
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Introduction The accessory pathway (AP) connecting the atrium and the ventricle has been anatomically proved to be an epicardial structure, which courses through the fibrofatty atrioventricular (AV) grooves on the epicardial aspect of the annulus1. Nevertheless, the locations of most APs are still within the range of the lesion created by radiofrequency (RF) energy applied endocardially, and thus can be managed by radiofrequency catheter ablation (RFCA) with a high success rate2. However, the AP connecting the right atrial appendage (RAA) and the right ventricle (RV), which was firstly recognized by Milstein et al3, makes the “true” epicardial connection since its location is superficial in the fat pad and distant from the annulus, which can be eliminated by open chest surgical ablation3 or dissection4 and RF ablation through epicardial access5. The efficacy to interrupt this special AP by targeting the atrial insertion site at the RAA was reported by a few case reports6, 7. The characteristics of this special AP and its RFCA are largely unknown. Therefore, we sought to investigate the feature of the APs connecting the RAA and the RV and the efficacy and safety of RFCA via the endocardial access. Methods Study Population Of a total of 684 patients with 722 right-sided APs who were managed at our center between January 2003 and December 2014, 14 patients were confirmed to have 14 APs connecting the RAA and the RV in the electrophysiological study and were managed by 15 procedures. Electrophysiological study The study was approved by institutional review committee at Fuwai Hospital, and all patients gave written informed consent. None of the patients had previously taken amiodarone. After withdrawal of antiarrhythmic drugs for at least 5 half-lives, all patients underwent electrophysiological study in fasting state under This article is protected by copyright. All rights reserved.
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minimal sedation. Catheters were introduced into the RV apex, at the His bundle electrogram region (HBE) and into the coronary sinus (CS). Twelve-lead surface electrocardiograms (ECGs) and intracardiac electrograms were recorded simultaneously by a digital multichannel system (LabSystem PRO, Bard Electrophysiology, Lowell, MA), filtered at 30-500 Hz for bipolar electrograms and at 0.05-500 Hz for unipolar electrograms. Standard electrophysiological criteria were used to diagnose right AP2. A 3.5-mm open irrigated tip ablation catheter (Navstar ThermoCool or Celsius thermocouple, Biosense Webster, Diamond bar, CA, USA) was advanced via an SR0 long sheath (Medtronic, Minneapolis, MN, USA) introduced through the right femoral vein to the right atrium (RA). We searched and ablated earliest site of retrograde atrial activation during orthodromic atrioventricular reentrant tachycardia (AVRT) or during RV pacing with local atrial and ventricular electrogram amplitude ratio of 1:4 to 1:1 at the tricuspid annulus (TA). If ablation attempts failed, the adjacent atrium was mapped carefully for the retrograde earliest atrial activation (EAA) that was remote from the annulus. In two of the 15 sessions, using the CARTO XP or CARTO3 system, isochronal 3D electroanatomic maps of the RA were obtained during continuous RV pacing with stimulation signal as the reference, and isochronal 3D maps of the RV were obtained during sinus rhythm (SR), with the lowest point of QRS complex in lead V1 as the reference. Whenever the ventricular electrogram was recorded at the successful target, the atrial/ventricular electrogram amplitude was calculated. Also, ventriculoatrial (VA) interval during RV pacing was measured from the first deflection of the ventricular electrogram to the first deflection of the atrial electrogram.
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Localization of atrial insertion of AP Whenever the target was suspected to be related to the RAA, the morphology of the RAA was revealed by angiography using the SR0 sheath, which, alongside with landmarks of intracardiac electrodes, served as a fluoroscopic reference to judge the successful target location. Five RAAs had a long and prolapsed lower lobe besides a triangle main lobe as previously described8. The atrial insertion of AP was considered to be at the RAA when retrograde EAA recorded in the angiographically confirmed RAA and, acutely, successful ablation was achieved. The RAA were arbitrarily divided into the following sections: 1) the tip of the main lobe, 2) the floor of the main lobe, 3) the roof of the main lobe (Figure 1), with or without 4) the lower lobe. Also, the location of atrial insertion sites of AP relative to the TA in the left anterior oblique (LAO) projection that was parallel to the septum were recorded. The shortest distance between the atrial insertion site and the TA was measured in the right anterior oblique (RAO) projection that was perpendicular to the septum (Supplementary Figure 1). In the 2 patients who received CARTO 3D mapping, the shortest distance between the atrial insertion site and the TA was also measured on the electroanatomic map using built-in tools provided by the manufacturer. RFCA RF energy was delivered using a Stockert 70 RF Generator (Biosense Webster, Diamond Bar, CA). An impedance greater than 160 ohms before ablation was universally detected with ablation at the RAA. RF energy was delivered using a temperature limit of 43℃ and a saline irrigation at a flow rate of 17 to 30 ml/min. A power of 25-35 Watts was used. It was maintained for 60 seconds if the antegrade or retrograde conduction was blocked within 20 seconds and catheter dislodgement was not observed. An ablation procedure was regarded as acutely successful by the absence of antegrade or retrograde conduction over the AP during atrial and ventricular pacing with multiple cycle lengths 30 minutes after ablation despite infusion of isoproterenol (up to 6 mcg/min).
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Post-procedural management and follow-up After the procedure, patients were treated with oral aspirin (100mg/d) for 3 months. No antiarrhythmic drugs were administered in patients with successful ablation. ECG was recorded whenever there was a symptom of palpitation. Transthoracic echocardiography and Holter monitoring were performed at an interval of 3 months in the first year after the last successful RFCA procedure, and at an interval of 12 months thereafter. Statistical analysis Continuous variables are given as mean ± standard deviation or as median and range, depending on normality of distribution. Categorical variables are given as count and ratio. Analyses were performed using SAS ver.9.2 (SAS Institute, Inc., Cary, NC). Results Patient characteristics and electrophysiological findings Fourteen patients (median age 32.0 [range 17-50] years, 4 women) were included in the study, which suggested an incidence of 2.0% in 684 patients with right-sided APs. All patients had structurally normal hearts. Six patients had received prior ablation attempts at other institutions before referral to our center. The baseline ECG during SR before the electrophysiological test showed preexcitation, which suggested right free wall AP in 10 patients (Figure 2). In the electrophysiological lab, 14 APs were identified, which suggested an incidence of 1.9% in all 722 right-sided APs. Ten APs presented both antegrade and retrograde conduction property, while the other 4 APs presented solely retrograde conduction property. However, none of these APs had either antegrade or retrograde decremental conduction property. Fourteen AVRT mediated by the AP could be induced, of which 13 were orthodromic and 1 was antidromic. The details are shown in Table 1.
