Europace Advance Access originally published online on December 12, 2007
Europace 2008 10(1):105-109; doi:10.1093/europace/eum264
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
ELECTROCARDIOGRAPHY
Characterization of focal right atrial appendage tachycardia


Arrhythmia Section, Cardiology Department, Thorax Institute, Hospital Clinic, University of Barcelona, Villarroel 170, Barcelona 08036, Catalonia, Spain
Manuscript submitted 18 September 2007. Accepted after revision 7 November 2007.
* Corresponding author. Tel: +34 932275551; fax: +34 934513045. E-mail address: berruezo{at}clinic.ub.es
| Abstract |
|---|
|
|
|---|
Aims: Though right atrial appendage tachycardia (RAAT) has been described, no studies to date have focused on its clinical characterization. The aim of the present study was to analyze its clinical, electrocardiographic (ECG), and electrophysiologic (EP) characteristics and the results of radiofrequency ablation (RFA) in RAAT.
Methods and results: Out of 186 consecutive patients undergoing RFA for AT, 15 (8%) had focal RAAT. Mapping was performed using conventional catheters or a 3D electroanatomic mapping system. Patients with RAAT were more likely to be male (66 vs. 38%; P= 0.013) and younger (32 ± 12.6 vs. 55 ± 13.2 years; P < 0.001) than patients with AT originating elsewhere. They were also more likely to have dyspnea (27 vs. 7.6%; P = 0.03), incessant tachycardia (53 vs. 16%; P < 0.001), and left ventricular systolic dysfunction (27 vs. 5%; P = 0.018). RFA was effective in all patients (100 vs. 75%; P = 0.022) and no recurrences (0 vs. 8%; P = 0.31) were observed during a mean follow-up of 37 ± 36 months. A specific ECG pattern was identified, consisting of negative P-waves in leads V1–V2 and a transition to positivity in the rest of the precordial leads. This ECG pattern correctly identified RAAT with a sensitivity of 100%, a specificity of 98%, a positive predictive value of 88%, and a negative predictive value of 100%.
Conclusion: Right atrial appendage tachycardia is more prevalent in young male patients and is commonly associated with tachycardiomyopathy. RFA is effective over long-term follow-up. A characteristic ECG pattern identifies RAAT with a very high sensitivity and specificity.
Key Words: Atrial tachycardia, Radiofrequency ablation, Right atrial tachycardia
| Introduction |
|---|
|
|
|---|
Several recent publications have described the characteristics of different focal atrial tachycardias (AT). Some anatomic sites of AT origin show specific electrocardiographic (ECG), electrophysiologic (EP), and clinical characteristics that might help in identifying specific tachycardias (e.g. sinus tachycardia or AT originating in the pulmonary veins). The commonest foci of AT originating in the right atrium are crista terminalis,1
Although mapping and ablation techniques are the gold standard for location and treatment of AT,9
–14
some ECG algorithms based on P-wave morphology may help to localize the origin of the AT.15
–19
However, although AT originating in the RAA has been described in some case reports13
,16
,17
,19
and in papers about AT as a whole,20
only one recent paper provides ECG and EP data for this type of tachycardia.5
Information on the clinical profile and long-term outcomes of AT after radiofrequency ablation is still lacking, and little is known about its demographic, epidemiologic, electrocardiographic, and EP characteristics. The purpose of this study was to describe these characteristics as well as long-term outcome after radiofrequency ablation (RFA) of right atrial appendage tachycardia (RAAT) as compared with other AT, in order to identify a specific profile.
| Methods |
|---|
|
|
|---|
Patient population
One hundred and eighty-six consecutive patients with paroxysmal or persistent focal AT undergoing RFA between January 1998 and July 2006 were recruited. The RAA was the origin in 15 (8%) patients.
Electrophysiologic study
All patients underwent EP study after the provision of informed written consent. Patients were studied in the fasted awake state with minimal use of sedation. During the study, 12 surface ECG leads and intracardiac electrograms were registered and continuously recorded with an EP-TRACER (Cardio Tek bv, Maastricht, The Netherlands). A 6F quadripolar catheter was placed in the lateral wall of the RA under fluoroscopic guidance. A 4 mm (conventional, open irrigated or Navistar®) 7F quadripolar catheter was used for mapping and ablation. All antiarrhythmic drugs were withdrawn at least five half-lives before the start.
