Europace Advance Access originally published online on June 1, 2007
Europace 2007 9(9):785-789; doi:10.1093/europace/eum105
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
CATHETER ABLATION
Inducible supraventricular tachycardias in patients referred for catheter ablation of atrial fibrillation
1 Department of Cardiology, Athens Euroclinic, 9 Athanassiadou Street, Athens 11521, Greece; 2 Division of Cardiology, Medical College of Virginia, Richmond, VA, USA
Manuscript submitted 15 February 2007. Accepted after revision 24 April 2007.
* Corresponding author. Tel: +30 210 6416600; fax: +30 210 6416661. E-mail address: dkatritsis{at}euroclinic.gr/ dgkatr{at}otenet.gr
| Abstract |
|---|
|
|
|---|
Aims To investigate the prevalence of underlying, inducible supraventricular arrhythmias in patients referred for ablation of atrial fibrillation (AF).
Methods and results Electrophysiology study reports of 409 consecutive patients (18% female), aged 55 ± 9 years, who were referred for catheter ablation of AF, were studied. At electrophysiology study, arrhythmias other than AF were induced in 31 patients (7.6%). Cavotricuspid-dependent atrial flutter was induced in 15 patients (3.7%), slow-fast atrioventricular nodal re-entrant tachycardia (AVNRT) in seven patients (1.7%), atrioventricular re-entrant tachycardia (AVRT) due to an accessory pathway in five patients (1.2%), and atrial tachycardia (AT) in four patients (0.98%). Specific ablation aimed at elimination of the underlying arrhythmia only was performed in 13 patients, isolation of the pulmonary veins without additional ablation in three patients, and a combined procedure was performed in the remaining 15 patients. No significant association was observed between type of induced arrhythmia and type of ablation performed (P = 0.338). Slow pathway ablation without pulmonary vein isolation was more common among patients with AVNRT (five patients, 71%). AF recurrence was higher among patients in whom atrial flutter was induced at electrophysiology study (eight patients, 53%) compared to those with AVRT (no patient), AT (no patient), or AVNRT (one patient) (P = 0.03).
Conclusion Patients referred for ablation of paroxysmal AF should be investigated for evidence of underlying supraventricular arrhytmias. In patients with AVNRT, slow pathway ablation may be the only procedure that is necessary for cure of AF. Inducibility of atrial flutter appears to carry an increased risk of AF recurrence regardless of whether the cavotricuspid isthmus is also ablated.
Key Words: Atrial fibrillation, Supraventricular tachycardia, Radiofrequency ablation
| Introduction |
|---|
|
|
|---|
The association of atrial fibrillation (AF) with other forms of supraventricular tachycardia (SVT) is well described.1
The prevalence of underlying supraventricular arrhythmias in patients referred for ablation of AF is not known. This is, however, of clinical relevance, as ablation of the underlying arrhythmia may result in elimination of AF, particularly in the young, and in the absence of structural heart disease.4
,6
,9
We, therefore, analysed our database of patients referred for catheter ablation of permanent of paroxysmal over a 9-year period. The aims of the study were to: (i) investigate the prevalence of additional inducible arrhythmias in patients referred for AF ablation and (ii) examine the effect of ablation treatment on AF recurrence.
| Methods |
|---|
|
|
|---|
Patients
Databases in our institutions were searched throughout the period 1998–2006, and all patients who were referred for catheter ablation of AF were included in the study. Electrophysiology study and ablation reports as well as complete medical records of patients with symptomatic, paroxysmal AF (PAF) or permanent AF were reviewed for evidence of additional arrhythmias by the investigators. PAF was defined as recurrent episodes of AF lasting more than 2 min and <7 days,10
Electrophysiology study and catheter ablation
Electrophysiology assessment was carried out according to standard protocol. Right atrial and right ventricular refractory periods at one or more cycle lengths were performed as well as decremental pacing. Arrhythmia induction was facilitated by isoproterenol infusion at rates up to 10 µg/min. AF or other SVTs were considered inducible if its duration was >1 min. Bipolar electrograms were filtered at 30–500 Hz, amplified at gains of 20–80 mm/mV, and displayed and acquired, together with surface electrocardiograms.