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Mapping and RFCA Ablation targeting the sites at the TA had no impact on the AP conduction, even transiently in all patients. In the contrary, all patients were successfully managed by ablating the site with retrograde EAA during RV pacing or during orthodromic AVRT with as many as a median of 10.5 (range 5-28) RF applications. All ablation targets were located within the spectrum of 9 to 12 o’clock of the TA in the LAO projection, which corresponded to the relative position of the RAA to the TA. By angiography of the RAA, we located the atrial insertion sites of 10 APs at the floor of the RA, and the atrial insertion sites of the remaining 4 APs inside the lower lobe of the RAA (Figure 3 A, B and C). By angiography of the RA and the TA, the shortest distance between the atrial insertion site of the APs and the TA in the RAO projection was measured to be 19.7±4.0 mm (Table 2). All local electrograms at the successful targets showed high amplitude atrial electrogram and low amplitude or no ventricular electrogram. Noticeably, even if the targets were remote from the TA, a low amplitude ventricular electrogram could still be recorded in 8 patients, of which, 5 were near-field and the other 3 were far-field. In these 8 APs, local VA interval during RV pacing or during orthodromic AVRT was 54.8±22.7 ms, and the median local atrial and ventricular electrogram amplitude ratio during SR was 4.1 (range 2-11.1). Mapping for the ventricular insertion site was attempted in 3 patients (Patients 9, 11, 13), whose AP had antegrade conduction, and earliest ventricular activation (EVA) was localized to the corresponding site at supraventricular crest. Multiple ablation attempts targeting this site failed to eliminate the AP in these 3 patients. However, we didn’t perform systematical mapping for the ventricular insertion site in the other 7 patients who had preexcitation during SR. Two typical examples (Patients 14 and 9) were given. In Patient 14, mapping and ablation at the TA failed to eliminate the AP. Then, retrograde EAA, with stimulus to atrial activation interval of 76 ms, was mapped to be at the lower lobe of the RAA, manifested by angiography (Figure 3 B and C). During SR, the local ventricular activation preceded the onset of delta wave by 20 ms (Figure 3D). Successful ablation terminated the tachycardia by blocking retrograde conduction through the AP (Figure 3 E and F). In Patient 9, unfavorable targets were also identified at the TA (Figure 4A). The site where antegrade EVA was recorded in the RV was remote from the TA (Figures 4B, 5C and 6B); so was the site with retrograde EAA in the RA (Figures 4C, 5B and 6A). Multiple RF applications targeting the atrial insertion site at the floor of RAA finally abolished the AP conduction.
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Follow-up No acute complications occurred during periprocedural period. After an average of 1.1±0.3 procedures, no patients had tachycardia-associated symptom and no evidence of tachycardia was documented on surface ECG during a median follow-up period of 4.3 (range 0.2-11.8) years. Discussion Incidence of the APs connecting the RAA and the RV To our knowledge, there were only case reports on the APs connecting the RAA and the RV. Thus, the incidence of this kind of AP was unknown. Inferred from the report of Long et al9 that included 3 patients with APs connecting the RAA and the RV, the incidence was approximately 3%. Moreover, in patients with previously failed ablation10, the incidence can be as high as 50%. In our study, 14 cases of APs connecting the RAA and the RV were found in a series of 684 patients with 722 right-sided APs. The incidence was about 2%. However, our study was still subject to selection bias, i.e., 6 (42.9%) patients received 1 to 3 previously failed ablation at institutions with annual volume of >200 ablation cases before referral to our center. Therefore, this study may overestimate the incidence of this rare AP.
Correlative anatomy of the RAA and the RV and its implication in AP formation and location It is hypothesized that the direct overlapping of atrial and ventricular myocardium may increase the probability of AP formation11 because the deep groove between the RA and the RV allows the atrial wall to fold over the ventricular wall. In terms of APs connecting the RAA and the RV, Mah et al reported their surgical observation that both the RAA and the LAA were respectively adherent to the RV and the LV surface and AP conduction was blocked by severing the adherence.4 Suturing the RA to the RV in Fontan procedure can cause iatrogenic accessory AV connection,12-14 which also lends credence to this hypothesis. This article is protected by copyright. All rights reserved.
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None of the APs demonstrated decremental conduction in our study and in all prior reports3, 5-7. Thus, it was more reasonable that uninsulated muscular strand consisting of working myocardium but not specialized conduction tissue served as the connecting pathway, which did not travel too long in most situations. This required the spatial proximity between two structures for formation of AP connecting them. Furthermore, the atrial insertion site of the AP could only be found at the floor or the lower lobe of the RAA, which overlapped the nearby ventricular masses, especially the supraventricular crest and the lateral basal free wall of the RV. No connections had the atrial insertion site at the tip or the roof of the RAA. The successful target at the atrial insertion site at the RAA in this study had a distance averaged about 20 mm away from the TA. At this distance, it would be more understandable that no ventricular electrogram should be recorded, which was the fact in 6 patients. However, ventricular electrograms were still recorded in the rest 8 patients. These electrograms all had low amplitudes and 3 of them had a far-field appearance. This reflected the direct overlapping of the RV at the epicardial aspect of the RAA. Furthermore, as shown by Figure 5, the site of antegrade EVA at the supraventricular crest was very close to the site of retrograde EAA at the RAA when viewed fluoroscopically in both the LAO and the RAO projection. Therefore, we believe that the spatial proximity between the floor and the lower lobe of the RAA and the RV underlay the formation of the AP connecting the two. Consistent with former findings from sporadic case reports6, 7, our results found that 1) An ideal target at the TA could not be identified, and ablations targeting the sites at the TA failed to block the AP, even transiently, in all patients; 2) The sites with EVA recorded during pre-excitation was remote from the TA, and so was the successful target at the RAA; and 3) Local VA interval during RV pacing or during orthodromic AVRT recorded at the successful target was apparently longer than ordinary APs. All this electrophysiological evidence supports our belief that the APs we described in this study were located epicardially, as proved in open chest surgery3 and autopsy1. An illustration of the epicardial course of this special AP is shown in Supplementary Figure 2.
