(Circulation. 1996;93:960-968.)
© 1996 American Heart Association, Inc.
Articles |
Heterogeneity of Retrograde Fast-Pathway Conduction Pattern in Patients With Atrioventricular Nodal Reentry Tachycardia
Observations by Use of Simultaneous Multisite Catheter Mapping of Koch's Triangle
From Harvard-Thorndike Institute of Electrophysiology, Cardiology Division, Beth Israel Hospital, Harvard Medical School, Boston, Mass.
Correspondence to Mark E. Josephson, MD, Cardiovascular Division, Beth Israel Hospital, 330 Brookline Ave, Boston, MA 02215.
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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Background Selective ablation of either the fast or the slow pathway resulting in cure of AV nodal reentry tachycardia (AVNRT) has led to the concept that these pathways are discrete, anatomically defined structures. We hypothesized that if a discrete retrograde fast pathway exists, it should be possible to record a single focus of early atrial activation near the apex of Koch's triangle, with sequential spread of depolarization to the rest of the atria.
Methods and Results We evaluated 46 patients (33 women, 13 men; mean age, 45±17 years) undergoing electrophysiology study and catheter ablation for typical AVNRT. Retrograde atrial activation during AVNRT (337±43 ms) and ventricular pacing at a similar cycle length (352±51 ms) was recorded in the region of Koch's triangle with a decapolar catheter in the His bundle position, a multipolar catheter in the coronary sinus, and a deflectable quadripolar catheter along the tricuspid annulus anterior to the coronary sinus ostium. Earliest atrial activation was recorded at the apex of the triangle of Koch in 38 patients during ventricular pacing and in 43 patients during AVNRT. A broad wave front of atrial activation was recorded in 17 patients during ventricular pacing and in 26 patients during AVNRT. During AVNRT, only 2 patients had a single early site with focal and sequential activation along the tendon of Todaro. There was concordance in the pattern of atrial activation between ventricular pacing and AVNRT in only 21 of 46 patients.
Conclusions Retrograde atrial activation over the fast pathway is heterogeneous within Koch's triangle and the coronary sinus, both for the entire population and for individual patients during different modes of activation. These data do not support the concept of an anatomically discrete retrograde fast pathway.
Key Words: tachycardia • atrioventricular node • reentry
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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The success of catheter ablation in curing AV nodal reentry tachycardia (AVNRT) is now well established.1 2 3 4 5 6 7 8 9 10 11 Techniques for selective ablation of either the fast5 7 8 11 or the slow1 2 3 4 8 9 10 11 pathway have been reported, and spatial separation of successful ablation sites has fostered the concept that the fast and slow pathways are discrete anatomic structures.
Evidence exists, however, that a simplistic construct of anatomically defined pathways is not correct. Successful ablation of the fast pathway has been reported with use of a posterior approach, and slow-pathway conduction has been eliminated with ablation at anterior sites.2 11 Furthermore, histological studies have not confirmed the presence of discrete fast and slow AV nodal pathways. The posterior and anterior "inputs" into the region of the compact AV node are composed of a heterogeneous mixture of working myocardial cells and transitional cells.12 13 The manner in which atrial cells are coupled to these transitional cells is unknown. In fact, electrophysiological and anatomic correlates of rabbit and dog AV junction suggest that transitional cells enter the compact node.14 15 Thus, although the overall success rate for cure of AVNRT by either approach is beyond question, a precise anatomic and physiological correlation to explain the mechanism of the tachycardia is lacking.