Ablation of accessory pathways, slow pathway for AVNRT, and cavotricuspid isthmus for right atrial flutter was performed according to standard techniques. Catheter ablation for AF was accomplished via an ostial or circumferential approach, as described elsewhere.11
Induction of sustained supraventricular arrythmias other than AF was an indication for ablation of these SVTs, especially when initiation of AF was found either during the electrophysiology study or from an electrocardiographic recording to show that the AF arose directly from these SVTs. A combined approach with both SVT and AF ablation was performed in individuals when the relationship between SVT and AF was uncertain or undocumented.
Follow-up
Patients were followed-up by means of clinical assessment, ambulatory electrocardiographic monitoring, and trans-telephonic monitoring. Initial post-ablation follow-up took place at 1 and 3 months, and every 6 months thereafter. Beyond this interval, 6-month out-patient clinic visits with Holter monitoring were scheduled. All patients were instructed to maintain their personal records with descriptions of every episode of symptomatic palpitations and, in case of persistent arrhythmia episodes, to obtain trans-telephonic or electrocardiographic documentation of the underlying rhythm. A successful outcome over the follow-up period was defined as the lack of electrocardiographically recorded SVT or AF, and no PAF (duration >1 min) on Holter.
Statistical analysis
Data are presented as mean ± SD for continuous variables and as absolute and relative frequencies (in %) for categorical variables. The association between categorical variables (i.e. type of induced arrhythmia and clinical characteristics, type of ablation) was evaluated using Fisher's exact test, as the small sample size had as a consequence the occurrence of less than five observations in some cells. Moreover, the association between continuous variables and categorical variables was evaluated with Student's t-test and one-way analysis of variance, as appropriate. Simple and multiple logistic regression models were used to evaluate the association between type of induced arrhythmia and recurrence of AF. All reported P-values were based on two-sided tests and were compared to a significant level of 5%.
| Results |
|---|
|
|
|---|
Patients
In total, 409 patients (18% female), aged 55 ± 9 years, were included in the study. Fourteen patients had permanent AF, whereas the remainder presented with PAF. Analysis of medical records and electrophysiology study and ablation reports revealed 36 patients with an additional arrhythmia. In 31 patients (7.6%), an additional arrhythmia was induced at electrophysiology study preceding planed AF ablation (Figures 1 and 2). Clinical characteristics are presented in Table 1.
|
|
|
Inducible SVT and catheter ablation
Cavotricuspid-dependent atrial flutter was the most common arrhythmia induced at electrophysiology study, with an incidence of 3.7% (15 cases). Seven patients (1.7%) had typical, slow-fast AVNRT, five patients AVRT because of an accessory pathway (1.2%), and four patients atrial tachycardia (AT) (0.98%), without a history of prior SVT or AF ablation. Specific ablation aimed at elimination of the additional arrhythmia only was performed in 13 patients (Table 1). In three patients, isolation of the pulmonary veins without additional ablation was performed, whereas in the remaining 15 patients a combined procedure was accomplished, as indicated in Table 1. No significant association was observed between type of induced arrhythmia and type of ablation treatment (P = 0.338), although slow pathway ablation without pulmonary vein isolation was more common among patients with AVNRT (five patients, 71%). In all other types of induced arrhythmia, the combination of pulmonary vein isolation and specific ablation was more common.