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Difficulty in mapping and RFCA The immediate difficulty in the electrophysiological lab was to identify the existence of the AP connecting the RAA and the RV in a timely manner. This would save the electrophysiologists a lot of effort in abating the traditional AV balanced target at the TA. In our experience, localization of the AP to be at the 9 to 12 o’clock of the TA in the LAO projection, failure to identify an ideal target at the TA with balanced AV amplitude ratio, and failure to block the AP, even transiently, by multiple RF applications at the TA comprised the most important clues. Further mapping of the retrograde EAA at the atrial side or the antegrade EVA at the ventricular site remote from the TA established the diagnosis of this peculiar pathway. After the RAA morphology was revealed by angiography, the floor and the lower lobe, if present, should be the area of special interest when mapping the retrograde EAA. Another difficulty lay in the anatomical characteristics of the RAA and the AP. The RAA is a highly pliable structure, which influences the contact and stability of catheter8. Furthermore, the slow blood flow within the RAA, thus less convective cooling, limited the power delivery inside the RAA because of impedance rise6, 7. This has been largely overcome by 3D mapping system and open irrigated catheter. However, the broad-based nature of the AP4 still required multiple RF applications to abolish all connections6, 7. In our case series, after identification of the atrial insertion at the RAA, a median of 10.5 RF applications were needed to eliminate the AP. We also tried to ablate the ventricular insertion site by targeting antegrade EVA during preexcitation in 3 patients but achieved no success. A possible explanation was that the AP mostly branched into finer and diffuse strands at the ventricular insertion sites,11 and thus ablating one or a few of them was not sufficient to block the AP. Considering this evidence comprehensively, together with universal presence of retrograde conductions in this group of patients, we suggest that targeting retrograde EAA at the atrial insertion site should be an acceptable strategy. If this fails, epicardial mapping and ablation via subxiphoid access, or even open chest surgery or minimally invasive surgery, can be considered in patients who have high risk APs or are highly symptomatic.
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Limitations Our study also had following limitations: 1) Due to the retrospective nature of the study, only a few patients received 3D mapping. The distance measurement utilizing the fluoroscopic land marks may not be precise, but provided the best estimation in this study; 2) Intracardiac echocardiography was not utilized to identify the location of the catheter, due to product unavailability in China; 3) Ventricular insertion sites were not systematically mapped in patients with ventricular preexcitation. Whether ablation eliminating all EVA at the RV would be effective or not was not determined in our study. Conclusion The APs connecting the RAA and the RV had typical conduction properties. The retrograde conduction was universally present. The atrial insertion site favored the floor and the lower lobe, if present, of the RAA. Ablation targeting the atrial insertion sites proved to be effective and safe, albeit multiple RF applications were needed.
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References 1. Anderson RH, Ho SY: Structure and location of accessory muscular atrioventricular connections. J Cardiovasc Electrophysiol 1999;10:1119-1123. 2. Wood MA: Ablation of Free Wall Accessory Pathways In Huang SS, Wood MA, eds: Catheter Ablation of Cardiac Arrhythmias. Philadelphia: Elsevier Saunders, 2010, pp, 360-382. 3. Milstein S, Dunnigan A, Tang C, Pineda E: Right atrial appendage to right ventricle accessory atrioventricular connection: a case report. Pacing Clin Electrophysiol 1997;20:1877-1880. 4. Mah D, Miyake C, Clegg R, Collins KK, Cecchin F, Triedman JK, Mayer J, Walsh EP: Epicardial left atrial appendage and biatrial appendage accessory pathways. Heart Rhythm 2010;7:1740-1745. 5. Lam C, Schweikert R, Kanagaratnam L, Natale A: Radiofrequency ablation of a right atrial appendage-ventricular accessory pathway by transcutaneous epicardial instrumentation. J Cardiovasc Electrophysiol 2000;11:1170-1173. 6. Soejima K, Mitamura H, Miyazaki T, Miyoshi S, Murata M, Sato T, Shinagawa K, Takatsuki S, Ogawa S, Nakagawa H: Catheter ablation of accessory atrioventricular connection between right atrial appendage to right ventricle: a case report. J Cardiovasc Electrophysiol 1998;9:523-528. 7. Goya M, Takahashi A, Nakagawa H, Iesaka Y: A Case of Catheter Ablation of Accessory Atrioventricular Connection Between the Right Atrial Appendage and Right Ventricle Guided by a Three-Dimensional Electroanatomic Mapping System. J Cardiovasc Electrophysiol 1999;10:1112-1118. 8. Guo XG, Zhang JL, Ma J, Jia YH, Zheng Z, Wang HY, Su X, Zhang S: Management of focal atrial tachycardias originating from the atrial appendage with the combination of radiofrequency catheter ablation and minimally invasive atrial appendectomy. Heart Rhythm 2014;11:17-25. 9. Long D-Y, Dong J-Z, Liu X-P, Tang R-B, Ning MAN, Gao L-Y, Yu R-H, Fang D-P, Jiang C-X, Yuan Y-Q, Sang C-H, Yin X-D, Chen G, Zhang X-Y, Liang CUI, Ma C-S: Ablation of Right-Sided Accessory Pathways With Atrial Insertion Far From the This article is protected by copyright. All rights reserved.
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Tricuspid Annulus Using an Electroanatomical Mapping System. J Cardiovasc Electrophysiol 2011;22:499-505. 10. Schweikert RA, Saliba WI, Tomassoni G, Marrouche NF, Cole CR, Dresing TJ, Tchou PJ, Bash D, Beheiry S, Lam C, Kanagaratnam L, Natale A: Percutaneous pericardial instrumentation for endo-epicardial mapping of previously failed ablations. Circulation 2003;108:1329-1335. 11. Ho SY: Accessory atrioventricular pathways: getting to the origins. Circulation 2008;117:1502-1504. 12. Razzouk AJ, Gow R, Finley J, Murphy D, Williams WG: Surgically created Wolff-Parkinson-White syndrome after Fontan operation. Ann Thorac Surg 1992;54:974-977. 13. Case CL, Schaffer MS, Dhala AA, Gillette PC, Fletcher SE: Radiofrequency catheter ablation of an accessory atrioventricular connection in a Fontan patient. Pacing Clin Electrophysiol 1993;16:1434-1436. 14. Rosenthal E, Bostock J, Gill J: Iatrogenic atrioventricular bypass tract following a Fontan operation for tricuspid atresia. Heart 1997;77:283-285.
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Figure 1. Anatomy of the RAA with only a main lobe by angiography. Panel A. In the RAO projection, the main lobe of the RAA had a triangular shape and was arbitrarily divided into 3 sections: the tip (1), the floor (2) and the roof (3). Panel B. In the LAO projection, the main lobe of the RAA had an oval shape. The floor (2) is facing the RV. The tip (1) was the most superior portion.
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Figure 2. ECG during SR of patients with ventricular preexcitation.
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Figure 3. Examples of RA and RAA morphologies and ablation targets of Patient 14. Panels A. RA angiography. White broken line delineates the TA. Panel B. RAA angiography. White broken line delineates the silhouette of the RAA. A prolapsed, lower lobe can be seen clearly in the LAO projection. Panel C. Ablation target can be located to be inside the lower lobe of the RAA. Panel D. The electrogram recorded at the successful ablation target during SR and during RV pacing. The antegrade EVA preceded the onset of delta wave by 20ms, and the shortest retrograde stimulus to atrial electrogram interval was 76 ms. Panel E. The electrogram recorded at the successful ablation target during orthodromic AVRT with QRS to retrograde EAA interval of 64 ms. Panel F. RF response. Local VA interval lengthened gradually after 4 seconds of RF application and the tachycardia was terminated with block of retrograde conduction through AP. ABLd/p indicates distal/proximal electrodes of ablation catheter; CSd/p, distal/proximal pair of coronary sinus catheter; HBEd/p, distal/proximal electrodes of His bundle electrogram recording catheter; LAO, left anterior oblique projection; RAO, right anterior oblique projection; and RV, right ventricle catheter.