The purpose of the present study was to gain further insight into the details of retrograde fast-pathway conduction in patients with typical AVNRT by use of simultaneous multisite catheter mapping of Koch's triangle and adjacent coronary sinus. We hypothesized that if a discrete retrograde fast pathway exists, it should be possible to record a single focus of early atrial activation with sequential spread to the rest of the atria. In contrast, variability in the site of earliest retrograde atrial activation and discordance in atrial activation during AVNRT and ventricular pacing would suggest the presence of a functionally determined circuit with multiple and heterogeneous potential pathways of retrograde conduction.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Study Population
The study population included 46 patients undergoing electrophysiology study and catheter ablation for typical AVNRT. AVNRT was defined by previously published standard criteria.16 17 18 19 20 There were 33 women and 13 men, with a mean age of 45±17 years. Forty-two patients had no identifiable structural heart disease, 3 had coronary artery disease, and 1 had dilated cardiomyopathy. One patient had mild hypertension. All studies were performed in the postabsorptive state after all antiarrhythmic medications had been stopped for at least five half-lives. Informed written consent was obtained from each patient before the study in accordance with institutional guidelines.
Atrial Recording Sites
Transvenous intracardiac
multielectrode catheters were
positioned as follows: Quadripolar catheters with 5-mm interelectrode
distance were positioned in the high right atrium and the right
ventricle. A decapolar catheter with 2-mm interelectrode distance was
placed across the tricuspid valve and positioned to obtain the largest
His bundle deflection in the distal electrode pair, and the remaining
electrodes were positioned in contact with the atrium along the tendon
of Todaro (His bundle electrogram [HBE] catheter). Efforts were made
to ensure that atrial potentials could be recorded from each
bipolar pair during sinus rhythm, ventricular pacing, and
AVNRT. A hexapolar, octapolar, or decapolar catheter with 5-mm
interelectrode distance was placed in the coronary sinus with
the proximal electrode at the ostium. A steerable quadripolar catheter
(interelectrode distance, 2/5/2 mm) was positioned along the tricuspid
annulus approximately at the level of the coronary sinus
ostium. The ratio of atrial:ventricular electrogram
amplitude recorded from the distal electrode pair during sinus
rhythm at this site was <1 for all patients. The positioning of this
catheter was not dictated by the presence of slow-pathway
potential, nor was it necessarily at the site of subsequent successful
ablation. Rather, this position was chosen anatomically to standardize
the recording site for the entire study population. The
distance between the proximal HBE recording electrodes and the
closest electrodes on the catheter in the posterior triangle of Koch
ranged from 1 to 3 cm, with an average of 2 cm. Data were
analyzed from the five HBE bipolar pairs, the distal
slow-pathway electrode pair, and the coronary sinus bipolar
pair that recorded the earliest atrial electrogram. A schematic
diagram of the recording sites relative to Koch's triangle is
presented in Fig 1
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Measurement of Atrial Activation
Bipolar electrograms were
filtered at 40 to 400 Hz. An
analog to digital sampling rate of 1000 Hz was applied before digital
storage and analysis. Ventricular pacing was
performed at twice diastolic threshold with a programmable
stimulator (Bloom Assoc). Measurements of atrial activation were made
at a sweep speed of 200 mm/s by use of electronic calipers on a digital
electrophysiology recording system in 32 patients; in the
remaining 14 patients, analog signals sampled at 4000 Hz were
analyzed by handheld calipers. Atrial activation was
recorded during ventricular pacing and AVNRT at similar
cycle lengths in each patient. Recordings were performed first
during AVNRT and immediately thereafter during ventricular
pacing to avoid changes in autonomic tone. In those patients who
required isoproterenol and/or atropine for initiation of sustained
AVNRT, measurements of atrial activation were made in close temporal
proximity after these agents had been administered.
Measurements were
made with the onset of the atrial electrogram. There
was no difference in the qualitative patterns of retrograde atrial
activation when the largest deflection that crossed the isoelectric
baseline was used. When atrial and ventricular activation
occurred simultaneously, single or double
ventricular premature depolarizations were delivered to
separate the individual components (Fig 2). Care was
taken to ensure that the ventricular premature
depolarization did not affect the tachycardia circuit.
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The site of earliest atrial activation was recorded during AVNRT and during ventricular pacing for each patient. This site was assigned a reference time of zero, and the timing of all other sites was measured relative to this.