Clinical outcome
During the follow-up period (2.9 ± 2 years), eight patients had AF recurrence (in seven of them, repeat AF ablation was performed) and one patient developed permanent AF. No statistically significant association was observed between type of ablation treatment for the underlying arrhythmia and AF recurrence (P = 0.312), although AF recurrence occurred in 40% of patients who had undergone a combined procedure (specific ablation for the underlying arrhythmia and pulmonary vein isolation), in 23% of these who had undergone only specific ablation for the additional arrhythmia, and in none of the patients who had been subjected only to pulmonary vein isolation. Regarding the type of additional arrhythmia, AF recurrence was significantly higher among patients in whom atrial flutter was induced at electrophysiology study [eight patients (53%) compared to those with AVRT (no patient), AT (no patient), or AVNRT (one patient) (P = 0.03)]. Merging patients with AVRT, AVNRT, and AT in one group, we observed that the AF recurrence risk was statistically significantly lower in these patients when compared with patients with atrial flutter (odds ratio = 17.1, 95% CI: 1.8–164.9, P = 0.014). After adjustment for age, hypertension, and ischaemic heart disease, patients with atrial flutter continued to have higher risk of AF recurrence even though the estimate did not reach statistically significance.
| Discussion |
|---|
|
|
|---|
Our data indicated that in 7.6% of patients referred for AF ablation, a detailed electrophysiology study may reveal an underlying arrhythmia, the specific cure of which may also abolish PAF. Atrial flutter appears to be the most common arrhythmia in this respect, followed by AVNRT, AVRT, and AT.
Although AF, typical, and atypical atrial flutter appear to represent separate clinical entities, recent electrophysiologic data indicate important interrelationships between these arrhythmias.2
,12
,13
Approximately 30% of patients undergoing successful ablation of atrial flutter may develop AF at follow-up,14
,15
whereas a similar proportion of patients subjected to pulmonary vein ablation for AF may experience isthmus-dependent atrial flutter following the procedure.16
It appears that atrial flutter may play a more important role in the pathogenesis of AF,13
whereas AF may create the conditions for the development of a functional line of block between the venae cavae and thus promote induction of isthmus-dependent atrial flutter.2
Interestingly, isthmus-dependent atrial flutter may present with atypical ECG characteristics,17
particularly when it occurs following the PV isolation for AF.18
Both typical and atypical forms may respond to cavotricuspid isthmus ablation.19
,20
Kumagai et al.21
have also reported on isthmus ablation that resulted in a 75% success rate of preventing PAF with an organized pattern around the tricuspid annulus. We and others have previously reported on patients with simultaneous episodes of AF alternating with atrial flutter.1
,2
This patient group, which at electrophysiology study, is identified by the recording of flutter waves from the right atrium and AF from the left atrium, may benefit by ablation of the cavotricuspid isthmus.1
In the present series, two out of four patients with PAF and additional atrial flutter responded to cavotricuspid isthmus ablation only. It seems, however, that in a significant proportion of patients who present with clinical AF and inducible atrial flutter at electrophysiology study, cavotricuspid isthmus ablation, even when combined with pulmonary vein isolation, may not be enough to eliminate AF recurrences. These patients appear to carry an adverse prognosis because of the need for further ablations, indicating more significant substrate disease.
Several reports have described the association of AVNRT with AF.3
–6
Sauer et al.6
have reported a 4.3% incidence of inducible AVNRT among patients referred for AF ablation. In 13 of their patients, slow pathway ablation abolished AF recurrences. It seems that in a considerable proportion of such patients, particularly in the young, elimination of AVNRT results in abolition of the AF episodes as well. The exact relationship between the AVNRT and the triggering mechanism(s) for AF cannot be deduced from our study. Palma et al.5
and Sauer et al.6
detected AF triggers in over half of the patients with AF and AVNRT. We have been unable to identify AF triggers with certainty in our patients. It is of interest, however, that in four patients, ablation of the slow pathway resulted in clinical improvement without any further PAF episodes. In our series, a combined approach with both SVT and AF ablation was adopted when the relationship between SVT and AF was uncertain, and this decision was left to the operator's discretion.