A conventional fluoroscopic system was used for the majority of the procedures. Location of catheters for radiofrequency application was assessed using oblique projections when necessary. If patients were in sinus rhythm at the onset of the ablation procedure, tachycardia was induced using a standard electrical stimulation protocol and burst atrial pacing. If this was unsuccessful, isoproterenol was infused (1–6 µg/min). Standard electrophysiological criteria were used to diagnose AT.22
When patients were in AT, global mapping of the atria was undertaken in order to identify the mechanism.
For patients in whom the CARTOTM system (Biosense Webster, USA) was used, the construction of activation maps during tachycardia started with the identification of anatomical structures. Local activation times were then recorded by manually marking the earliest onset of bipolar potentials. Focal AT were characterized by activation maps showing a wavefront originating from a circumscribed region, from where it spread in a radial fashion to the rest of the atrium. A focal origin was also suggested when, after careful mapping of the atria during tachycardia, only a limited portion of the cycle length (<30%) was covered.23
For patients in whom the CARTO system was not used, the activation sequence maps were evaluated by means of point by point mapping. The precocity of the intracardiac signal registered with the distal bipole of the mapping catheter with respect to the earliest surface P-wave was measured, until the earliest site of endocardial activity was reached. The density of point mapping was particularly high in the regions with the earliest endocardial activation.
Atrial tachycardias was judged to originate in the RAA when the earliest activation was recorded there and successful ablation was achieved inside the triangulated portion of the RAA. The triangulated component of the RAA was mapped in all patients. In all cases of RAAT, the position of the catheter was assessed using fluoroscopic oblique projections. In patients in whom the origin of the AT was far from the tip (>15 mm), CARTO was used to identify the triangulated portion of the RAA.
Radiofrequency energy was applied at the earliest local endocardial activation point relative to the onset of the P-wave. Power output was set at 40–50 W and temperature feedback control of power output was used with a target temperature of 50–60°C (45°C when an irrigated catheter was used). Successful RFA was defined as the termination of the tachycardia with the absence of spontaneous or inducible tachycardia despite isoproterenol infusion.
Electrocardiographic analysis
Surface 12-lead P-wave morphology analysis was performed when AT was present. P-wave morphology was classified into four groups: positive or negative when a predominant polarity was observed and biphasic or isoelectric when no predominant polarity could be determined. P-wave morphology was evaluated and based on consensus between two observers who were blinded to the tachycardia location.
Statistical analysis
Continuous data are expressed as mean ± SD. Means were compared with Students t-test for unpaired data. Categorical variables were compared with a
2 test. A value of P < 0.05 was considered significant.
| Results |
|---|
|
|
|---|
From a total of 186 patients with focal AT, 15 patients (8%) presented AT originating in the triangulated portion of the RAA. Thus, a total of 171 (92%) focal AT originating outside the RAA were collected. Clinical data were obtained from 165 patients with other AT and all patients with RAAT. Basal characteristics of the two types of tachycardias are shown in Table 1.
|
Clinical and echocardiographic data
Patients with RAAT were younger than those with other locations of focal AT (32 ± 12.6 vs. 55 ± 16.3 years, P < 0.001) and a higher proportion were male (66 vs. 38%, P = 0.013).
Clinical presentation also differed in patients with RAAT and with other AT. The most frequent symptoms in both groups were palpitations (60 vs. 88%, P = 0.63), but dyspnea was present between 27% of patients with RAAT and in only 7.6% of those with other types of focal AT (P = 0.006). Tachycardia was incessant in 53% of RAAT cases but only in 16% of patients with other AT locations (P < 0.001). Right atrial appendage tachycardia mean heart rate was 157 ± 24 bpm compared with 148 ± 17 bpm for other AT (P = 0.067).
Echocardiographic analysis showed that left ventricular dysfunction, defined as left ventricular ejection fraction (LVEF) lower than 50%, was more prevalent in RAAT (27 vs. 5%, P = 0.002), probably due to its incessant nature, which explained the greater proportion of patients with tachycardiomyopathy. Mean LVEF of patients with left ventricular dysfunction was 21 ± 5.9%, and the mean LVEF of the whole group of RAAT was also lower than that of the rest of AT (44 ± 6 vs. 58 ± 4%; P = 0.01).
Electrophysiologic study
The origin of AT foci was identified during the EP study. The right atrium was the origin in 132 patients (71%) and the left atrium in 54 patients (29%). The anatomic distribution of right AT foci was Crista terminalis (22%, n = 41), perisinusal (high cristal tachycardias) (15%, n = 28), tricuspid annulus (12%, n = 22), right atrial appendage (8%, n = 15), parahisian (8%, n = 15), and coronary sinus (6%, n = 11).