To characterize the pattern of atrial activation, the following categories were defined along the His bundle catheter: (1) sequential wave front: earliest atrial activation at one or two adjacent bipole pairs with sequential spread to the remaining electrode pairs; (2) broad wave front: three or more adjacent bipolar pairs of the HBE catheter within 5 ms.
Over the entire Koch's triangle, the following categories were defined: (1) multiple early sites: (a) two or more activation times along the HBE catheter within 5 ms separated by two later sites, and (b) one or more sites on the HBE catheter and any other catheter within 5 ms; (2) single early site: sites that did not fulfill criteria for multiple early sites.
For each patient, the site of earliest atrial activation as well as the qualitative pattern of atrial activation over the Koch's triangle was compared during ventricular pacing and AVNRT.
To ensure the reproducibility of the measurement, tracings were analyzed in a blinded manner three times by two different investigators 2 weeks apart. The retrograde atrial activation sequence was assessed by use of at least three beats with stable cycle length. Although differences in the absolute timing of atrial electrograms could differ up to 10 ms, qualitative assessment of relative atrial activation did not vary between investigators.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Activation times at each site and the qualitative patterns of atrial activation during both ventricular pacing and tachycardia are shown in Table 1
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Sites of Earliest Atrial Activation
The sites of earliest
atrial activation during
ventricular pacing and AVNRT are summarized in Fig 3.
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During Ventricular Pacing
Earliest atrial activation was
recorded in one of the two
distal HBE electrode pairs in 38 patients (82.6%), whereas activation
in the remaining 8 patients was distributed evenly over the other
recording sites. Multiple sites of earliest atrial activation
were recorded in 10 patients (21.7%). Earliest atrial activation
was simultaneous in the coronary sinus and in the
HBE in 2 patients; in the coronary sinus, in the HBE, and at
the base of the triangle of Koch in 4 patients; and in the HBE and at
the base of the triangle of Koch in 4 patients (Fig 4).
In 1 patient, the earliest atrial activation was recorded at the
base of the triangle of Koch.
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During AVNRT
Earliest
atrial activation was recorded in one of the
two distal HBE electrode pairs in the majority of patients (40 of 46;
87%). However, multiple sites of earliest atrial depolarization were
found in 8 patients (17.4%), and in 2 patients, the earliest site was
in the coronary sinus or at the base of the triangle of Koch
(Fig 3
).
In only 18 (39.1%) of the 46 patients, the earliest atrial site of activation was identical during ventricular pacing and typical AVNRT.
Pattern of Atrial Activation
During Ventricular Pacing
Twenty-nine patients demonstrated a sequential pattern in the
HBE catheter, whereas a broad wave front was recorded in 17
patients. Fifteen patients (32.6%) had only a single early site of
atrial activation, and 31 patients (67.4%) demonstrated multiple sites
of early breakthrough in the area of the triangle of Koch.
During AVNRT
Twenty patients had a sequential
pattern and 26 patients had
a broad wave front of activation. Fifteen patients (32.6%) showed
early activity at a single site, and 31 patients (67.4%) had multiple
early breakthrough sites recorded over the area of the triangle of
Koch.
Only 21 patients (45.7%) demonstrated concordance in the qualitative pattern of atrial activation within Koch's triangle during both AVNRT and ventricular pacing. Representative intracardiac recordings from 2 patients with discordant patterns and from 1 patient with a concordant pattern of retrograde atrial activation between AVNRT and ventricular pacing are presented in Figs 4, 5, and 6.
