Europace Advance Access originally published online on January 10, 2006
Europace 2006 8(2):129-133; doi:10.1093/europace/euj037
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ELECTROPHYSIOLOGY
Long-term safety and efficacy of slow pathway ablation in patients with atrioventricular nodal re-entrant tachycardia and pre-existing prolonged PR interval
Service de Cardiologie A, Hopital Arnaud de Villeneuve, Centre Hospitalier Universitaire, 34295 Montpellier Cedex 5, France
Manuscript submitted 29 October 2003. Revision received 9 November 2005. Corresponding author. Tel: +33 4 67 33 61 89; fax: +33 4 67 33 61 96. E-mail address: jl-pasquie{at}chu-montpellier.fr
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Abstract |
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The association of atrioventricular nodal re-entrant tachycardia (AVNRT) and pre-existing prolonged PR interval is unusual. Radiofrequency (RF) ablation in such patients may be associated with an increased risk of immediate and delayed AV block. The aim of our study is to assess the long-term efficacy and safety of slow pathway ablation in this population. We studied 10 patients (4 males and 6 females) with pre-existing prolonged PR interval of 68 consecutive patients with AVNRT. All had slow–fast subtype of AVNRT. The mean PR interval was 222±15 ms before RF. The patients with pre-existing prolonged PR were older (69±15 vs. 54±17, P=0.008) and their tachycardias were slower (387±102 vs. 323±73 ms; P<0.05). Transient complete AV block (<5 s) occurred in two patients. None had permanent complete AV block. One patient had a significant increase in PR interval (from 220 to 320 ms). The mean post-RF PR interval was 232±37 ms (P=n.s.). Over a mean follow-up of 39±21 months, none had a recurrence of tachycardia nor developed higher degree AV block. In conclusion, in patients with AVNRT and pre-existing prolonged PR interval, a slow pathway ablation appeared efficient and safe. From our data, no delayed AV block developed on a long follow-up. Most of the patients with periprocedural transient AV block had no evidence of dual AV node physiology, suggesting that, in this population, absence of dual AV node physiology may be associated with a higher risk of AV block during slow pathway ablation.
Key Words: Atrioventricular nodal re-entrant tachycardia, Follow-up, Atrioventricular block, Radiofrequency ablation
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Introduction |
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Atrioventricular nodal re-entrant tachycardia (AVNRT) is one of the most common causes of paroxysmal supraventricular tachycardia. Slow pathway radiofrequency (RF) catheter ablation has become the reference therapy for cure of AVNRT and has been widely reported as efficient and safe1
,2 with a 1.5% atrioventricular block incidence.1–3 Association of AVNRT with pre-existing prolonged PR interval is rather unusual. Such association was found in 2–3% of the patients referred for AVNRT ablation in all previously reported series.4–8 Slow pathway ablation was the most common target in these patients4–6 and appeared efficient and safe. As an increased risk of delayed AV block was recently reported in such patients,6 the aim of our study is to assess the long-term efficiency and safety of slow pathway ablation in patients with AVNRT and pre-existing prolonged PR interval. |
Methods |
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Population
In our institution, 68 consecutive patients underwent slow pathway ablation for AVNRT from May 1997 to May 2002. Of these patients, 10 had a pre-existing PR interval of
200 ms.
Electrophysiological study
All electrophysiological studies were performed under light sedation (nalbuphin IV) after discontinuation of all antiarrhythmic drugs for at least five half-lives. Two quadripolar electrode catheters (St Jude Medical, St Paul, MN, USA) were inserted via the femoral vein and positioned at the His bundle and either the high right atrium or the right ventricle apex. Standard electrophysiological intervals were measured before and after ablation. The atrioventricular nodal effective refractory period was determined in all patients at a cycle length of 600 ms. Dual atrioventricular nodal physiology was defined as a sudden prolongation of the AH interval (50 ms) in response to a 10 ms decrease in the AA interval. Programmed atrial stimulation (up to two extrastimuli) and atrial or ventricular burst pacing were performed in order to induce AVNRT. If tachycardia could not be induced at baseline, isoprenaline was infused and the same stimulation protocol repeated until tachycardia was induced. Typical slow–fast AVNRT was considered when retrograde atrial activity was shown before or inside the QRS complex on the 12-lead ECG and with endocardial recordings exhibiting an almost simultaneous recording of atrial and ventricular electrograms (short HA interval and relatively long AH interval) with the earliest retrograde atrial activity recorded in the His bundle region.