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Figure 4. Electrograms of Patient 9. Panel A. Electrograms recorded at the TA. Antegrade ventricular activation did not precede the onset of the delta wave and there was initial positive deflection on unipolar electrogram. Ablation attempts at these sites failed to eliminate the AP. Panel B. Antegrade EVA was recorded at the supraventricular crest, which preceded the onset of the delta wave by 20 ms. Unipolar electrogram at this site presented as QS pattern. Panel C. Retrograde EAA at the floor of the RAA. Only a vague and low amplitude ventricular electrogram was recorded locally.
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Figure 5. Morphology of the RAA and ablation target of Patient 9. Panel A. Angiography of the RAA. Broken lines delineate the silhouette of the RAA. Panel B. Successful ablation site targeting the atrial insertion at the floor of the RAA. Panel C. Unsuccessful ablation site targeting antegrade EVA at the supraventricular crest. ABL, ablation catheter; HBE, His bundle electrogram catheter; CS, coronary sinus catheter; HRA, high right atrium catheter; RV, right ventricle catheter; RAO, right anterior oblique; LAO, left anterior oblique.
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Figure 6. 3D electroanatomic map of the RA and RV of Patient 9. Panel A. Electroanatomic map of the RA. Open arrow head indicates the successful ablation target at the floor of the RAA. Panel B. Electroanatomic map of the RV. Open arrow indicates unsuccessful ablation target at the TA. Solid arrow indicates the EVA during ventricular pre-excitation. The red tags indicate ablation sites and the yellow tag indicates HBE recording site. RA, right atrium; RV, right ventricle; RAO, right anterior oblique; LAO, left anterior oblique.
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Table 1. Clinical characteristics and electrophysiological features. RFCA sessions at Pre-excited AVRT AP Conduction Follow-up other institution/at during SR induced property* (yr) our center 1 F/26 10 0/1 Yes Orthodromic Bidirectional 11.8 2 F/38 2 0/1 Yes Orthodromic Bidirectional 11 3 M/33 10 0/1 Yes Orthodromic Bidirectional 8.5 4 M/25 10 1/1 Yes Orthodromic Bidirectional 8 5 F/45 1 0/1 No Orthodromic Only retrograde 5 6 M/31 5 2/1 Yes Orthodromic Bidirectional 5 7 M/42 30 1/1 Yes Orthodromic Bidirectional 4.5 8 F/21 14 0/1 No Orthodromic Only retrograde 4 9 M/22 10 0/2 Yes Orthodromic Bidirectional 1.8 10 M/50 1 1/1 No Orthodromic Only retrograde 1.5 11 M/17 6 3/1 No Orthodromic Only retrograde 1 12 M/30 16 2/1 Yes Orthodromic Bidirectional 0.8 13 M/34 0.2 0/1 Yes Antidromic Bidirectional 0.3 14 M/41 20 0/1 Yes Orthodromic Bidirectional 0.2 AP, accessory pathway; AVRT, atrioventricular reentrant tachycardia; RFCA, radiofrequency catheter ablation; SR, sinus rhythm. *No decremental properties were detected. Patient Sex/Age no. (yr)
History (yr)
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Table 2. Features of atrial insertion of AP and RFCA
Patient no.
Location relative to the RAA
Location
Shortest distance
Shortest distance
Local AV
relative to the
to the TA in the
to the TA in the
interval
TA in the LAO
RAO fluoroscopic
electroanatomic
during
projection
projection (mm)
map (mm)
SR (ms)
Local VA interval during RV pacing or during orthodromic AVRT
Local atrial and ventricular electrogram amplitude ratio
1
Floor
12 o’clock
23
n/a*
n/a‡
n/a‡
n/a‡
2
Lower lobe
9 o’clock
25
n/a*
n/a‡
n/a‡
n/a‡
3
Floor
9 o’clock
22
n/a*
70
64
6.2
4
Floor
9 o’clock
12
n/a*
44
40
4.1
5
Floor
9 o’clock
20
n/a*
n/a†
n/a‡
n/a‡
6
Lower lobe
9 o’clock
20
n/a*
28
24
8.5
7
Floor
9 o’clock
20
n/a*
n/a‡
n/a‡
n/a‡
8
Floor
9 o’clock
15
n/a*
n/a†
70
4.1
9
Floor
10 o’clock
19
23.6
72
50
11.1
10
Floor
11 o’clock
16
n/a*
n/a†
70
2.5
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22
11
Floor
9 o’clock
14
14.6
n/a†
90
2.3
12
Floor
9 o’clock
27
n/a*
n/a‡
n/a‡
n/a‡
13
Lower lobe
9 o’clock
18
n/a*
n/a‡
n/a‡
n/a‡
14
Lower lobe
9 o’clock
14
n/a*
38
30
2
AVRT, atrioventricular reentrant tachycardia; LAO, left anterior oblique; RAA, right atrial appendage; RAO, right anterior oblique; RF, radiofrequency; RV, right ventricle; TA, tricuspid annulus. n/a=not available or not associated. *No 3D electroanatomic mapping was performed. †APs
had no antegrade conductions.
‡
No ventricular electrogram was recorded at successful target.
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Xiao-gang Guo, MD1; Qi Sun, MD1; Jian Ma, MD1*; Xu Liu, MD1; Gong-bu Zhou, MD1; Jian-du Yang, MD1; Shu Zhang, MD1.
1State
Key Laboratory of Cardiovascular Disease, Arrhythmia Center, Fuwai
Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Short title: AP connecting the RAA and the RV
*Corresponding author: State Key Laboratory of Cardiovascular Disease, Arrhythmia Center, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, 100037 Beijing, China. E-mail: [email protected]. Phone: +8618811213672. Fax: +8601088398435. Disclosures: None
This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1111/jce.12693. This article is protected by copyright. All rights reserved.