Ablation of an accessory pathway may also abolish AF recurrences, particularly in the young. In the series of Dagres et al.9
12% of patients with AF in the context of an accessory pathway and younger than 50-years old experienced AF recurrence following ablation of the pathway, as opposed to 55% of those older than 60. Ablation therapy of the underlying arrhythmia may not necessarily eliminate future AF recurrences.4
,7
,22
Study limitations
Two are the main limitations of our study. First, our numbers are small. Second, the majority of our patients with additional SVT, such as AVNRT, AT, or atrial flutter had no evidence of a transition from SVT to AF, so no precise conclusions could be drawn regarding the relationship between the SVT and the AF and the potential benefit of ablating only the SVT on AF recurrence were therefore not determined.1
,6
,21
In conclusion, patients referred for ablation of PAF should be investigated for evidence of underlying supraventricular arrhythmias such as atrial flutter, AT, AVNRT, or AVRT triggering the fibrillation episodes. In certain patients, specific SVT ablation may be the only procedure that is necessary for cure of AF. Patients with AVNRT, in particular, can be treated by slow pathway ablation alone with elimination of AF recurrences. Inducibility of atrial flutter appears to carry an increased risk of AF recurrence regardless of the method of ablation adopted.
Conflict of interest: none declared.
| References |
|---|
|
|
|---|
[1] Katritsis D, Iliodromitis E, Fragakis N, Adamopoulos S, Kremastinos D. Ablation therapy of type I atrial flutter may eradicate paroxysmal atrial fibrillation. Am J Cardiol (1996) 78:345–7.[CrossRef][Web of Science][Medline]
[2] Horvath G, Goldberger JJ, Kadish AH. Simultaneous occurrence of atrial fibrillation and atrial flutter. J Cardiovasc Electrophysiol (2000) 11:849–58.[Web of Science][Medline]
[3] Brugada J, Mont L, Matas M, Navarro-Lopez F. Atrial fibrillation induced by atrioventricular nodal reentrant tachycardia. Am J Cardiol (1997) 79:681–2.[CrossRef][Web of Science][Medline]
[4] Delise P, Gianfranchi L, Paparella N, Brignole M, Menozzi C, Themistoclakis S, et al. Clinical usefulness of slow pathway ablation in patients with both paroxysmal atrioventricular nodal reentrant tachycardia and atrial fibrillation. Am J Cardiol (1997) 79:1421–3.[CrossRef][Web of Science][Medline]
[5] Palma EC, Ferrick KJ, Gross JN, Kim SG, Fisher JD. Transition from atrioventricular node reentry tachycardia to atrial fibrillation begins in the pulmonary veins. Circulation (2000) 102:937.
[6] Sauer WH, Alonso C, Zado E, Cooper JM, Lin D, Dixit S, et al. Atrioventricular nodal reentrant tachycardia in patients referred for atrial fibrillation ablation: response to ablation that incorporates slow-pathway modification. Circulation (2006) 114:191–5.
[7] Wathen M, Natale A, Wolfe K, Yee R, Klein G. Initiation of atrial fibrillation in the Wolff-Parkinson-White syndrome: the importance of the accessory pathway. Am Heart J (1993) 125:753–9.[CrossRef][Web of Science][Medline]
[8] Sung RJ, Castellanos A, Mallon SM, Bloom MG, Gelband H, Myerburg RJ. Mechanisms of spontaneous alternation between reciprocating tachycardia and atrial flutter-fibrillation in the Wolff-Parkinson-White syndrome. Circulation (1977) 56:409–16.
[9] Dagres N, Clague JR, Lottkamp H, Hindricks G, Breithardt G, Borggrefe M. Impact of radiofrequency catheter ablation of accessory pathways on the frequency of atrial fibrillation during long-term follow-up: high recurrence rate of atrial fibrillation in patients older than 50 years of age. Eur Heart J (2001) 22:423–7.
[10] McNamara RL, Brass LM, Drozda JP Jr, Go AS, Halperin JL, Kerr CR, et al, American College of Cardiology; American Heart Association. ACC/AHA key data elements and definitions for measuring the clinical management and outcomes of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Data Standards (Writing Commitee to Develop Data Standards on Atrial Fibrillation). J Am Coll Cardiol (2004) 44:475–95.