RF catheter ablation
A standard 4 mm-tip temperature-controlled ablation catheter (D curve, Biosense Webster, Worcester, MA, USA) was used in all patients. A 500 kHz RF ablation unit (Stockert EP Shuttle, Biosense Webster) was used for ablation. The defined target of RF application was the slow pathway in all patients, assessed by recording of slow pathway potentials on the ablation catheter. The defined endpoint of the procedure was non-inducibility of tachycardia and less than two nodal echoes during control stimulation. Slow pathway ablation was started low and posteriorly, moving higher and more anteriorly if no specific potentials could be found or if RF application was not associated with slow junctional rhythm. The current was initially applied at a power output of 20 W and increased to a maximum of 30 W, if no junctional rhythm occurred within 10 s of RF application. RF application was immediately stopped in the case of prolongation of AV conduction times or VA block during junctional rhythm. Isoprenaline infusion was used to test ablation success only if it was initially necessary to induce tachycardia before ablation.
Follow-up
Patients were discharged the day after the procedure. All patients had ECG at 1 month and every 3 months after ablation with a 24 h Holter recording at 1 month and every 6 months. The referring cardiologists were contacted by telephone and asked about the ‘rhythmic’ status of the patients. All patients were contacted by telephone to confirm their clinical status.
Statistical analysis
Continuous variables were expressed as mean±standard deviation (SD). The comparisons within groups were assessed using a paired Student's t-test. The comparisons between groups were assessed using one-way analysis of variance. A value of P<0.05 was considered significant.
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Results |
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Clinical characteristics of the patients
Among 68 consecutive patients who underwent slow pathway ablation in our centre, 10 had a pre-existing prolonged PR interval. The clinical characteristics of these patients are reported in Tables 1 and 2. All of them complained of palpitations, and most of them had underlying heart disease. On the contrary, none of the patients with AVNRT and normal PR interval had structural heart disease. Patient 3 had surgery for ostium primum atrial septal defect 15 years before and had persistent grade II mitral insufficiency. Patient 5 had a dual-chamber pacemaker 1 year before for symptomatic sinus node dysfunction. Patient 10 had surgery for left atrial myxoma 10 years before. This patient also suffered from paroxysmal atrial fibrillation and had been treated with amiodarone. As described in Table 2, the patients with pre-existing prolonged PR interval were older and had a tachycardia with a longer cycle length.
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Electrophysiological data and ablation results
All of the patients were in sinus rhythm at the beginning of the EP study. Baseline electrocardiographic data of the patients are reported in Table 2. Associated intraventricular conduction disturbances were found in 5 of 10 patients. Electrophysiological data and characteristics of the ablation procedures are reported in Tables 3 and 4. The slow–fast common form of AVNRT was the clinical tachycardia and was induced in all patients. In Patients 5, 7, 8, and 10, AVNRT was almost incessant during EP study and re-started on each pacing protocol after an AH jump. A slow–slow form of AVNRT was also induced in Patient 6. A slow pathway ablation procedure was achieved in all patients with complete elimination of the slow pathway in six patients and persistence of one nodal echo in four. However, transient conduction disturbances were noted in three patients: one blocked P wave during RF application in Patient 2 and complete AV block for <5 s in Patients 3 and 5. Patient 9 had a dramatic and permanent increase in PR interval from 240 to 320 ms during RF application.
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Characteristics of patients with transient conduction disturbances
Considering the three patients with severe conduction disturbances (Patients 3, 5, and 9), their mean age was identical (69.3±23.4) with identical PR interval (233.3±11.5 ms). Their clinical tachycardia was a slow–fast form of AVNRT with a slower cycle length (446.7±81.4 ms) and a longer retrograde VA interval (46.7±11.5 ms). Two of these three patients had no evidence of conduction jump, and no slow pathway potentials could be found in these three patients. No significant difference was observed in procedure and X-ray durations. In the same manner, RF application time was similar (83.3±47.3 s). Patient 9 had a coronary sinus ostium very close to the site of His recording. Ablation resulted in rather rapid junctional rhythm related probably to a very high approach, resulting in a lesion of the fast pathway. In the two other patients, the RF application showed evidence of slow junctional rhythm with occurrence of block of retrograde AV conduction. Despite interruption of RF pulse, complete AV block occurred for a few seconds (<5 s).
