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Europace Advance Access originally published online on May 3, 2007
Europace 2007 9(7):458-465; doi:10.1093/europace/eum067
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© The European Society of Cardiology 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

ELECTROPHYSIOLOGY

Retrograde slow pathway conduction in patients with atrioventricular nodal re-entrant tachycardia

Demosthenes G. Katritsis1,*, Kenneth A. Ellenbogen2, Anton E. Becker3 and A. John Camm4

1 Department of Cardiology, Athens Euroclinic, 9 Athanassiadou St., Athens 11521, Greece; 2 Division of Cardiology, Medical College of Virginia, Richmond, VA, USA; 3 Academic Medical Center, University of Amsterdam, Amsterdam, The, Netherlands; 4 Cardiac and Vascular Sciences, St George's, University of London, London, UK

Manuscript submitted 22 February 2007. Revision received 21 March 2007. * Corresponding author. Tel: +30 210 6416600; fax: +30 210 6819779/6416661. E-mail address: dkatritsis{at}euroclinic.gr


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Study limitations
 Acknowledgements
 References
 
Aims To study retrograde slow pathway conduction by means of right- and left-sided septal mapping.

Methods and results Nineteen patients with slow–fast atrioventricular nodal re-entrant tachycardia (AVNRT) were studied before and after slow pathway ablation. Simultaneous His bundle recordings from right and left sides of the septum, using trans-aortic and trans-septal electrodes, were made during right ventricular pacing. Pre-ablation, decremental retrograde ventriculo-atrial (VA) conduction without jumps or discontinuities was recorded in eight patients (group 1). In six patients, retrograde conduction jumps were demonstrated (group 2) and in the remaining four patients, there was minimal prolongation of stimulus to atrium (St-A) intervals (group 3). The maximal difference ({Delta}St-A) between St-A intervals obtained with pacing at a constant cycle length of 500 ms and at the cycle length with maximal retrograde VA prolongation was significantly longer measured from the right His compared with the left His (122 ± 25 vs. 110 ± 33 ms, P = 0.02, respectively) in group 1 and group 2 (140 ± 23 vs. 110 ± 35 ms, P = 0.03), but not in group 3 (10 ± 4 vs. 13 ± 8 ms, P = 0.35). Post-ablation, {Delta}St-A intervals were similar between right and left His recordings (77 ± 37 vs. 76 ± 33 ms, P = 0.53, respectively) in group 1, (100 ± 24 vs. 103 ± 21 ms, P = 0.35) group 2, and (63 ± 32 vs. 66 ± 33 ms, P = 0.35) group 3.

Conclusion In patients with typical AVNRT, retrograde conduction through the slow pathway results in earliest retrograde atrial activation on the left side of the septum and catheter ablation in the right inferoparaseptal area abolishes this pattern. These findings are compatible with the concept of slow pathway conduction by means of the inferior AV nodal extensions.

Key Words: Atrioventricular node, Slow pathway, Tachycardia, Ablation


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Study limitations
 Acknowledgements
 References
 
Little data exist describing the physiology of retrograde conduction over the slow pathway in patients with typical (slow–fast) atrioventricular nodal re-entrant tachycardia (AVNRT) before and after ablation. Initial studies have demonstrated continuous ventriculo-atrial (VA) conduction curves with either fixed or minimal prolongation of the VA interval in patients with typical, slow–fast AVNRT.1Go–3Go This has traditionally been explained by attributing all retrograde conduction to the fast pathway.4Go Decremental conduction or retrograde dual pathways, however, may also occur,5Go–8Go although retrograde dual pathway conduction is demonstrated in only 4–23% of patients with slow–fast AVNRT.7Go The role, therefore, of retrograde slow pathway conduction as the cause of decremental VA conduction is unknown. Retrograde conduction through the slow pathway is associated with a change in the retrograde atrial activation sequence, with a switch from earliest activation in the septal right atrium to earliest activation recorded at the coronary sinus (CS) ostium.5Go,9Go However, although the atrioventricular (AV) node represents a true septal structure, no detailed mapping of the left septum has been performed during ventricular pacing.