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Abstract BACKGROUND The accessory pathway (AP) connecting the right atrial appendage (RAA) and the right ventricle (RV) is rare. OBJECTIVE We sought to investigate the feature of the AP connecting the RAA and the RV and the efficacy of radiofrequency catheter ablation via the endocardial access. METHODS We retrospectively analyzed 14 consecutive patients with 14 APs connecting the RAA and the RV managed by 15 procedures between January 2003 and December 2014. RESULTS Ten patients presented as preexcitation during sinus rhythm. All APs had retrograde conduction. None had either antegrade or retrograde decremental conduction property. Ablation targeting the sites at the tricuspid annulus failed in all patients. They were successfully managed by ablating the atrial insertion sites with a median of 10.5 (range 5-28) radiofrequency applications. Electrograms at the successful target showed high amplitude atrial electrogram and low amplitude or no ventricular electrogram. The atrial insertion sites were at the floor of the RAA in 10 patients and inside the lower lobe of the RAA in the remaining 4 patients. The shortest distance between the successful target and the tricuspid annulus in the right anterior oblique projection was 19.7±4.0 mm. There were no complications or recurrence during a median follow-up period of 4.3 (range 0.2-11.8) years. CONCLUSION The APs connecting the RAA and the RV had typical conduction properties. The atrial insertion site favored the floor and the lower lobe of the RAA. Ablation targeting the atrial insertion sites was effective and safe, albeit multiple radiofrequency applications were needed. KEYWORDS: accessory pathway; right atrial appendage; radiofrequency catheter ablation; WPW syndrome; right atrial appendage accessory pathway
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Abbreviations and Acronyms AP
=
accessory pathway
AV
=
atrioventricular
AVRT
=
atrioventricular reentrant tachycardia
CS
=
coronary sinus
EAA
=
earliest atrial activation
ECG
=
electrocardiogram
EVA
=
earliest ventricular activation
HBE
=
His bundle electrogram
LAO
=
left anterior oblique
RA
=
right atrium
RAA
=
right atrial appendage
RAO
=
right anterior oblique
RF
=
radiofrequency
RFCA
=
radiofrequency catheter ablation
RV
=
right ventricle
SR
=
sinus rhythm
TA
=
tricuspid annulus
VA
=
ventriculoatrial
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Introduction The accessory pathway (AP) connecting the atrium and the ventricle has been anatomically proved to be an epicardial structure, which courses through the fibrofatty atrioventricular (AV) grooves on the epicardial aspect of the annulus1. Nevertheless, the locations of most APs are still within the range of the lesion created by radiofrequency (RF) energy applied endocardially, and thus can be managed by radiofrequency catheter ablation (RFCA) with a high success rate2. However, the AP connecting the right atrial appendage (RAA) and the right ventricle (RV), which was firstly recognized by Milstein et al3, makes the “true” epicardial connection since its location is superficial in the fat pad and distant from the annulus, which can be eliminated by open chest surgical ablation3 or dissection4 and RF ablation through epicardial access5. The efficacy to interrupt this special AP by targeting the atrial insertion site at the RAA was reported by a few case reports6, 7. The characteristics of this special AP and its RFCA are largely unknown. Therefore, we sought to investigate the feature of the APs connecting the RAA and the RV and the efficacy and safety of RFCA via the endocardial access. Methods Study Population Of a total of 684 patients with 722 right-sided APs who were managed at our center between January 2003 and December 2014, 14 patients were confirmed to have 14 APs connecting the RAA and the RV in the electrophysiological study and were managed by 15 procedures. Electrophysiological study The study was approved by institutional review committee at Fuwai Hospital, and all patients gave written informed consent. None of the patients had previously taken amiodarone. After withdrawal of antiarrhythmic drugs for at least 5 half-lives, all patients underwent electrophysiological study in fasting state under This article is protected by copyright. All rights reserved.
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minimal sedation. Catheters were introduced into the RV apex, at the His bundle electrogram region (HBE) and into the coronary sinus (CS). Twelve-lead surface electrocardiograms (ECGs) and intracardiac electrograms were recorded simultaneously by a digital multichannel system (LabSystem PRO, Bard Electrophysiology, Lowell, MA), filtered at 30-500 Hz for bipolar electrograms and at 0.05-500 Hz for unipolar electrograms. Standard electrophysiological criteria were used to diagnose right AP2. A 3.5-mm open irrigated tip ablation catheter (Navstar ThermoCool or Celsius thermocouple, Biosense Webster, Diamond bar, CA, USA) was advanced via an SR0 long sheath (Medtronic, Minneapolis, MN, USA) introduced through the right femoral vein to the right atrium (RA). We searched and ablated earliest site of retrograde atrial activation during orthodromic atrioventricular reentrant tachycardia (AVRT) or during RV pacing with local atrial and ventricular electrogram amplitude ratio of 1:4 to 1:1 at the tricuspid annulus (TA). If ablation attempts failed, the adjacent atrium was mapped carefully for the retrograde earliest atrial activation (EAA) that was remote from the annulus. In two of the 15 sessions, using the CARTO XP or CARTO3 system, isochronal 3D electroanatomic maps of the RA were obtained during continuous RV pacing with stimulation signal as the reference, and isochronal 3D maps of the RV were obtained during sinus rhythm (SR), with the lowest point of QRS complex in lead V1 as the reference. Whenever the ventricular electrogram was recorded at the successful target, the atrial/ventricular electrogram amplitude was calculated. Also, ventriculoatrial (VA) interval during RV pacing was measured from the first deflection of the ventricular electrogram to the first deflection of the atrial electrogram.
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Localization of atrial insertion of AP Whenever the target was suspected to be related to the RAA, the morphology of the RAA was revealed by angiography using the SR0 sheath, which, alongside with landmarks of intracardiac electrodes, served as a fluoroscopic reference to judge the successful target location. Five RAAs had a long and prolapsed lower lobe besides a triangle main lobe as previously described8. The atrial insertion of AP was considered to be at the RAA when retrograde EAA recorded in the angiographically confirmed RAA and, acutely, successful ablation was achieved. The RAA were arbitrarily divided into the following sections: 1) the tip of the main lobe, 2) the floor of the main lobe, 3) the roof of the main lobe (Figure 1), with or without 4) the lower lobe. Also, the location of atrial insertion sites of AP relative to the TA in the left anterior oblique (LAO) projection that was parallel to the septum were recorded. The shortest distance between the atrial insertion site and the TA was measured in the right anterior oblique (RAO) projection that was perpendicular to the septum (Supplementary Figure 1). In the 2 patients who received CARTO 3D mapping, the shortest distance between the atrial insertion site and the TA was also measured on the electroanatomic map using built-in tools provided by the manufacturer. RFCA RF energy was delivered using a Stockert 70 RF Generator (Biosense Webster, Diamond Bar, CA). An impedance greater than 160 ohms before ablation was universally detected with ablation at the RAA. RF energy was delivered using a temperature limit of 43℃ and a saline irrigation at a flow rate of 17 to 30 ml/min. A power of 25-35 Watts was used. It was maintained for 60 seconds if the antegrade or retrograde conduction was blocked within 20 seconds and catheter dislodgement was not observed. An ablation procedure was regarded as acutely successful by the absence of antegrade or retrograde conduction over the AP during atrial and ventricular pacing with multiple cycle lengths 30 minutes after ablation despite infusion of isoproterenol (up to 6 mcg/min).