Follow-up
On a follow-up of 39.1±20.7 months (median: 50 months), no patients experienced tachycardia recurrence. Patient 3 suffered from palpitations, but no tachycardia was registered despite repeated ECG Holter recordings. A second EP study was attempted in this patient and no tachycardia could be induced despite isoprenaline infusion. No patient developed grade II or III AV block in the whole follow-up. An increase in PR interval from 220 to 240 ms was found 3 months after ablation in Patient 6 (Table 5).
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Discussion |
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The present study showed in a mean 39-month follow-up that ablation of the slow pathway could be successfully achieved in patients with AVNRT and pre-existing prolonged PR interval without tachycardia recurrence and without delayed high degree AV block even in those with transient periprocedural AV block. In these patients, absence of dual AV node physiology may be associated with a higher risk of periprocedural AV block and requires a very cautious ablation procedure.
In our study, patients presenting with pre-existing prolonged PR interval were older than commonly found in patients with AVNRT and normal PR interval. This finding was similar to the studies of Natale et al.5 and Li et al.6 On the contrary, Sra et al.4 reported a mean age of 31 in their series of seven patients. This older age in our study may explain the higher incidence of AVNRT associated with prolonged PR interval when compared with previous series reporting a 2–3% incidence of the patients referred for AVNRT ablation,4–8 the largest series reporting the outcome of 18 of 346 patients with AVNRT.6 This increase in PR interval associated with a slower tachycardia cycle length is probably related to diffuse disease of the conduction system related to age. Five patients, i.e. 50%, had bundle branch block assessing a more distal conduction tissue disease and six had structural heart disease when compared with none in our group with AVNRT and normal PR interval.
Ablation of the slow pathway has become the first-line therapy in patients with AVNRT.1,2 In patients with pre-existing prolonged PR interval, this approach has been shown efficient in small series of 74,5 and 18 patients.6 Other authors preferred to target the retrograde fast pathway7,8 in three8 and five patients.7 In our study, six of our patients had evidence of dual AV node physiology with longer conduction times probably related to ageing of the conduction pathways, and we postulated that the slow pathway would be the appropriate target for ablation even in the absence of overt dual nodal physiology.
No significant change in conduction times and refractory periods was found in our study, as reported by Sra et al.4 On the contrary, Natale et al.5 showed a shortening of AH interval after slow pathway ablation probably due to the resolution of electrotonic interaction. These changes may be related to complete ablation of the slow pathway as suggested by Strickberger et al.9
The main complication of slow pathway ablation for AVNRT is AV block. This risk of immediate AV block was 
1.5% in the initial reports,1,2 as well as in the French experience.3 In our small series, no permanent complete AV block occurred during the ablation procedure, nor did it occur in the other reported series.4–6 However, three patients had short-lasting transient high degree AV block, and another patient without evidence of dual nodal physiology had a permanent dramatic increase in PR interval. Risk factors of such immediate complications were suggested to be related to total elimination of the slow pathway6 or to occur in patients with very long pre-existing PR intervals.8 In these cases, some authors have suggested ablation of the retrograde fast pathway,7 especially when PR>300 ms,8 or if there was no evidence of the existence of an anterograde fast pathway, i.e. no dual AV node physiology.8 However, this approach is at high risk of AV block, as ablation of the fast pathway may be associated with a much higher incidence of AV block.3 More recently, percutaneous cryotherapy has been demonstrated to be efficient in the ablation of the slow pathway for AVNRT.10 The ability to test the ablation site before producing a permanent lesion may eliminate inadvertent AV block. This technique could be of particular interest in patients with prolonged PR interval. Considering our four patients with transient or permanent impairment in conduction, three had no conduction jump, suggesting the absence of efficient dual antegrade pathways. Thus, ablation of the slow pathway in patients without a conduction jump, i.e. without dual AV node physiology, may be considered at particularly high risk of periprocedural AV block. The occurrence of AV block during slow pathway ablation in these patients may be related to anterograde AV conduction through intranodal pathways other than the fast pathway.4
In patients with pre-existing prolonged PR interval, an increased risk of delayed AV block has been reported.6 However, this risk was much higher in patients with total elimination of the slow pathway than in patients with modification of the slow pathway.6 In our study, only one patient had a delayed slight increase in PR interval. This increase was early in the follow-up as in the series of Li et al.,6 in which 33% developed AV block within 1 month. Moreover, older age, underlying structural heart disease, and pre-existing diffuse His-Purkinje disease might be the associated risk factors of delayed AV block.6 However, in our study with the longest follow-up reported so far in that very particular population, no delayed AV block was detected in the long-term, even in patients with structural heart disease or diffuse conduction disorders.