Table 2 summarizes the qualitative patterns of atrial
activation during ventricular pacing and AVNRT. Note that
the pattern of a single early site with sequential activation along the
HBE catheter was seen in only six patients during
ventricular pacing and in two patients during AVNRT.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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The major finding of this study is that fast retrograde atrial activation is heterogeneous within the area of Koch's triangle in patients with AVNRT both during tachycardia and during ventricular pacing. We hypothesized that if the retrograde fast pathway is an anatomically discrete structure similar to an accessory pathway, then atrial activation should demonstrate a single early site with focal and sequential spread proceeding from the apex of Koch's triangle to posterior atrial sites. Our results showed, however, that this type of pattern was rare (ventricular pacing=6 patients, AVNRT=2 patients). In fact, multiple sites of early breakthrough in the triangle of Koch as well as a broad wave front of activation in the His bundle catheter were frequent (31 and 17 patients during ventricular pacing, 31 and 26 patients during AVNRT, respectively). Since discordance in the retrograde atrial activation sequence was present between ventricular pacing and AVNRT, the retrograde fast pathway appears to be not only variable in different patients but also dynamic for each individual.
Previous Studies
Early studies on retrograde atrial
activation during
ventricular pacing and typical AVNRT were performed with
use of bipolar recordings of the right atrial septum, high
lateral right atrium, and "proximal" and "distal"
coronary sinus (neither of which was specifically localized or
standardized). Retrograde activation measured in a small number of
patients revealed that the right atrial septum was the earliest site of
retrograde atrial activation and preceded activation of the
"proximal" coronary sinus and high lateral right
atrium.21 22 The sequence of retrograde atrial
activation
was further characterized by Sung et al23 in seven
patients with dual AV nodal pathways during ventricular
pacing and typical AVNRT. Earliest atrial activation was recorded
at the apex of the triangle of Koch in all of the patients.
Recently, McGuire et al24 reported results of intraoperative high-resolution mapping of Koch's triangle in patients with AVNRT. These investigators used a plaque with 60 unipolar electrodes to record atrial activation in the region surrounding the AV node in 13 patients undergoing surgery for AVNRT. In 9 patients with typical AVNRT in whom atrial activation was recorded during ventricular pacing, a single site of earliest activation was seen in 7 patients. In 1 patient, however, almost the entire area of Koch's triangle was activated simultaneously. In 2 patients, dual sites of earliest atrial activation were observed. Recordings made during AVNRT demonstrated earliest breakthrough anteriorly at the apex of Koch's triangle in 9 of 10 patients.
Current Results
Our series demonstrated that multiple sites
of earliest atrial
activation were present in 21.7% of patients during
ventricular pacing and in 17.4% of patients during typical
AVNRT, with only 39.1% concordance in the site of earliest activation.
We defined multiple sites of early breakthrough to describe a pattern
in which atrial depolarization at the coronary sinus or
slow-pathway region was recorded too early to have been a
consequence of sequential activation from the apex of the triangle of
Koch. By this definition, multiple sites of early breakthrough were
recorded in two thirds of patients during both
ventricular pacing and AVNRT. Moreover, a broad wave front
of HBE activation was recorded in 37% and 56.5% of patients
during ventricular pacing and AVNRT, respectively.
Concordance in the pattern of activation was present in only 45.7%
of the patients.
Several factors may explain the discrepancies between previous studies and our results. Previous series that used catheter mapping were limited by the small number of recording sites used.21 22 23 Therefore, the possibility of multiple areas of breakthrough could not be excluded. In the McGuire series,24 the use of unipolar recordings may have confounded results by the detection of far-field signals. Even though they did not specifically address secondary breakthrough sites, they did note qualitative differences in retrograde conduction in different patients, similar to our findings. Furthermore, earliest retrograde atrial activation was recorded over 6 mm or more (simultaneous in three poles 3 mm apart) in several patients who showed intracardiac recordings of typical AVNRT.24 This corresponds to our definition of a broad wave front of activation and supports the presence of heterogeneity of fast retrograde conduction. The isochrons drawn from such maps demonstrate anisotropic propagation, not a sequential loop of activation.