We hypothesized that retrograde slow pathway conduction in patients with typical AVNRT can be mapped by analysis of the retrograde atrial activation pattern. We further hypothesized that if the slow pathway represents a distinct anatomical entity, ablation of the slow pathway in patients with AVNRT should result in a change in the retrograde VA conduction and the retrograde atrial activation sequence. The purpose of this study was to perform detailed characterization of retrograde slow pathway conduction in patients with AVNRT by means of right and left septal mapping before and after slow pathway ablation.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Study limitations
 Acknowledgements
 References
 
Patients
Nineteen patients with discontinuous AV nodal conduction curves and inducible typical slow–fast AVNRT were studied before and after successful completion of the ablation procedure. Atrioventricular nodal re-entrant tachycardia was diagnosed according to standard criteria.10Go Slow pathway ablation was accomplished by a combined anatomic and electrogram recording approach from the right side in all patients.11Go,12Go Patients were studied in the post-absorptive state, under sedation with diazepam and diamorphine, and after all antiarrhythmic agents had been discontinued more than 5 days. No patient had received amiodarone for the preceding 3 months. The study received approval from our institutional review board, and all patients signed written, informed consent.

Electrophysiological study
Electrodes were introduced into the right atrium, across the tricuspid valve to record a right-sided His bundle electrogram, the CS, the right ventricular apex, and retrograde through the non-coronary cusp of the aortic valve to record a left-sided His bundle electrogram (Figure 1A–C) as described elsewhere.13Go–15Go As retrograde positioning of the left septal catheter through the non-coronary cusp inevitably results in mapping of the anterior part of the septum, a trans-septal approach that should allow additional mapping of the left side of the septum was also attempted in 10 patients. Deflectable decapolar catheters with 2/5/2 mm interelectrode distance with 2 mm interelectrode separation were positioned to record the His bundle electrogram on both the right and left sides of the septum. A deflectable decapolar catheter with 2/5/2 mm interelectrode separation was used for mapping the CS with the proximal pair of electrodes negotiating the ostium of the CS. Ventricular pacing was performed at a constant cycle length of 500 ms and stepwise decremented by 10 ms until AV nodal refractoriness was reached. Stimuli of 1 ms duration were delivered at twice the diastolic threshold. Care was taken to ensure catheter stability during recordings by means of continuous verification against stored fluoroscopic images and electrogram characteristics (Figure 2A and B).


Figure 1
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  		Figure 1 (A–C) Positioning of recording electrodes on the right and left septa through a trans-aortic and trans-septal approach, and the coronary sinus at the anteroposterior (A), 30° left anterior oblique (LAO) (B), and 30° right anterior oblique (RAO) (C) projections; R His, right His bundle recording electrode; TA His, trans-aortic left His bundle electrode; TS His, trans-septal left His bundle electrode.

 


Figure 2
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  		Figure 2 (A and B) Verification of catheter position. Following the last ventricular extra-stimulus at 220 ms, there are both retrograde and anterograde (seen on sinus beat as well as following drive train) His bundle potentials on the right and left His catheters through the aorta. (A) No His can be seen on the trans-septal catheter. (B) No retrograde His is recorded, but anterograde His bundle potentials are seen in the following sinus beat on all three His-recording catheters. Recordings are at 100 mm/s. I, lead I of the surface ECG; II, lead II of the surface ECG; R His, right His bundle recording electrode; TA His, trans-aortic left His bundle recording; TS His, trans-septal left His bundle recording; CS, coronary sinus.

 
Bipolar electrograms were filtered at 30–500 Hz, amplified at gains of 20–80 mm/mV, and displayed and acquired on a physiological recorder (Bard LabSystem Duo and Pro; Bard, Billerica, MA, USA), together with surface electrocardiograms. All measurements were accomplished at a speed of 200 mm/s using the on-line automated caliper system. Measurements were analysed by two different investigators at separate time intervals to assess inter-observer reproducibility. To assess temporal reproducibility, all measurements were made during repeated episodes of right ventricular pacing.

Definitions
Stimulus to atrium (St-A) intervals at constant pacing cycle lengths were measured from the stimulus artefact to the initial deflection of the atrial electrogram on the His bundle recording. Stimulus to atrium values obtained at retrograde VA maximal conduction decrement (St-Amax D) were also recorded. Ventriculo-atrial conduction jumps or maximum decrement associated with change of retrograde atrial activation sequence were considered to indicate conduction via AV nodal inputs that engage fibres with slow pathway conduction properties (Figure 3). Retrograde conduction jumps were diagnosed using the criterion of an increase of at least 50 ms in the VA interval for a 10 ms decrease in the ventricular coupling interval.10Go For comparative purposes, the difference ({Delta}St-A) between St-A and St-Amax D was also used as a measure of slow pathway conduction.13Go Post-ablation, St-A values obtained at constant pacing and at maximal retrograde VA conduction decrement were measured.


