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Tex Heart Inst J. 2010; 37(6): 706–709.
PMCID: PMC3014113

Quadruple Atrioventricular Nodal Pathways

Involved in Orthodromic Atrioventricular Reentrant Tachycardia

Abstract

Supraventricular tachycardia can be caused by multiple atrioventricular nodal pathways or atrioventricular accessory pathways. Herein, we report the case of a patient who was diagnosed with an orthodromic atrioventricular reentrant tachycardia that was caused by an unusual combination of quadruple atrioventricular nodal pathways and an atrioventricular accessory pathway. Radiofrequency catheter ablation of the accessory pathway successfully eliminated the arrhythmias and the patient's symptoms. Careful analysis of complete electrophysiologic studies can help in the diagnosis of such rare clinical presentations.

Key words: Atrioventricular node/physiopathology, cardiac electrophysiology, catheter ablation, diagnosis, differential, electrocardiography, tachycardia, atrioventricular reentry/complications/diagnosis/epidemiology/physiopathology/therapy, tachycardia, supraventricular/diagnosis, treatment outcome

The existence of either multiple atrioventricular (AV) nodal pathways or AV accessory pathways can lead to conditions that cause supraventricular tachycardia (SVT). Herein, we describe the case of a patient with an orthodromic AV reentrant tachycardia (AVRT, a form of SVT) that was caused by an unusual combination of quadruple AV nodal pathways and an AV accessory pathway.

Case Report

In 2008, a 34-year-old man was admitted to the hospital with a 5-year history of paroxysmal palpitations. A 12-lead electrocardiogram (ECG) revealed a sinus rhythm of 70 beats/min and 2 distinct changes in the PR interval and QRS complex (Fig. 1). The 1st change was a PR interval of 0.26 sec with normal QRS complexes. The 2nd change, a shortened PR interval of 0.1 sec, was associated with a widened QRS complex of 0.16 sec and an obvious delta wave that slurred the upstroke of the QRS and the secondary ST segment-T wave. We concluded that the patient had a type B intermittent pre-excitation syndrome with possible 1st-degree AV block.

figure 26FF1
Fig. 1 A 12-lead electrocardiogram indicates a type B intermittent pre-excitation syndrome, with possible 1st-degree atrioventricular block.

Transesophageal atrial pacing was used to clarify the mechanisms of the patient's symptomatic episodes. A bipolar electrode was introduced through the patient's nasal passages and was positioned within the esophagus. An esophageal electrogram and a 12-lead surface ECG simultaneously recorded changes in cardiac electrical activity. Incremental atrial pacing was begun when it reached 110 pulses/min, the interval from the stimuli to the onset of QRS complex was 140 ms, and the characteristics of the pre-excitation were progressively unmasked (Fig. 2). Tachycardia was induced when the pacing rate reached 130 pulses/min (Fig. 3). The ECG recorded a heart rate of 143 beats/min and a ventriculoatrial (VA) interval of 140 ms, which was shorter than the AV interval of 280 ms. The reentrant P (P') waves were inverted in leads I and aVL but were upright in leads II, III, and aVF. The morphology of the QRS complex was normal. The ECG, recorded after tachycardia was induced, revealed orthodromic AVRT. The sinus electrical impulse propagated in usual fashion from the atria to the AV node and the ventricles; however, the impulse then propagated in the reverse direction—from the ventricles to the atria via an accessory pathway—completing a tachycardia reentrant loop (Fig. 4). From the results of the 2 tests, we established a diagnosis of type B pre-excitation syndrome and orthodromic AVRT with a rare finding of upright retrograde P' waves.

figure 26FF4
Fig. 4 A 12-lead electrocardiogram, recorded after tachycardia was induced, reveals orthodromic atrioventricular reentrant tachycardia.
figure 26FF3
Fig. 3 A 12-lead electrocardiogram, obtained when tachycardia was induced at an incremental atrial pacing rate of 130 pulses/min, with a resultant heart rate of 143 beats/min, a ventriculoatrial (VA) interval of 140 ms, and an atrioventricular (AV) interval ...
figure 26FF2
Fig. 2 A 12-lead electrocardiogram shows that, at an incremental atrial pacing rate of 110 pulses/min, the interval from the stimuli to the onset of QRS complex is 140 ms. The characteristics of pre-excitation are progressively unmasked.