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Post-procedural management and follow-up After the procedure, patients were treated with oral aspirin (100mg/d) for 3 months. No antiarrhythmic drugs were administered in patients with successful ablation. ECG was recorded whenever there was a symptom of palpitation. Transthoracic echocardiography and Holter monitoring were performed at an interval of 3 months in the first year after the last successful RFCA procedure, and at an interval of 12 months thereafter. Statistical analysis Continuous variables are given as mean ± standard deviation or as median and range, depending on normality of distribution. Categorical variables are given as count and ratio. Analyses were performed using SAS ver.9.2 (SAS Institute, Inc., Cary, NC). Results Patient characteristics and electrophysiological findings Fourteen patients (median age 32.0 [range 17-50] years, 4 women) were included in the study, which suggested an incidence of 2.0% in 684 patients with right-sided APs. All patients had structurally normal hearts. Six patients had received prior ablation attempts at other institutions before referral to our center. The baseline ECG during SR before the electrophysiological test showed preexcitation, which suggested right free wall AP in 10 patients (Figure 2). In the electrophysiological lab, 14 APs were identified, which suggested an incidence of 1.9% in all 722 right-sided APs. Ten APs presented both antegrade and retrograde conduction property, while the other 4 APs presented solely retrograde conduction property. However, none of these APs had either antegrade or retrograde decremental conduction property. Fourteen AVRT mediated by the AP could be induced, of which 13 were orthodromic and 1 was antidromic. The details are shown in Table 1.
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Mapping and RFCA Ablation targeting the sites at the TA had no impact on the AP conduction, even transiently in all patients. In the contrary, all patients were successfully managed by ablating the site with retrograde EAA during RV pacing or during orthodromic AVRT with as many as a median of 10.5 (range 5-28) RF applications. All ablation targets were located within the spectrum of 9 to 12 o’clock of the TA in the LAO projection, which corresponded to the relative position of the RAA to the TA. By angiography of the RAA, we located the atrial insertion sites of 10 APs at the floor of the RA, and the atrial insertion sites of the remaining 4 APs inside the lower lobe of the RAA (Figure 3 A, B and C). By angiography of the RA and the TA, the shortest distance between the atrial insertion site of the APs and the TA in the RAO projection was measured to be 19.7±4.0 mm (Table 2). All local electrograms at the successful targets showed high amplitude atrial electrogram and low amplitude or no ventricular electrogram. Noticeably, even if the targets were remote from the TA, a low amplitude ventricular electrogram could still be recorded in 8 patients, of which, 5 were near-field and the other 3 were far-field. In these 8 APs, local VA interval during RV pacing or during orthodromic AVRT was 54.8±22.7 ms, and the median local atrial and ventricular electrogram amplitude ratio during SR was 4.1 (range 2-11.1). Mapping for the ventricular insertion site was attempted in 3 patients (Patients 9, 11, 13), whose AP had antegrade conduction, and earliest ventricular activation (EVA) was localized to the corresponding site at supraventricular crest. Multiple ablation attempts targeting this site failed to eliminate the AP in these 3 patients. However, we didn’t perform systematical mapping for the ventricular insertion site in the other 7 patients who had preexcitation during SR. Two typical examples (Patients 14 and 9) were given. In Patient 14, mapping and ablation at the TA failed to eliminate the AP. Then, retrograde EAA, with stimulus to atrial activation interval of 76 ms, was mapped to be at the lower lobe of the RAA, manifested by angiography (Figure 3 B and C). During SR, the local ventricular activation preceded the onset of delta wave by 20 ms (Figure 3D). Successful ablation terminated the tachycardia by blocking retrograde conduction through the AP (Figure 3 E and F). In Patient 9, unfavorable targets were also identified at the TA (Figure 4A). The site where antegrade EVA was recorded in the RV was remote from the TA (Figures 4B, 5C and 6B); so was the site with retrograde EAA in the RA (Figures 4C, 5B and 6A). Multiple RF applications targeting the atrial insertion site at the floor of RAA finally abolished the AP conduction.
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Follow-up No acute complications occurred during periprocedural period. After an average of 1.1±0.3 procedures, no patients had tachycardia-associated symptom and no evidence of tachycardia was documented on surface ECG during a median follow-up period of 4.3 (range 0.2-11.8) years. Discussion Incidence of the APs connecting the RAA and the RV To our knowledge, there were only case reports on the APs connecting the RAA and the RV. Thus, the incidence of this kind of AP was unknown. Inferred from the report of Long et al9 that included 3 patients with APs connecting the RAA and the RV, the incidence was approximately 3%. Moreover, in patients with previously failed ablation10, the incidence can be as high as 50%. In our study, 14 cases of APs connecting the RAA and the RV were found in a series of 684 patients with 722 right-sided APs. The incidence was about 2%. However, our study was still subject to selection bias, i.e., 6 (42.9%) patients received 1 to 3 previously failed ablation at institutions with annual volume of >200 ablation cases before referral to our center. Therefore, this study may overestimate the incidence of this rare AP.
Correlative anatomy of the RAA and the RV and its implication in AP formation and location It is hypothesized that the direct overlapping of atrial and ventricular myocardium may increase the probability of AP formation11 because the deep groove between the RA and the RV allows the atrial wall to fold over the ventricular wall. In terms of APs connecting the RAA and the RV, Mah et al reported their surgical observation that both the RAA and the LAA were respectively adherent to the RV and the LV surface and AP conduction was blocked by severing the adherence.4 Suturing the RA to the RV in Fontan procedure can cause iatrogenic accessory AV connection,12-14 which also lends credence to this hypothesis. This article is protected by copyright. All rights reserved.
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None of the APs demonstrated decremental conduction in our study and in all prior reports3, 5-7. Thus, it was more reasonable that uninsulated muscular strand consisting of working myocardium but not specialized conduction tissue served as the connecting pathway, which did not travel too long in most situations. This required the spatial proximity between two structures for formation of AP connecting them. Furthermore, the atrial insertion site of the AP could only be found at the floor or the lower lobe of the RAA, which overlapped the nearby ventricular masses, especially the supraventricular crest and the lateral basal free wall of the RV. No connections had the atrial insertion site at the tip or the roof of the RAA. The successful target at the atrial insertion site at the RAA in this study had a distance averaged about 20 mm away from the TA. At this distance, it would be more understandable that no ventricular electrogram should be recorded, which was the fact in 6 patients. However, ventricular electrograms were still recorded in the rest 8 patients. These electrograms all had low amplitudes and 3 of them had a far-field appearance. This reflected the direct overlapping of the RV at the epicardial aspect of the RAA. Furthermore, as shown by Figure 5, the site of antegrade EVA at the supraventricular crest was very close to the site of retrograde EAA at the RAA when viewed fluoroscopically in both the LAO and the RAO projection. Therefore, we believe that the spatial proximity between the floor and the lower lobe of the RAA and the RV underlay the formation of the AP connecting the two. Consistent with former findings from sporadic case reports6, 7, our results found that 1) An ideal target at the TA could not be identified, and ablations targeting the sites at the TA failed to block the AP, even transiently, in all patients; 2) The sites with EVA recorded during pre-excitation was remote from the TA, and so was the successful target at the RAA; and 3) Local VA interval during RV pacing or during orthodromic AVRT recorded at the successful target was apparently longer than ordinary APs. All this electrophysiological evidence supports our belief that the APs we described in this study were located epicardially, as proved in open chest surgery3 and autopsy1. An illustration of the epicardial course of this special AP is shown in Supplementary Figure 2.