Right atrial appendage tachycardia was identified using conventional catheters and fluoroscopic guidance in 12 patients (80%) and a three-dimensional mapping system in three patients (20%) in order to delimit the triangulated portion of the RAA (Figure 1). In nine patients (60%), the origin of the tachycardia was located in the tip of the appendage and in six patients (40%), the origin was at the base of the RAA triangulated portion.
|
For RAAT, tachycardia cycle length varied from 318 to 444 ms (364 ± 25.7 ms). At the RAA, endocardial atrial activation preceded the onset of the P-wave by a mean of 28.4 ± 13 ms. Tachycardia was spontaneous in 10 patients (66%), required isoproterenol alone in three patients (22%) and required both isoproterenol and programmed electrical stimulation in two (11%).
Radiofrequency ablation was effective in 100% of patients with RAAT and in 75% of patients with other AT (P = 0.027). The differences were significant for both left-sided AT (100 vs. 65%; P = 0.003), and right-sided AT (100 vs. 80.5%, P = 0.05). Radiofrequency ablation was initially attempted with conventional ablation catheters in all patients. Five patients with RAAT (33%) required irrigated ablation catheters in order to achieve adequate power—a significantly higher figure than in other AT (33 vs. 12%, P = 0.03). No procedure-related complications were observed. The mean procedure time was 110 ± 31 min and fluoroscopy time was 32 ± 18 min.
Finally, no evidence of recurrence was reported in the RAA group, compared with a recurrence rate of 8% in the group of AT from other origins over a mean follow-up of 37 ± 36 months, P = 0.31. All patients with left ventricular systolic dysfunction recovered LVEF within the normal range (62 ± 4%) within 6 months after RFA.
P-wave morphology
Electrocardiographic during tachycardia was very characteristic of RAAT, which showed negative P-waves in leads V1–V2 and a transition to positivity in the other precordial leads in all patients Figure 2. Other ECG characteristics were positive P-waves in lead DI (14 of 15 patients, 92%), negative P-waves in lead aVR (13 of 15 patients, 85%), and positive P-waves in inferior leads (10 of 15 patients, 66%).
|
P-wave morphology of AT from other locations was also analyzed in order to evaluate the sensitivity and specificity of a RAAT ECG criterion. The ECG criterion was defined and tested prospectively by two blinded observers. Considering P-wave negativity in leads V1–V2 as the ECG criterion for diagnosis of RAAT, we obtained a sensitivity of 100%, a specificity of 87%, a PPV of 40%, and a NPV of 100%. Reduction of specificity was basically due to AT from tricuspid annuls, since, in most cases, these AT presented negative P-waves in all precordial leads.2
| Discussion |
|---|
|
|
|---|
Although RAAT have been described in the majority of general AT papers, only one report has specifically assessed this origin,5
Right atrial appendage tachycardia represents not only a particular anatomic origin of AT but also a group of tachycardias with specific clinical, ECG, and EP characteristics. Compared with other AT, RAAT were more likely to be present in younger male patients and are more frequently incessant. This characteristic probably explains why a much higher proportion of patients presented left ventricular systolic dysfunction and dyspnea as clinical manifestations of a tachycardiomyopathy, especially since there was a small difference in mean heart rate between RAAT and the rest of AT (157 ± 24 vs. 148 ± 17 bpm, P = 0.067).
Other EP characteristics included a greater proportion of successful ablations and a lower incidence of recurrence. In our series, RAAT were successfully ablated in all cases and other AT in 75% (P = 0.027). The success rate of RFA for the rest of the AT was very similar to those reported previously.13
,24
Moreover, whereas no relapses of RAAT were observed, other AT had a recurrence rate of 8%.
Most of our findings were in agreement with the recent paper published by Roberts-Thomson et al.5
However, some differences were observed: a slightly younger age at presentation, and a greater prevalence. Moreover, the greater long-term follow-up after RFA allowed us to demonstrate the complete recovery of LVEF in all patients with tachymyocardiopathy and the absence of recurrence over a mean follow-up of 3 years.
The geometry of the RAA may be related to the better ablation efficacy since it is conducive to a stable and firm ablation catheter contact. This better ablation efficacy may also be related to the incessant nature of RAAT, since inconsistent inducibility is a well known limitation of ablation in AT. In contrast, trabeculation of the RAA may be involved in the inadequate power delivery of conventional ablation catheters and the need of irrigated ones.5
However, such a high use of irrigated catheters could also be involved with a higher success ablation rate in RAAT group. On the other hand, the absence of manifest structural atrial disease in all patients may also be an important explanatory factor in the low recurrence rate over long-term follow-up.