[11] Katritsis D, Wood MA, Shepard RK, Giazitzoglou E, Kourlaba G, Ellenbogen KA. Atrial arrhythmias following ostial or circumferential pulmonary vein ablation. J Interv Card Electrophysiol (2006) 16:123–30.[CrossRef][Web of Science][Medline]
[12] Waldo AL. The interrelationship between atrial fibrillation and atrial flutter. Prog Cardiovasc Dis (2005) 48:41–56.[CrossRef][Web of Science][Medline]
[13] Nabar A, Rodriguez LM, Timmermans C, van den Dool A, Smeets JL, Wellens HJ. Effect of right atrial isthmus ablation on the occurrence of atrial fibrillation: observations in four patient groups having type I atrial flutter with or without associated atrial fibrillation. Circulation (1999) 99:1441–5.
[14] Phillipon F, Plumb VJ, Epstein AE, Kay GN. The risk of atrial fibrillation following radiofrequency catheter ablation of atrial flutter. Circulation (1995) 92:430–5.
[15] Hsieh MH, Tai CT, Chiang CE, Tsai CF, Yu WC, Chen YJ, et al. Recurrent atrial flutter and atrial fibrillation after catheter ablation of the cavotricuspid isthmus: a very long-term follow-up of 333 patients. J Interv Card Electrophysiol (2002) 7:225–31.[CrossRef][Web of Science][Medline]
[16] Scharf C, Veerareddy S, Ozaydin M, Chugh A, Hall B, Cheung P, et al. Clinical significance of inducible atrial flutter during pulmonary vein isolation in patients with atrial fibrillation. J Am Coll Cardiol (2004) 43:2057–62.
[17] Milliez P, Richardson AW, Obioha-Ngwu O, Zimetbaum PJ, Papageorgiou P, Josephson ME. Variable electrocardiographic characteristics of isthmus-dependent atrial flutter. J Am Coll Cardiol (2002) 40:1125–32.
[18] Chugh A, Latchamsetty R, Oral H, Elmouchi D, Tschopp D, Reich S, et al. Characteristics of cavotricuspid isthmus-dependent atrial flutter after left atrial ablation of atrial fibrillation. Circulation (2006) 113:609–15.
[19] Tai CT, Chen SA, Chiang CE, Lee SH, Ueng KC, Wen ZC, et al. Electrophysiologic characteristics and radiofrequency catheter ablation in patients with clockwise atrial flutter. J Cardiovasc Electrophysiol (1997) 8:24–34.[Web of Science][Medline]
[20] Yang Y, Mangat I, Glatter KA, Cheng J, Scheinman MM. Mechanism of conversion of atypical right atrial flutter to atrial fibrillation. Am J Cardiol (2003) 91:46–52.[CrossRef][Web of Science][Medline]
[21] Kumagai K, Tojo H, Noguchi H, Yasuda T, Tamari H, Matsumoto N, et al. Effects of cavotricuspid isthmus catheter ablation on paroxysmal atrial fibrillation. Jpn Heart J (2001) 42:79–89.[CrossRef][Medline]
[22] Weiss R, Knight BP, Bahu M, Zivin A, Souza J, Goyal R, et al. Long-term follow-up after radiofrequency ablation of paroxysmal supraventricular tachycardia in patients with tachycardia-induced atrial fibrillation. Am J Cardiol (1997) 80:1609–10.[CrossRef][Web of Science][Medline]
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
A. Shiroshita-Takeshita, H. Mitamura, S. Ogawa, and S. Nattel Rate-dependence of atrial tachycardia effects on atrial refractoriness and atrial fibrillation maintenance Cardiovasc Res, January 1, 2009; 81(1): 90 - 97. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. G. Katritsis Catheter Ablation of Atrial Fibrillation: For Whom and How? Angiology, August 1, 2008; 59(2_suppl): 103S - 106S. [Abstract] [PDF] |
||||
![]() |
A. C.P. Wiesfeld Key questions are helpful to prevent an unnecessary pulmonary veins isolation ablation procedure Europace, January 1, 2008; 10(1): 121 - 121. [Full Text] [PDF] |
||||
![]() |
D. Katritsis and K. A. Ellenbogen Key questions are helpful to prevent an unnecessary pulmonary veins isolation ablation procedure: reply Europace, January 1, 2008; 10(1): 121 - 121. [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||