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Difficulty in mapping and RFCA The immediate difficulty in the electrophysiological lab was to identify the existence of the AP connecting the RAA and the RV in a timely manner. This would save the electrophysiologists a lot of effort in abating the traditional AV balanced target at the TA. In our experience, localization of the AP to be at the 9 to 12 o’clock of the TA in the LAO projection, failure to identify an ideal target at the TA with balanced AV amplitude ratio, and failure to block the AP, even transiently, by multiple RF applications at the TA comprised the most important clues. Further mapping of the retrograde EAA at the atrial side or the antegrade EVA at the ventricular site remote from the TA established the diagnosis of this peculiar pathway. After the RAA morphology was revealed by angiography, the floor and the lower lobe, if present, should be the area of special interest when mapping the retrograde EAA. Another difficulty lay in the anatomical characteristics of the RAA and the AP. The RAA is a highly pliable structure, which influences the contact and stability of catheter8. Furthermore, the slow blood flow within the RAA, thus less convective cooling, limited the power delivery inside the RAA because of impedance rise6, 7. This has been largely overcome by 3D mapping system and open irrigated catheter. However, the broad-based nature of the AP4 still required multiple RF applications to abolish all connections6, 7. In our case series, after identification of the atrial insertion at the RAA, a median of 10.5 RF applications were needed to eliminate the AP. We also tried to ablate the ventricular insertion site by targeting antegrade EVA during preexcitation in 3 patients but achieved no success. A possible explanation was that the AP mostly branched into finer and diffuse strands at the ventricular insertion sites,11 and thus ablating one or a few of them was not sufficient to block the AP. Considering this evidence comprehensively, together with universal presence of retrograde conductions in this group of patients, we suggest that targeting retrograde EAA at the atrial insertion site should be an acceptable strategy. If this fails, epicardial mapping and ablation via subxiphoid access, or even open chest surgery or minimally invasive surgery, can be considered in patients who have high risk APs or are highly symptomatic.
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Limitations Our study also had following limitations: 1) Due to the retrospective nature of the study, only a few patients received 3D mapping. The distance measurement utilizing the fluoroscopic land marks may not be precise, but provided the best estimation in this study; 2) Intracardiac echocardiography was not utilized to identify the location of the catheter, due to product unavailability in China; 3) Ventricular insertion sites were not systematically mapped in patients with ventricular preexcitation. Whether ablation eliminating all EVA at the RV would be effective or not was not determined in our study. Conclusion The APs connecting the RAA and the RV had typical conduction properties. The retrograde conduction was universally present. The atrial insertion site favored the floor and the lower lobe, if present, of the RAA. Ablation targeting the atrial insertion sites proved to be effective and safe, albeit multiple RF applications were needed.
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References 1. Anderson RH, Ho SY: Structure and location of accessory muscular atrioventricular connections. J Cardiovasc Electrophysiol 1999;10:1119-1123. 2. Wood MA: Ablation of Free Wall Accessory Pathways In Huang SS, Wood MA, eds: Catheter Ablation of Cardiac Arrhythmias. Philadelphia: Elsevier Saunders, 2010, pp, 360-382. 3. Milstein S, Dunnigan A, Tang C, Pineda E: Right atrial appendage to right ventricle accessory atrioventricular connection: a case report. Pacing Clin Electrophysiol 1997;20:1877-1880. 4. Mah D, Miyake C, Clegg R, Collins KK, Cecchin F, Triedman JK, Mayer J, Walsh EP: Epicardial left atrial appendage and biatrial appendage accessory pathways. Heart Rhythm 2010;7:1740-1745. 5. Lam C, Schweikert R, Kanagaratnam L, Natale A: Radiofrequency ablation of a right atrial appendage-ventricular accessory pathway by transcutaneous epicardial instrumentation. J Cardiovasc Electrophysiol 2000;11:1170-1173. 6. Soejima K, Mitamura H, Miyazaki T, Miyoshi S, Murata M, Sato T, Shinagawa K, Takatsuki S, Ogawa S, Nakagawa H: Catheter ablation of accessory atrioventricular connection between right atrial appendage to right ventricle: a case report. J Cardiovasc Electrophysiol 1998;9:523-528. 7. Goya M, Takahashi A, Nakagawa H, Iesaka Y: A Case of Catheter Ablation of Accessory Atrioventricular Connection Between the Right Atrial Appendage and Right Ventricle Guided by a Three-Dimensional Electroanatomic Mapping System. J Cardiovasc Electrophysiol 1999;10:1112-1118. 8. Guo XG, Zhang JL, Ma J, Jia YH, Zheng Z, Wang HY, Su X, Zhang S: Management of focal atrial tachycardias originating from the atrial appendage with the combination of radiofrequency catheter ablation and minimally invasive atrial appendectomy. Heart Rhythm 2014;11:17-25. 9. Long D-Y, Dong J-Z, Liu X-P, Tang R-B, Ning MAN, Gao L-Y, Yu R-H, Fang D-P, Jiang C-X, Yuan Y-Q, Sang C-H, Yin X-D, Chen G, Zhang X-Y, Liang CUI, Ma C-S: Ablation of Right-Sided Accessory Pathways With Atrial Insertion Far From the This article is protected by copyright. All rights reserved.
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Tricuspid Annulus Using an Electroanatomical Mapping System. J Cardiovasc Electrophysiol 2011;22:499-505. 10. Schweikert RA, Saliba WI, Tomassoni G, Marrouche NF, Cole CR, Dresing TJ, Tchou PJ, Bash D, Beheiry S, Lam C, Kanagaratnam L, Natale A: Percutaneous pericardial instrumentation for endo-epicardial mapping of previously failed ablations. Circulation 2003;108:1329-1335. 11. Ho SY: Accessory atrioventricular pathways: getting to the origins. Circulation 2008;117:1502-1504. 12. Razzouk AJ, Gow R, Finley J, Murphy D, Williams WG: Surgically created Wolff-Parkinson-White syndrome after Fontan operation. Ann Thorac Surg 1992;54:974-977. 13. Case CL, Schaffer MS, Dhala AA, Gillette PC, Fletcher SE: Radiofrequency catheter ablation of an accessory atrioventricular connection in a Fontan patient. Pacing Clin Electrophysiol 1993;16:1434-1436. 14. Rosenthal E, Bostock J, Gill J: Iatrogenic atrioventricular bypass tract following a Fontan operation for tricuspid atresia. Heart 1997;77:283-285.