Many investigators have emphasized the importance of slow-pathway potentials in localizing the anatomic site of the slow pathway.1 3 Although it has been theorized that these potentials represent activation of a structurally discrete pathway of slow conduction, recent observations contradict this hypothesis. Josephson25 reported that in 30% of patients, ablation at sites just above the coronary sinus in the posterior triangle, an area in which slow-pathway potentials were often recorded, resulted in elimination of fast-pathway conduction. McGuire et al26 demonstrated a similar area over which slow-pathway potentials could be recorded in dogs. These potentials represented far-field potentials from the atrial septum and deeper local potentials from transitional cells close to the tricuspid annulus and did not correspond to a well-defined area of slow conduction. Our results provide confirmation as to the heterogeneity of conduction properties at sites in the posterior aspect of the Koch's triangle and may further undermine the significance of high-frequency potentials recorded at these sites as specific electrophysiological markers.
Clinical Implication
Despite extensive experience in radio
frequency ablation of AVNRT
during the past several years, many clinical observations relating to
fast- and slow-pathway conduction remain unexplained. Complete
heart block complicates up to 1% of
cases1 2 3 4 when the
slow pathway is targeted and up to 2% to 10% of cases when the fast
pathway is targeted.7 27 28 Elimination
of
fast-pathway conduction has been reported at posterior sites of
ablation,25 and complete heart block can complicate cases
in which ablation is performed distant from the compact AV
node.1 2 3 4 These
observations are difficult to reconcile
with a model of AVNRT in which distinct pathways of conduction exist in
anatomically determined sites. Our results emphasize the anatomic
heterogeneity and potentially dynamic properties of
retrograde AV nodal conduction and stand in contrast to a strictly
anatomically determined model. This complexity may underlie the
unexpected outcomes observed during AVNRT radiofrequency ablation.
Study Limitations
Subtle degrees of catheter movement between
AVNRT and
ventricular pacing protocols potentially could have
affected the comparison of results. However, to minimize this
possibility, frequent fluoroscopic images and review of electrogram
characteristics were obtained, with concurrence of stability by two
observers. Slight repositioning was occasionally necessary and was
guided by stored fluoroscopic images and electrogram morphology.
We systematically introduced ventricular premature depolarizations during AVNRT to advance the ventricular electrogram and to fully expose the atrial electrogram. The absolute timing of the atrial electrogram could vary by up to 10 ms between the different investigators during the different measurements. However, the qualitative assessment of the relative atrial activation and the pattern assigned did not differ.
Although retrograde atrial activation during ventricular pacing and during typical AVNRT were analyzed at cycle lengths that were as similar as possible, these cycle lengths were not identical for all the patients. However, conduction over the fast pathway was ensured through analysis of the retrograde ventriculoatrial conduction curves.
Conclusions
Successful cure of AVNRT is now possible in
nearly all patients.
However, the mechanism of the tachycardia is still not
fully understood. Whereas a single radiofrequency lesion may cure the
tachycardia, retrograde AV nodal conduction is highly
complex. The analogy of retrograde AV nodal conduction to accessory
pathway conduction appears to be overly simplistic. Our data and those
of other investigators have shown that retrograde atrial activation is
heterogeneous and not fully determined by discrete anatomic
pathways. We believe that these data are most consistent with a
subatrial reentrant circuit (which may be temporally "fixed"
during the tachycardia) with variable propagation to
the atrium due to heterogeneous nodal-atrial coupling.
Further studies are needed to better define the determinants of this
variability in retrograde AV nodal conduction.
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Acknowledgments |
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Dr Anselme was supported by a grant from La Federation Francaise de Cardiologie. The authors gratefully acknowledge the excellent technical assistance of Philippa Beswick and the active participation of Panos Papageorgiou, Noel Boyle, and Claudio Schuger.
Received June 23, 1995; revision received October 11, 1995; accepted October 16, 1995.