Figure 3
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  		Figure 3 Shift of the earliest retrograde atrial activation sequence at retrograde conduction jump. During constant ventricular pacing, atrial activation on the right His precedes that recorded at other His catheters. At decremental retrograde conduction (S1–S2=280 ms), the left (trans-aortic) atrial activation slightly precedes that of the right (216 compared with 218 ms) (left panel). At retrograde conduction jump (S1–S2=270 ms), the earliest atrial activation is recorded on the left septum by the trans-aortic electrode and precedes that of the right His by 12 ms (259–247 ms) (right panel). At maximum conduction decrement (S1–S2=240 ms), this difference became 19 ms, as indicated in Figure 5. Recordings are at 200 mm/s. Abbreviations are as in Figure 2.

 
Statistical analysis
Differences between St-A measured from the His bundle electrogram recorded from the right septum (R His) and the His bundle electrogram recorded from the left septum (TA His), and between St-A measured from R His and proximal coronary sinus electrode (pCS), were evaluated through the sign-rank test. This analysis was repeated for St-Amax D and {Delta}St-A. Intra-observer reproducibility of activation patterns was evaluated using the Bland–Altman method,16Go which indicates the smallest detectable difference (i.e. the amount of detectable change above the random measurement error). The 95% confidence interval was estimated using the method described by Shrout and Fleiss.17Go Concordance between observers was assessed using the kappa coefficient. All reported P-values are based on two-sided tests and compared with a significant level of 5%. SPSS version 11.0 (SPSS Inc., USA) software was used for all statistical calculations.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Study limitations
 Acknowledgements
 References
 
Electrophysiological study and ablation
Nineteen patients (11 men) with a median age of 41 years (range: 32–51) were studied before and after successful completion of the ablation procedure. All patients had normal left ventricular function, without evidence of underlying structural heart disease. Atrioventricular nodal conduction jumps and typical slow–fast AVNRT were reproducibly induced by atrial pacing in all patients. Ventricular pacing induced tachycardia in only two patients. Recording of a reproducible His bundle electrode from the trans-aortic approach was feasible in 18 patients. Recording of the His bundle electrogram from the trans-septal catheter was possible in only three out of the 10 patients in whom the technique was applied, despite prolonged mapping efforts. Comparisons between right and left His recordings, therefore, were mainly made by considering the left His recorded from the trans-aortic electrode. Slow pathway ablation was successfully accomplished in all patients, with elimination of inducibility of tachycardia and prevention of induction of echo beats. Continuous VA nodal conduction curves were documented in all patients after successful ablation.

Slow pathway retrograde conduction
Pre-ablation
Pre-ablation, three patterns of retrograde conduction were noted. In eight patients (group 1), decremental retrograde VA conduction without jumps or discontinuities was recorded (Figure 4). In six patients (group 2), typical retrograde conduction jumps with a discontinuous conduction curve were demonstrated (Figure 5). In the remaining four patients (group 3), there was minimal prolongation of St-A times (Figure 6). Induction of tachycardia with ventricular pacing was possible in two patients from group 3. Stimulus to atrium and St-Amax D intervals with ventricular extra-stimulation are presented in Tables 1–3. Considering {Delta}St-A times, there were significantly longer {Delta}St-A intervals on the right His compared with the left His (122 ± 25 vs. 110 ± 33 ms, P = 0.02, respectively) in group 1 and group 2 (140 ± 23 vs. 110 ± 35 ms, P = 0.03), but not in group 3 (10 ± 4 vs. 13 ± 8 ms, P = 0.35). No statistically significant differences were seen in {Delta}St-A intervals on the right His compared with those on the pCS in group 1 (122 ± 25 vs. 118 ± 20 ms, P = 0.10), group 2 (140 ± 23 vs. 115 ± 47 ms, P = 0.21), and group 3 (10 ± 4 vs. 10 ± 4 ms, P = 0.72).