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Figure 1. Anatomy of the RAA with only a main lobe by angiography. Panel A. In the RAO projection, the main lobe of the RAA had a triangular shape and was arbitrarily divided into 3 sections: the tip (1), the floor (2) and the roof (3). Panel B. In the LAO projection, the main lobe of the RAA had an oval shape. The floor (2) is facing the RV. The tip (1) was the most superior portion.
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Figure 2. ECG during SR of patients with ventricular preexcitation.
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Figure 3. Examples of RA and RAA morphologies and ablation targets of Patient 14. Panels A. RA angiography. White broken line delineates the TA. Panel B. RAA angiography. White broken line delineates the silhouette of the RAA. A prolapsed, lower lobe can be seen clearly in the LAO projection. Panel C. Ablation target can be located to be inside the lower lobe of the RAA. Panel D. The electrogram recorded at the successful ablation target during SR and during RV pacing. The antegrade EVA preceded the onset of delta wave by 20ms, and the shortest retrograde stimulus to atrial electrogram interval was 76 ms. Panel E. The electrogram recorded at the successful ablation target during orthodromic AVRT with QRS to retrograde EAA interval of 64 ms. Panel F. RF response. Local VA interval lengthened gradually after 4 seconds of RF application and the tachycardia was terminated with block of retrograde conduction through AP. ABLd/p indicates distal/proximal electrodes of ablation catheter; CSd/p, distal/proximal pair of coronary sinus catheter; HBEd/p, distal/proximal electrodes of His bundle electrogram recording catheter; LAO, left anterior oblique projection; RAO, right anterior oblique projection; and RV, right ventricle catheter.
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Figure 4. Electrograms of Patient 9. Panel A. Electrograms recorded at the TA. Antegrade ventricular activation did not precede the onset of the delta wave and there was initial positive deflection on unipolar electrogram. Ablation attempts at these sites failed to eliminate the AP. Panel B. Antegrade EVA was recorded at the supraventricular crest, which preceded the onset of the delta wave by 20 ms. Unipolar electrogram at this site presented as QS pattern. Panel C. Retrograde EAA at the floor of the RAA. Only a vague and low amplitude ventricular electrogram was recorded locally.
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Figure 5. Morphology of the RAA and ablation target of Patient 9. Panel A. Angiography of the RAA. Broken lines delineate the silhouette of the RAA. Panel B. Successful ablation site targeting the atrial insertion at the floor of the RAA. Panel C. Unsuccessful ablation site targeting antegrade EVA at the supraventricular crest. ABL, ablation catheter; HBE, His bundle electrogram catheter; CS, coronary sinus catheter; HRA, high right atrium catheter; RV, right ventricle catheter; RAO, right anterior oblique; LAO, left anterior oblique.
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Figure 6. 3D electroanatomic map of the RA and RV of Patient 9. Panel A. Electroanatomic map of the RA. Open arrow head indicates the successful ablation target at the floor of the RAA. Panel B. Electroanatomic map of the RV. Open arrow indicates unsuccessful ablation target at the TA. Solid arrow indicates the EVA during ventricular pre-excitation. The red tags indicate ablation sites and the yellow tag indicates HBE recording site. RA, right atrium; RV, right ventricle; RAO, right anterior oblique; LAO, left anterior oblique.
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Table 1. Clinical characteristics and electrophysiological features. RFCA sessions at Pre-excited AVRT AP Conduction Follow-up other institution/at during SR induced property* (yr) our center 1 F/26 10 0/1 Yes Orthodromic Bidirectional 11.8 2 F/38 2 0/1 Yes Orthodromic Bidirectional 11 3 M/33 10 0/1 Yes Orthodromic Bidirectional 8.5 4 M/25 10 1/1 Yes Orthodromic Bidirectional 8 5 F/45 1 0/1 No Orthodromic Only retrograde 5 6 M/31 5 2/1 Yes Orthodromic Bidirectional 5 7 M/42 30 1/1 Yes Orthodromic Bidirectional 4.5 8 F/21 14 0/1 No Orthodromic Only retrograde 4 9 M/22 10 0/2 Yes Orthodromic Bidirectional 1.8 10 M/50 1 1/1 No Orthodromic Only retrograde 1.5 11 M/17 6 3/1 No Orthodromic Only retrograde 1 12 M/30 16 2/1 Yes Orthodromic Bidirectional 0.8 13 M/34 0.2 0/1 Yes Antidromic Bidirectional 0.3 14 M/41 20 0/1 Yes Orthodromic Bidirectional 0.2 AP, accessory pathway; AVRT, atrioventricular reentrant tachycardia; RFCA, radiofrequency catheter ablation; SR, sinus rhythm. *No decremental properties were detected. Patient Sex/Age no. (yr)
History (yr)
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Table 2. Features of atrial insertion of AP and RFCA
Patient no.
Location relative to the RAA
Location
Shortest distance
Shortest distance
Local AV
relative to the
to the TA in the
to the TA in the
interval
TA in the LAO
RAO fluoroscopic
electroanatomic
during
projection
projection (mm)
map (mm)
SR (ms)
Local VA interval during RV pacing or during orthodromic AVRT
Local atrial and ventricular electrogram amplitude ratio
1
Floor
12 o’clock
23
n/a*
n/a‡
n/a‡
n/a‡
2
Lower lobe
9 o’clock
25
n/a*
n/a‡
n/a‡
n/a‡
3
Floor
9 o’clock
22
n/a*
70
64
6.2
4
Floor
9 o’clock
12
n/a*
44
40
4.1
5
Floor
9 o’clock
20
n/a*
n/a†
n/a‡
n/a‡
6
Lower lobe
9 o’clock
20
n/a*
28
24
8.5
7
Floor
9 o’clock
20
n/a*
n/a‡
n/a‡
n/a‡
8
Floor
9 o’clock
15
n/a*
n/a†
70
4.1
9
Floor
10 o’clock
19
23.6
72
50
11.1
10
Floor
11 o’clock
16
n/a*
n/a†
70
2.5
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22
11
Floor
9 o’clock
14
14.6
n/a†
90
2.3
12
Floor
9 o’clock
27
n/a*
n/a‡
n/a‡
n/a‡
13
Lower lobe
9 o’clock
18
n/a*
n/a‡
n/a‡
n/a‡
14
Lower lobe
9 o’clock
14
n/a*
38
30
2
AVRT, atrioventricular reentrant tachycardia; LAO, left anterior oblique; RAA, right atrial appendage; RAO, right anterior oblique; RF, radiofrequency; RV, right ventricle; TA, tricuspid annulus. n/a=not available or not associated. *No 3D electroanatomic mapping was performed. †APs
had no antegrade conductions.
‡
No ventricular electrogram was recorded at successful target.
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