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References |
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TopAbstractIntroductionMethods Results Discussion References |
|---|
1. Jackman WM, Beckman KH, McClelland JH, Wang X, Friday K, Roman C, Moulton K, Twidale N, Hazlitt H, Prior M, Oren J, Overholt E, Lazzara R. Treatment of supraventricular tachycardia due to atrioventricular nodal reentry by radiofrequency ablation of slow-pathway conduction. N Engl J Med. 1992;327:313-318. [Abstract]
2.
Kay GN, Epstein AE, Dailey SM, Plumb VJ.
Selective radiofrequency ablation of the slow pathway for the treatment
of atrioventricular nodal reentrant
tachycardia: evidence for involvement of perinodal
myocardium within the reentrant circuit.
Circulation. 1992;85:1675-1688.
3.
Haissaguerre M, Gaita F, Fisher B, Commenges D,
Montserrat P, d'Ivernois C, Lemetayer P, Warin J. Elimination
of atrioventricular nodal reentrant
tachycardia using discrete slow potentials to guide
application of radiofrequency energy.
Circulation. 1992;85:2162-2175.
4.
Jazayeri MR, Hempe SL, Sra JS, Dhala AA, Blank Z,
Deshpande SS, Avitall B, Krum DP, Gilbert CJ, Akhtar M.
Selective transcatheter ablation of the fast and slow
pathways using radiofrequency energy in patients with
atrioventricular nodal reentrant
tachycardia. Circulation. 1992;85:1318-1328.
5.
Epstein L, Scheinman M, Langberg J, Chilson D,
Goldberg H, Griffin J. Percutaneous catheter
modification of the atrioventricular node: a potential
cure for atrioventricular nodal
tachycardia. Circulation. 1989;80:757-768.
6. Goy J, Fromer M, Schaepfer J, Kappenberger L. Clinical efficacy of radiofrequency current in the treatment of patients with atrioventricular node reentrant tachycardia. J Am Coll Cardiol. 1990;16:418-423. [Abstract]
7.
Lee M, Morady F, Kadish A, Schamp DJ, Chin MC,
Scheinman MM, Griffin JC, Lesh MD, Pederson D, Goldberger J, Calkins H,
de Buitleir M, Kou WH, Rosenheck S, Sousa J, Langberg JJ.
Catheter modification of the atrioventricular junction
using radiofrequency energy for control of
atrioventricular nodal reentry
tachycardia. Circulation. 1991;83:827-835.
8. Mitrani RD, Klein LS, Hackett FK, Zipes DP, Miles WM. Radiofrequency ablation for atrioventricular node reentrant tachycardia: comparison between fast (anterior) and slow (posterior) pathway ablation. J Am Coll Cardiol. 1993;21:432-441. [Abstract]
9. Wathen M, Natale A, Wolfe K, Yee R, Newman D, Klein G. An anatomically guided approach to atrioventricular node slow pathway ablation. Am J Cardiol. 1992;70:886-889. [Medline] [Order article via Infotrieve]
10. Wu D, Yeh SJ, Wang CC, Wen MS, Lin FC. A simple technique for selective radiofrequency ablation of the slow pathway in atrioventricular node reentrant tachycardia. J Am Coll Cardiol. 1993;21:1612-1621. [Abstract]
11.
Langberg JJ, Leon A, Borganelli M, Kalbfleisch SJ,
El-Atassi R, Calkins H, Morady F. A randomized, prospective
comparison of anterior and posterior approaches to radiofrequency
catheter ablation of atrioventricular nodal reentry
tachycardia. Circulation. 1993;87:1551-1556.
12. Becker AE, Anderson RH. Morphology of the human atrioventricular junctional area. In: Wellens HJJ, Lie KI, Janse MJ, eds. The Conduction System of the Heart: Structure, Function and Clinical Implications. Leiden, Netherlands: Stenfert Kroese BV; 1976:263-286.
13. Anderson RH, Becker AE, Brechenmacher C, Davies MJ, Rossi L. The human atrioventricular junctional area: a morphological study of the AV node and bundle. Eur J Cardiol. 1975;3:11-25. [Medline] [Order article via Infotrieve]
14.