Figure 4
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  		Figure 4 Example of decremental retrograde conduction. Following the last ventricular extra-stimulus at 220 ms, there is a shift of retrograde atrial activation from the right to the left side of the septum, and {Delta}St-A on the right His is 232–112 = 120 ms, whereas in the left His becomes 211–108 = 103 ms. Recordings are at 200 mm/s. Abbreviations are as in Figure 2.

 


Figure 5
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  		Figure 5 Example of discontinuous retrograde conduction. Following the last ventricular extra-stimulus at 240 ms, there is a shift of the earliest retrograde atrial activation from the right to the left side of the septum, and {Delta}St-A is 152 ms (278–126) on the right and 129 ms (259–130) on the left His. Recordings are at 200 mm/s. Abbreviations are as in Figure 2.

 


Figure 6
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  		Figure 6 Example of non-decremental retrograde conduction. Following the last ventricular extra-stimulus, there is no shift of retrograde atrial activation sequence, and {Delta}St-A is 8 ms on the right and 11 ms on the left His. Recordings are at 200 mm/s. Abbreviations are as in Figure 2.

 


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  		Table 1 Group 1. Decremental retrograde conduction

 


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  		Table 2 Group 2. Discontinuous retrograde conduction (ventriculo-atrial jumps)

 


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  		Table 3 Group 3. Non-decremental retrograde conduction

 
Post-ablation
Post-ablation, all patients demonstrated decremental VA conduction without conduction jumps (Tables 1–3 and Figure 7). Considering {Delta}St-A times, no significant differences between the right and left His were noted (77 ± 37 vs. 76 ± 33 ms, P = 0.53, respectively) in group 1, (100 ± 24 vs. 103 ± 21 ms, P = 0.35) group 2, and (63 ± 32 vs. 66 ± 33 ms, P = 0.35) group 3. Similarly, no significant differences were found between {Delta}St-A times obtained from the right His and pCS (77 ± 37 vs. 80 ± 38 ms, P = 0.26) in group 1, (100 ± 24 vs. 107 ± 18 ms, P = 0.25) group 2, and (63 ± 32 vs. 58 ± 40 ms, P = 0.35) group 3.


Figure 7
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  		Figure 7 Effect of catheter ablation. Same recording as in Figure 5. Following the last ventricular extra-stimulus at 220 ms, there is no shift of the earliest retrograde atrial activation, and {Delta}St-A is 110 ms on the right and 108 ms on the left His. Recordings are at 200 mm/s. Abbreviations are as in Figure 2.

 
Reproducibility of activation patterns
The sequence of atrial activation was reproducible during ventricular pacing, with no change in the retrograde atrial activation sequence when analysed at separate time intervals and by two different observers. Using the 95% limits of agreement that provided from the Bland and Altman method, we observed that 88% of the values were within the interval of agreement. High concordance was also found between the two observers (kappa statistic = 0.84, P < 0.01).


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Study limitations
 Acknowledgements
 References
 
Our results indicate that in patients with typical AVNRT, retrograde VA activation patterns compatible with both fast and slow pathway retrograde conduction can be observed during ventricular pacing, depending on the retrograde-effective refractory periods of the two pathways. The fact that initiation of tachycardia by ventricular pacing was possible in only two of our patients who demonstrated retrograde conduction decrement or dual pathways suggests that the retrograde refractory period of the slow pathway is usually shorter than that of the fast pathway. In 12–30% of patients with AVNRT, tachycardia can be initiated by ventricular extra-stimuli.4Go,7Go This mode of tachycardia initiation requires that the slow pathway has a retrograde refractory period longer than that of the fast pathway. Consequently, the ventricular extra-stimulus blocks in the slow pathway and is conducted over the fast one, thus preventing the demonstration of any retrograde jump or significant decrement.

When a retrograde conduction jump or maximum decrement occurs, there is a shift of retrograde activation with significantly shorter Stim-A intervals on the left septum, thus indicating that fibres from the slow pathway are primarily responsible for retrograde conduction. In this respect, our findings are compatible with the observation that the leftward inferior extension is shorter in length than the rightward inferior extension18Go and support our earlier reports that the inferior nodal extensions may play a role in slow pathway conduction.13Go–15Go Damage to this area through radiofrequency ablation resulted in abolition of these differences. Catheter ablation in the right inferoparaseptal area has been shown to affect the right inferior atrial extension.19Go In a previous case report, histopathological examination of the septum following slow pathway ablation showed a white endocardial patch at the site of ablation in the apex of Koch's triangle, a remnant of the inferior extension beyond the scar, and also distinct endocardial thickening on the left ventricular septal surface.19Go Thus, ablation targeting the slow pathway from the right side of the septum may well affect the left nodal extension as well. These observations provide a rationale for the well-documented observation that a successful ablation procedure may not result in complete slow pathway elimination.20Go–22Go

Our data provide further evidence in support of the initial hypothesis of Becker and co-workers13Go–15Go,18Go supporting the role of the inferior AV nodal extensions as the anatomic substrate of the slow pathway in human.