When the tachycardia was allowed to continue for another 30 sec, its characteristics changed (Fig. 5). The rhythm became irregular and the heart rate varied; however, the P' wave remained evident. Although the VA interval was consistently 140 ms, 4 different types of AV intervals were observed: the AV1,3,5,7,9,11,13,15,17,19,21 intervals were 280 ms; the AV4,6,10,16,18 intervals were 380 ms; the AV2,8,12,20 intervals were 440 ms; and the AV14 interval was 540 ms. The differences between these 4 intervals were 100, 60, and 100 ms, respectively. The changes in interval were obvious, and the ease with which the tachycardia was induced and maintained clearly excluded the influence of vagal tone. The different AV intervals repeated themselves with no Wenckebach periodicity, and the VA interval remained constant at 140 ms. On the basis of these findings, we inferred that quadruple AV nodal pathways precipitated the patient's SVT.

figure 26FF5
Fig. 5 In the esophageal electrogram and recordings of lead II and lead V1 that were all obtained during tachycardia, rhythm becomes irregular and heart rate varies; however, the reentrant P wave remains evident and the ventriculoatrial interval is consistently ...

In this type of tachycardia reentry circuit, anterograde conduction proceeded down the 4 AV nodal pathways at the AV intervals stated above, followed by retrograde conduction through the accessory AV connection—completing the tachycardia reentrant loop and leading to an irregular heart rhythm. In order to observe the changes more clearly, we continuously recorded lead V1 by means of surface ECG (Fig. 6). The heart rhythm changed from regular to irregular and then reverted to sinus rhythm. On the basis of these results, our diagnosis was quadruple AV nodal pathways that involved orthodromic AVRT.

figure 26FF6
Fig. 6 Continuous recording of electrocardiographic lead V1 shows rhythm changes from regular to irregular and back to sinus rhythm.

An intracardiac electrophysiologic (EP) study confirmed orthodromic AVRT that was mediated by the right posteroseptal accessory pathway. Radiofrequency catheter ablation of the accessory pathway was performed. Afterwards, no further tachycardia was induced with repetitive stimuli, 12-lead ECG showed that the pre-excitation pattern was eliminated (Fig. 7A), and intracardiac ECG revealed VA dissociation (Fig. 7B). As of October 2010, the patient had no further SVT or other arrhythmias, and he no longer needed to take antiarrhythmic medications.

figure 26FF7
Fig. 7 A) The 12-lead electrocardiogram shows elimination of the pre-excitation pattern after accessory pathway ablation. B) Intracardiac recordings reveal ventriculoatrial dissociation during burst stimulation at the cycle length of 400 ms after ablation ...

Discussion

Dual or multiple AV nodal pathways are common phenomena that could provide an EP basis for the development of irregular arrhythmia.1-3 Because of the net-like structure of the AV node, multiple and distinct pathways can easily form. These can be identified through careful EP study.4 Differences in EP attributes can lead to multiple AV nodal pathways with 3 distinct manners of conduction: anterograde, retrograde, and bidirectional.5 In a study of 500 patients who had multiple AV nodal pathways, the incidence of quadruple anterograde AV nodal pathways was 1%.4 Richter and colleagues1 reported the cases of 2 patients who had irregular SVT that was due to 3 different anterograde slow AV nodal pathways in an alternating sequence. In most patients, only 1 slow AV nodal pathway is usually operative in anterograde conduction during tachycardia. In our patient with orthodromic AVRT, the continuation of tachycardia uniquely depended upon the involvement of 4 different anterograde AV nodal pathways and 1 retrograde accessory pathway. We speculate that it is very rare for quadruple AV nodal pathways to all be involved in AVRT.