Right atrial appendage tachycardia also presented a typical ECG pattern showing negative P-waves in leads V1–V2 and a variable but always present transition to positivity of P-wave polarity on the rest of the precordial leads in all patients. This ECG pattern identified RAAT with a very high sensitivity (100%), specificity (98%), PPV (88%) and NPV (100%). Perisinusal AT had the most similar ECG appearance, and all false positives (2%) with our proposed ECG criteria were due to this focal AT. On the other hand, tricuspid annulus AT presented negative P-waves in leads V1–V2 in most cases, but the persistent negativity of P-waves along all precordial leads2
,19
allowed a good differentiation from RAAT. In contrast to AT from the left atrial appendage,8
not all RAAT seemed to present positive P-waves in inferior leads probably due to the anatomic relationship of the right atrium which is inferior with respect to the left atrium.
Previous AT algorithms based on P-wave morphology are also useful in order to identify the RAA origin.15
–19
However, applying the algorithm published by Kistler et al.19
in our series, RAAT could only be identified in 80% of patients when compared with 98% using our ECG criteria.
Study limitations
The main limitation of the study is the difficulty of precisely identifying the anatomic limits of the triangulated portion of the RAA. However, in the case of a tip origin, the use of oblique projections allowed us to make an accurate localization and firm and stable contact, thanks to the favourable geometry of the RAA. When the origin was at the base, CARTO mapping was used in order to define the RAAs boundary. However, we cannot conclusively rule out the possibility that a very small proportion of the RAAT actually originate slightly outside the triangulated portion of the RAA.
| Conclusions |
|---|
|
|
|---|
Right atrial appendage tachycardia is an uncommon form of focal AT which appears most frequently in young male patients. This type of AT is frequently incessant, producing dyspnea and left ventricular systolic dysfunction secondary to tachymyocardiopathy. A highly sensitive and specific ECG pattern can be used to identify it. Radiofrequency ablation is effective and the recurrence rate is low.
| Footnotes |
|---|
The first two authors contributed equally to this study. | References |
|---|
|
|
|---|
[1] Kalman JL, Olgin JE, Karch MR, Hamdan M, Lee RJ, Lesh MD. Cristal Tachycardias: origin of right atrial tachycardias from the crista terminalis identified by intracardiac ecocardiography. J Am Coll Cardiol (1998) 31:451–9.
[2] Morton JB, Sanders P, Das A, Vohra JK, Sparks PB, Kalman JM. Focal atrial tachycardia arising from the tricuspid annulus: electrophysiologic and electrocardiographic characteristics. J Cardiovasc Electrophysiol (2001) 12:653–9.[CrossRef][Web of Science][Medline]
[3] Badhwar N, Kalman JM, Sparks PB, Kistler PM, Attari M, Berger M, et al. Atrial tachycardia arising from the coronary sinus musculatura. J Am Coll Cardiol (2005) 46:1921–30.
[4] Kistler PM, Fynn SP, Haqqani H, Stevenson IH, Vohra JK, Morton JB, et al. Focal atrial tachycardia from the ostium of the coronary sinus. J Am Coll Cardiol (2005) 45:1488–93.
[5] Roberts-Thomson KC, Kistler PM, Haqqani HM, McGavigan AD, Hillock RJ, Stevenson IH, et al. Focal Atrial tachycardias arising from the right atrial appendage: electrocardiographic and electrophysiologic characteristics and radiofrequency ablation. J Cardiovasc Electrophysiol (2007) 18:367–72. [Epub 7 February 2007].[CrossRef][Web of Science][Medline]
[6] Kistler PM, Sanders P, Hussin A, Morton JB, Vohra JK, Sparks PB, et al. Focal atrial tachycardia arising from the mitral annulus: electrocardiographic and electrophysiologic characterization. J Am Coll Cardiol (2003) 41:2212–9.
[7] Kistler PM, Sanders P, Fynn SP, Stevenson IH, Hussin A, Vohra JK, et al. Electrophysiological and electrocardiographic characteristics of focal atrial tachycardia originating from the pulmonary veins: acute and long-term outcomes of radiofrequency ablation. Circulation (2003) 108:1968–75.