   Study limitations
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Study limitations
Acknowledgements
 References
 
First, our patient numbers are small to allow detailed comparisons between the three groups. Perhaps unavoidably, the nature of this study had made recruitment extremely difficult. Secondly, our findings depend on conventional catheter mapping techniques, and we cannot exclude subtle catheter movements affecting our results. Nevertheless, retrograde activation patterns were shown to be consistent and reproducible. Thirdly, while performing right ventricular pacing, it may be difficult to obtain recordings of the retrograde His bundle potential. In the literature, retrograde conduction properties of the fast and slow pathways have been derived indirectly by analysing the conduction curves (V1–V2/A1–A2). Thus, in cases of discontinuous retrograde curves, the longest V1–V2 interval in which conduction fails in the fast pathway is assumed to be the retrograde-effective refractory period of the fast pathway, and the shortest attainable A1–A2 interval on the fast pathway conduction curves is assumed to be its functional refractory period. Similarly, analysis of curves left of the discontinuity, which represent slow pathway conduction, provides the refractory periods of the slow pathway.4Go This method assumes that no other causes of discontinuities in VA conduction, such as intraventricular conduction delays, exist. Of course, retrograde refractoriness of the His-Purkinje system may also be an important factor with respect to VA conduction patterns. Anatomic slow pathway ablation, however, does not affect conduction in the His bundle.

In summary, our study has shown that in patients with typical AVNRT, VA activation patterns compatible with both fast and slow pathway retrograde conduction can be obtained. Retrograde conduction through the slow pathway results in the earliest retrograde atrial activation on the left side of the septum, and catheter ablation in the right inferoparaseptal area results in abolition of this pattern. These findings are compatible with the concept of slow pathway conduction by means of the inferior AV nodal extensions.


   Acknowledgements
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Study limitations
 Acknowledgements
References
 
We are grateful to D. Panagiotakos, PhD, and G. Kurlaba, BSc, for their help with statistical analysis.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Study limitations
 Acknowledgements
 References
 
[1] Wu D, Denes P, Amat-y-Leon F, Dhingra R, Wyndham CR, Bauernfeind R, et al. Clinical, electrocardiographic and electrophysiologic observations in patients with paroxysmal supraventricular tachycardia. Am J Cardiol (1978) 41:1045–51.[CrossRef][Web of Science][Medline]

[2] Gomes JAC, Dhatt MS, Damato AN, Akhtar M, Holder CA. Incidence, determinants and significance of fixed retrograde conduction in the region of the atrioventricular node: evidence for retrograde atrioventricular nodal bypass tracts. Am J Cardiol (1979) 44:1089–98.[CrossRef][Web of Science][Medline]

[3] Wu D. Dual atrioventricular nodal pathway: a reappraisal. PACE (1982) 5:72–7.[Medline]

[4] Wu D, Kou HC, Yeh SJ, Lin FC, Hung JS. Determinants of tachycardia induction using ventricular stimulation in dual pathway atrioventricular nodal reentrant tachycardia. Am Heart J (1984) 108:44–55.[CrossRef][Web of Science][Medline]

[5] Sung RJ, Waxman HL, Saksena S, Juma Z. Sequence of retrograde atrial activation in patients with dual atrioventricular nodal pathways. Circulation (1981) 64:1059–67.[Abstract/Free Full Text]

[6] Reddy CP, McAllister RG Jr. Effect of verapamil on retrograde conduction in atrioventricular nodal reentrant tachycardia. Am J Cardiol (1984) 54:535–43.[CrossRef][Web of Science][Medline]