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Limitations |
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One of the major limitations of our study is the absence of patients with a very long PR interval and, particularly, with PR >300 ms. Only two studies reported the results of slow pathway11
or retrograde fast pathway ablation in three patients with PR >300 ms.8 These patients generally have no dual AV node physiology because of the absence of conduction through the fast pathway. In these patients with very long PR interval, the antegrade conduction goes through ‘intermediate’ pathways other than the fast pathway. It appears, clearly, that periprocedural AV block is of higher risk in these patients as demonstrated by Ridgen et al.,11 with a 30% incidence of AV block (two of seven patients). This risk appeared much lower in patients with moderate increase in PR interval as in our study and other published studies.4–7 On the basis of the limited data presented in this study, no firm guidelines can be proposed. However, absence of dual AV node physiology at baseline as well as under isoprenaline infusion may be considered to be associated with a higher risk of AV block during slow pathway ablation.
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References |
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[1] Jackman WM, Beckman KJ, McClelland JH, et al. Treatment of supraventricular tachycardia due to atrioventricular nodal reentry by radiofrequency catheter ablation of slow pathway conduction. N Eng J Med 1992; 327: 313–8.[Abstract]
[2] HaÏssaguerre M, Gaita F, Fischer B, et al. Elimination of atrioventricular nodal reentrant tachycardia using discrete slow potentials to guide applications of radiofrequency energy. Circulation 1992; 85: 655–6.
[3] Groupe de Rythmologie de la Socièté Française de Cardiologie. Complications des ablations par radiofréquence. Expérience Française. Arch Mal C
ur 1996; 89: 1599–605.
[4] Sra JS, Jazayeri MR, Blanck Z, Deshpande S, Dhala AA, Akhtar M. Slow pathway ablation in patients with atrioventricular nodal reentrant tachycardia and a prolonged PR interval. J Am Coll Cardiol 1994; 24: 1064–8.[Abstract]
[5] Natale A, Greenfield RA, MJ Geiger, et al. Safety of slow pathway ablation in patients with long PR interval: further evidence of fast and slow pathway interaction. Pacing Clin Electrophysiol 1997; 20: 1698–703.[Medline]
[6] Li YG, Grönefeld G, Bender B, Machura C, Hohnloser SH. Risk of development of delayed atrioventricular block after slow pathway modification in patients with atrioventricular nodal reentrant tachycardia and a pre-existing prolonged PR interval. Eur Heart J 2001; 22: 89–95.
[7] Reithmann C, Hoffmann E, Grünewald A, et al. Fast pathway ablation in patients with common atrioventricular nodal reentrant tachycardia and prolonged PR interval during sinus rhythm. Eur Heart J 1998; 19: 929–35.
[8] Verdino RJ, Burke MC, Kall JG, et al. Retrograde fast pathway ablation for atrioventricular nodal reentry associated with markedly prolonged PR interval. Am J Cardiol 1999; 83: 455–8.[CrossRef][Web of Science][Medline]
[9] Strickberger SA, Daoud E, Niebauer M, et al. Effects of partial and complete ablation of the slow pathway on fast pathway properties in patients with atrioventricular nodal reentrant tachycardia. J Cardiovasc Electrophysiol 1994; 5: 645–9.[Web of Science][Medline]
[10] Skanes AC, Dubuc M, Klein GJ, Thibault B, Krahn AD, R Yee, et al. Cryothermal ablation of the slow pathway for the elimination of atrioventricular nodal reentrant tachycardia. Circulation 2000; 102: 2856–60.
[11] Ridgen LB, Kein LS, Mitrani RD, Zipes DP, Miles WM. Increased risk of heart block following slow pathway ablation for AV nodal reentrant tachycardia in patients with marked PR interval prolongation during sinus rhythm. (Abstract). Pacing Clin Electrophysiol 1995; 18: II-918.
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