[8] Yamada T, Murakami Y, Yoshida Y, Okada T, Yoshida N, Toyama J, et al. Electrophysiologic and electrocardiographic characteristics and radiofrequency catheter ablation of focal atrial tachycardia originating from the left atrial appendage. Heart Rhythm (2007) 4:1284–91. Epub 16 June 2007].[CrossRef][Web of Science][Medline]
[9] Tracy CM, Swartz JF, Fletcher RD, Hoops HG, Solomon AJ, Karasik PE, et al. Radiofrequency catheter ablation of ectopic atrial tachycardia using paced activation sequence mapping. J Am Coll Cardiol (1993) 21:910–7.[Abstract]
[10] Kay GN, Chong F, Epstein AE, Dailey SM, Plumb VJ. Radiofrequency ablation for treatment of primary atrial tachycardias. J Am Coll Cardiol (1993) 21:901–9.[Abstract]
[11] Walsh EP, Saul JP, Hulse JE, Rhodes LA, Hordof AJ, Mayer JE, et al. Transcatheter ablation of ectopic atrial tachycardia in young patients using radiofrequency current. Circulation (1992) 86:1138–46.
[12] Lesh MD, Van Hare GF. Status of ablation in patients with atrial tachycardia and flutter. Pacing Clin Electrophysiol (1994) 17:1026–33.[CrossRef][Medline]
[13] Chen SA, Tai CT, Chiang CE, Ding YA, Chang MS. Focal atrial tachycardia: reanalysis of the clinical and electrophysiologic characteristics and prediction of successful radiofrequency ablation. J Cardiovasc Electrophysiol (1998) 9:355–65.[Web of Science][Medline]
[14] Anguera I, Brugada J, Roba M, Mont L, Aguinaga L, Geelen P, et al. Outcomes after radiofrequency catheter ablation of atrial tachycardia. Am J Cardiol (2001) 87:886–90.[CrossRef][Web of Science][Medline]
[15] MacLean WA, Kart RB, Kouchoukos NT, James TN, Waldo AL. P waves during ectopic rhythms in man. Circulation (1975) 52:426–34.
[16] Zimerman Ll, Shenasa H, Sorrentino. Utility of p-wave morphology on predicting site of right atrial tachycardia. PACE (1995) 18:861.
[17] Tang CW, Scheinman MM, VanHare GF, Epstein LM, Fitzpatrick AP, Lee RJ, et al. Use of P wave configuration during atrial tachycardia to predict site of origin. J Am Coll Cardiol (1995) 26:1315–24.[Abstract]
[18] de Voogt WG, Mechelen R, Van den Bos A, Scheffer M, van Hemel NM, Levine PA. Electrical characteristics of low atrial septum pacing compared with right atrial appendage pacing. Europace (2005) 7:60–6.
[19] Kistler PM, Roberts-Thomson KC, Haqqani HM, Fynn SP, Singarayar S, Vohra JK, et al. P-wave morphology in focal atrial tachycardia: development of an algorithm to predict the anatomic site of origin. J Am Coll Cardiol (2006) 48:1010–7.
[20] Mizui S, Mori K, Kuroda Y. Ectopic atrial tachycardia due to aneurysm of the right atrial appendage. Cardiol Young (2001) 11:229–32.[CrossRef][Web of Science][Medline]
[21] Kubola T, Tsuchiya K, Hirano T. A case of tachycardia-induced cardiomyopathy caused by an ectopic atrial tachycardia originating from the right atrial appendage. Adv Electrocardiol (2004) (Proceedings of the 31st International Congress on Electrocardiology. World Scientific Publishing Co Pte. Ltd.)
[22] Saoudi N, Cosio F, Waldo A, Chen SA, Iesaka Y, Lesh M, et al. Working Group of Arrythmias of the European of Cardiology and the North American Society of Pacing and Electrophysiology. A classification of atrial flutter and regular atrial tachycardia according to electrophysiological mechanisms and anatomic bases: a statement from a Joint Expert Group from the Working Group of Arrhythmias of the European Society of Cardiology and the North AM Society of Pacing and Electrophysiol. Eur Heart J (2001) 22:1162–82.
[23] Shalganov TN, Vatasescu R, Paprika D, Kornyei L, Vanyi J, Geller L, et al. A simple algorithm for defining the mechanism and the chamber of origin in atrial tachycardias. J Electrocardiol (2006) 39:369–76.[CrossRef][Web of Science][Medline]
[24] Roberts-Thomson K, Kistler PM, Kalman JM. Focal atrial tachycardia II: management. Pacing Clin Electrophysiol (2006) 29:769–78.[CrossRef][Medline]
![]()
CiteULike
Connotea
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||