[7] Lee PC, Tai CT, Hwang B, Hsieh MH, Tsai CF, Chiang CE, et al. The electrophysiologic characteristics in patients with only ventricular-pacing inducible slow-fast form atrioventricular nodal reentrant tachycardia. J Interv Card Electrophysiol (2005) 14:153–7.[CrossRef][Web of Science][Medline]

[8] Lee PC, Hwang B, Tai CT, et al. The electrophysiological characteristics in patients with ventricular stimulation inducible fast-slow form atrioventricular nodal reentrant tachycardia. Pacing Clin Electrophysiol (2006) 29:1105–11.[CrossRef][Medline]

[9] Lockwood D, Otomo K, Wang Z. Electrophysiologic characteristics of atrioventricular nodal reentrant tachycardia: implications for the reentrant circuits. In: Cardiac Electrophysiology: From Cell to Bedside—Zipes DP, Jalife J, et al, eds. (2004) 3rd ed. Philadelphia, PA: W.B. Saunders Company. 537–57.

[10] Katritsis D, Camm AJ. Classification and differential diagnosis of atrioventricular nodal reentrant tachycardia. Europace (2006) 8:29–36.[Abstract/Free Full Text]

[11] Haissaguerre M, Gaita F, Fischer B, Commenges D, Montserrat P, d'Ivernois C, et al. Elimination of atrioventricular nodal reentrant tachycardia using discrete slow potentials to guide application of radiofrequency energy. Circulation (1992) 85:2162–75.[Abstract/Free Full Text]

[12] Kalbfleisch SJ, Strickberger SA, Williamson B, Vorperian VR, Man C, Hummel JD, et al. Randomized comparison of anatomic and electrogram mapping approaches to ablation of the slow pathway of atrioventricular node reentrant tachycardia. J Am Coll Cardiol (1994) 23:716–23.[Abstract]

[13] Katritsis D, Becker A, Ellenbogen K, Giazitzoglou E, Korovesis S, Karabinos I, et al. The right and left inferior extensions of the atrioventricular node may represent the anatomic substrate of the slow pathway in the human. Heart Rhythm (2004) 1:582–6.[CrossRef][Web of Science][Medline]

[14] Katritsis DG, Ellenbogen KA, Becker AE. Atrial activation during atrioventricular nodal reentrant tachycardia: studies on retrograde fast pathway conduction. Heart Rhythm (2006) 3:993–1000.[CrossRef][Web of Science][Medline]

[15] Katritsis DG, Becker AE, Ellenbogen KA, Giazitzoglou E, Korovesis S, Camm AJ. Effect of slow pathway ablation in atrioventricular nodal reentrant tachycardia on the electrophysiologic characteristics of the inferior atrial inputs to the human atrioventricular node. Am J Cardiol (2006) 97:860–5.[CrossRef][Web of Science][Medline]

[16] Bland JM, Altman DG. Statistical methods for assessing agreement between two methods for clinical measurement. Lancet (1986) 1:307–10.[CrossRef][Web of Science][Medline]

[17] Shrout PE, Fleiss JL. Intraclass coefficients: uses in assessing rater reliability. Psychol Bull (1979) 86:420–8.[CrossRef][Web of Science][Medline]

[18] Inoue S, Becker AE. Posterior extensions of the human compact atrioventricular node: a neglected anatomic feature of potential clinical significance. Circulation (1998) 97:188–93.[Abstract/Free Full Text]

[19] Inoue S, Becker AE, Riccardi R, Gaita F. Interruption of the inferior extension of the compact atrioventricular node underlies successful radio frequency ablation of atrioventricular nodal reentrant tachycardia. J Interv Card Electrophysiol (1999) 3:273–7.[CrossRef][Web of Science][Medline]

[20] Kalbfleisch SJ, Strickberger SA, Williamson B, Vorperian VR, Man C, Hummel JD, et al. Randomized comparison of anatomic and electrogram mapping approaches to ablation of the slow pathway of atrioventricular node reentrant tachycardia. J Am Coll Cardiol (1994) 23:716–23.[Abstract]

[21] Strickberger SA, Daoud E, Niebauer M, Williamson BD, Man KC, Hummel JD, 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]

[22] Jackman WM, Beckman KJ, McClelland JH, Wang X, Friday KJ, Roman CA, et al. Treatment of supraventricular tachycardia due to atrioventricular nodal reentry, by radiofrequency catheter ablation of slow-pathway conduction. N Engl J Med (1992) 327:313–8.[Abstract]


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