Anderson RH, Janse MJ, van Capelle FJL, Billette J,
Becker AE, Durrer D. A combined morphologic and
electrophysiologic investigation of the rabbit
atrioventricular node. Circ
Res. 1974;35:909-922.
15. Racker DK. Atrioventricular node and input pathways: a correlated gross anatomical and histological study of canine atrioventricular junctional area. Anat Res. 1989;224:336-354. [Medline] [Order article via Infotrieve]
16. Josephson ME. Supraventricular tachycardias. In: Josephson ME, ed. Clinical Cardiac Electrophysiology. Philadelphia, Pa: Lea & Febiger; 1993:181-274.
17.
Akhtar M, Jazayeri MR, Sra J, Blanck Z, Deshpande S,
Dhala A. Atrioventricular nodal reentry:
clinical, electrophysiological, and
therapeutic considerations. Circulation. 1993;88:282-295.
18. Josephson ME, Kastor JA. Supraventricular tachycardia: mechanisms and management. Ann Intern Med. 1977;87:346-358.
19. Josephson ME. Paroxysmal supraventricular tachycardia: an electrophysiologic approach. Am J Cardiol. 1978;41:1123-1126. [Medline] [Order article via Infotrieve]
20. Akhtar M. Supraventricular tachycardias. In: Josephson ME, Wellens HJJ, eds. Tachycardias: Mechanisms, Diagnosis, Treatment. Philadelphia, Pa: Lea & Febiger; 1984:137-169.
21.
Amat-y-Leon F, Dhingra RC, Wu D, Denes P, Wyndham
C, Rosen KM. Catheter mapping of retrograde atrial activation:
observations during ventricular pacing and AV nodal
re-entrant paroxysmal tachycardia. Br
Heart J. 1976;38:355-362.
22.
Agha AS, Befeler B, Castellanos AM, Sung RJ, Castillo
CA, Myerburg RJ, Castellanos A. Bipolar catheter electrograms
for study of retrograde atrial activation pattern in patients without
pre-excitation syndromes. Br Heart J. 1976;38:641-645.
23.
Sung JR, Harvey LW, Saksena S, Juma Z. Sequence
of retrograde atrial activation in patients with dual
atrioventricular nodal pathways.
Circulation. 1981;64:1059-1067.
24.
McGuire MA, Bourke JP, Robotin MC, Johnson DC,
Meldrum-Hanna W, Nunn GR, Uther JB, Ross DL. High resolution
mapping of Koch's triangle using 60 electrodes in humans with
atrioventricular junctional (AV nodal) reentrant
tachycardia. Circulation. 1993;88:2315-2328.
25. Josephson ME. Surgical and nonsurgical ablation in the therapy of arrhythmias. In: Josephson ME, ed. Clinical Cardiac Electrophysiology. Philadelphia, Pa: Lea & Febiger; 1993:726-821.
26.
McGuire MA, de Backer JMT, Vermeulen JT, Opthof T,
Becker AE, Janse MJ. Origin and significance of double
potentials near the atrioventricular node: correlation
of extracellular potentials, intracellular potentials, and
histology. Circulation. 1994;89:2351-2360.
27. Haisaguerre M, Warin JF, Lemetayer P, Saoudi N, Guillem JP, Blanchot P. Closed-chest ablation of retrograde conduction in patients with atrioventricular nodal reentrant tachycardia. N Engl J Med. 1989;320:426-433. [Abstract]
28. Calkins H, Sousa J, el-Atassi R, Rosenheck S, de Buitleir M, Kou WH, Kadish AH, Langberg JJ, Morady F. Diagnosis and cure of the Wolff-Parkinson-White syndrome or paroxysmal supraventricular tachycardias during a single electrophysiology test. N Engl J Med. 1991;324:1612-1618.[Abstract]
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