Our patient's AVRT was conducted anterograde through the 4 distinct AV nodal pathways and retrograde through the right posteroseptal accessory pathway. During the tachycardia, a regular rhythm was observed only when the anterograde conduction proceeded through the fast AV nodal pathway. However, when the anterograde conduction proceeded down all 4 AV nodal pathways, an irregular rhythm was apparent. That rhythm, which resulted from the quadruple AV nodal anterograde-conduction pathways (AV interval of 280 ms = 1st fast, 380 ms = 2nd fast, 440 ms = 1st slow, and 540 ms = 2nd slow), terminated when the retrograde P' wave conduction was stopped and the QRS complex disappeared (Fig. 6). The VA interval remained consistent at 140 ms and was significantly longer than that in AV nodal reentrant tachycardia. This means that the ventricles were also involved in the reentry circuit, which is characteristic of an orthodromic AVRT.6 Furthermore, the EP study revealed the existence of a right posteroseptal accessory pathway; and after successful accessory pathway ablation, the pre-excitation pattern was eliminated and tachycardia could not be induced. This evidence ruled out the possibility of AV nodal reentrant tachycardia; therefore, we did not perform further EP studies. Because the AV interval of the 1st fast-pathway conduction during reentrant tachycardia was 280 ms, this patient was diagnosed with a type B intermittent pre-excitation syndrome with 1st-degree AV block.

Transesophageal atrial pacing is a noninvasive means of studying cardiac EP function. It has proved to be highly effective and accurate for the characterization and diagnosis of various mechanisms of arrhythmia, especially during the induction and termination of reentrant SVT. We could not fully identify our patient's tachycardia by using surface ECG alone—using transesophageal atrial pacing and intracardiac EP enabled us to explore the mechanisms of the tachycardia thoroughly and evaluate its properties fully. Accordingly, we were able to define the appropriate treatment for our patient and to gain valuable insight into SVT that is induced through multiple AV nodal pathways. In regard to identifying rare mechanisms of arrhythmia, we emphasize the importance of carefully analyzing the results of a complete EP study—including surface ECG, transesophageal atrial pacing, and invasive EP.

Footnotes

Address for reprints: Qiaohua Li, MD, Department of Cardiology, Xiangya Second Hospital, Central South University, Changsha 410011, Hunan, PRC

E-mail: moc.anis@auhoaiq;f5000x#&il

References

1. Richter S, Berruezo A, Mont L, Boussy T, Sarkozy A, Brugada P, Brugada J. Pseudo-atrial fibrillation, rare manifestation of multiple anterograde atrioventricular nodal pathways. Am J Cardiol 2007;100(1):154–6. [PubMed]
2. Dixit S, Callans DJ, Gerstenfeld EP, Marchlinski FE. Reentrant and nonreentrant forms of atrio-ventricular nodal tachycardia mimicking atrial fibrillation. J Cardiovasc Electrophysiol 2006;17(3):312–6. [PubMed]
3. Otomo K, Nagata Y, Uno K, Fujiwara H, Iesaka Y. Irregular atypical atrioventricular nodal reentrant tachycardia: incidence, electrophysiological characteristics, and effects of slow pathway ablation. Heart Rhythm 2007;4(12):1507–22. [PubMed]
4. Tai CT, Chen SA, Chiang CE, Lee SH, Chiou CW, Ueng KC, et al. Multiple anterograde atrioventricular node pathways in patients with atrioventricular node reentrant tachycardia. J Am Coll Cardiol 1996;28(3):725–31. [PubMed]
5. Chen YJ, Chen SA, Chiang CE, Tai CT, Lee SH, Chiou CW, et al. Dual AV node pathway physiology in patients with Wolff-Parkinson-White syndrome. Int J Cardiol 1996;56(3): 275–81. [PubMed]
6. Zhu LH, Fang BS, Zhang WF. Special topic of electrocardiogram. Tianjin, China: Tianjin Science & Technology Press; 2004. p. 47–90.

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