Atypical atrioventricular Wenckebach periodicity caused by conduction through triple atrioventricular junctional pathway as a probable mechanism

Journal of Electrocardiology Vol. 36 No. 1 2003

Case Report

Atypical Atrioventricular Wenckebach Periodicity Caused By Conduction Through Triple Atrioventricular Junctional Pathway as a Probable Mechanism Takakazu Katoh, MD,* Shinji Kinoshita, MD,† Yoshinori Tsujimura, MD,‡ and Yoshihiko Sasaki, MT¶

Abstract: Electrocardiograms were taken from an 84-year-old man with right bundle branch block in whom atypical atrioventricular Wenckebach periodicity was frequently occurred. The electrocardiographic findings as mentioned below suggested that the atypical periodicity was caused by conduction through triple atrioventricular junctional pathways as a probable mechanism. When a P wave was blocked after a markedly prolonged PR interval of 0.64 s, the RP interval containing this blocked P wave ranged between 0.84 s and 0.86 s, and the next P wave was followed by a QRS complex of the same configuration, with the PR interval of 0.35 s. On the other hand, when a P wave was blocked after a PR interval of 0.49 s or 0.52 s, the RP interval containing this blocked P wave was comparatively long, ie, 0.95 s or 0.98 s, and the next P wave was followed by a QRS complex of somewhat different configuration showing borderline left axis deviation, with a shorter PR interval of 0.21 s or 0.23 s. These findings suggest that longitudinal dissociation occurred not only in the atrioventricular junction but also in the His bundle. This is the first report suggesting triple atrioventricular junctional pathways probably associated with longitudinal dissociation in the His bundle. Key words: Triple atrioventricular junctional pathways, atypical atrioventricular Wenckebach periodicity, longitudinal dissociation in the His bundle.

The presence of dual atrioventricular (AV) pathways has been shown in many reports (1). The

presence of triple AV nodal pathways has been shown in previous reports (2-9). In the present report, a case of atypical AV Wenckebach periodicity is shown in which conduction through triple AV nodal pathways is the suggested mechanism. A likely interpretation of the electrocardiographic data suggests that longitudinal dissociation occurred not only in the AV node but also in the His bundle (10-12) as an additional mechanism. The presence of such triple AV nodal pathways associ-

From the *Katoh Cardiovascular Clinic, Ohtsu; †Hokkaido Women’s University, Ebetsu, Hokkaido; ‡Division of Cardiology; and ¶Central Laboratory, Ohtsu Municipal Hospital, Ohtsu; Japan. Reprint requests: Takakazu Katoh, MD, Katoh Cardiovascular Clinic, Taishogun 3-Chome 8-16, Ohtsu 520-2145, Japan. Copyright 2003, Elsevier Science (USA). All rights reserved. 0022-0736/03/3601-0010$35.00/0 doi:10.1054/jelc.2003.50000

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Fig. 1. The 12-lead electrocardiogram during sinus rhythm with first-degree atrioventricular block. The QRS complex shows right bundle branch block with normal axis, and the PR interval measures 0.40 s.

ated with longitudinal dissociation in the His bundle has never been reported before.

Case Report Electrocardiograms were taken from an 84-yearold man with hypertension and hyperlipemia in whom atypical AV Wenckebach periodicity was frequently found. He did not experience any symptoms associated with the arrhythmia. His chest X-ray showed mild emphysema and his echocardiogram showed mild left ventricular hypertrophy with the posterior wall thickness of 11 mm. Figure 1 shows the 12-lead electrocardiogram during sinus rhythm with first degree AV block, in which the PR interval is markedly long (0.40 s) and right bundle branch block (RBBB) with the QRS interval of 0.16 s is found. Figure 2 shows part of a long continuous recording. In Figure 2, the upper 3 strips (A) in leads I, II, and V1 were recorded simultaneously. The strips A

and the lower strips B and C in lead II are continuous, which were recorded at a high sensitivity of 2 cm/mV. Numerals above and below the tracings in lead II indicate PR and RP intervals in hundredths of a second, respectively. Figure 2A shows that AV Wenckebach periodicity occurs in which sudden marked prolongation of the second PR interval in an AV Wenckebach period is found, as is seen in PR of 0.44 s after PR of 0.35 s; and PR of 0.42 s after PR of 0.22 s. This suggests occurrence of atypical AV Wenckebach periodicity of variant IIb as was defined by Kinoshita and Konishi (13). Namely, in a Wenckebach period, the second PR interval is much longer than the first one; the increment of this PR interval is the largest in the period; and the RR interval containing this PR interval is the longest in the period. The occurrence of such atypical AV Wenckebach periodicity suggests the presence of longitudinal dissociation in the AV junction including the His-Purkinje system. In Figure 2A, a P wave on the ST segment of the first QRS complex is blocked, and is nonconducted

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Fig. 2. Atypical atrioventricular Wenckebach periodicity of variant IIb. Strips A were recorded simultaneously in leads I, II, and V1. Strips B and C were recorded only in lead II. Strips A, B and C are continuous. The numerals above and below the tracings in lead II indicate PR and RP intervals in hundredths of a second, respectively. All strips were recorded with a high sensitivity of 2 cm/mV. In the ladder diagram, solid lines, dashed lines and dot lines represent conduction of impulses through the fast pathway ␣, the slow pathway ␤, and the slowest pathway ␥, respectively. A, atria; AV, atrioventricular junction; V, ventricles.

to the ventricles. The RP interval containing this blocked P wave is 0.86 s. After this RP interval, a P wave is followed by a QRS complex of the same configuration as that of the first QRS complex, with a PR interval of 0.35 s. The P wave on the ST segment of the fourth QRS complex is blocked again. The RP interval containing this blocked P wave is 0.97 s, which is considerably longer than the above-mentioned RP interval of 0.86 s. After this longer RP interval of 0.97 s, the P wave is followed by a considerably different QRS complex in configuration showing borderline left axis deviation, with a comparatively short PR interval of 0.22 s. The same features as the above were found throughout the continuous recording including

strips B and C in Figure 2. Namely, when a P wave was blocked after a markedly prolonged PR interval of 0.64 s, the RP interval containing this blocked P wave ranged between 0.84 sand 0.86 s. The next P wave was followed by a QRS complex of the same configuration, with a PR interval of 0.35 s. On the other hand, when a P wave was blocked after a PR interval of 0.49 s or 0.52 s, the RP interval containing this blocked P wave was comparatively long, ie, 0.95 s or 0.98 s, and the next P wave was followed by a QRS complex of somewhat different configuration showing borderline left axis deviation, with a shorter PR interval of 0.21 s or 0.23 s. Figure 3 shows part of another recording. In the figure, 2 escape QRS complexes R8 and R9 occur in succession, which are the same in configuration as

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Fig. 3. Part of a long recording in which two escape QRS complexes with normal axis occur in succession. The escape impulse originates from ectopic pacemaker E1 represented by solid squares. P10 is conducted retrogradely through the slow pathway ␥. Abbreviations are the same as in Figure 2.

the basic QRS complexes. The escape complexes originate from an escape pacemaker represented by solid squares (E1) with an escape cycle of 1.28 s. A retrograde P wave (P10) conducted from the first escape impulse is found. It seems that P9 fails to be conducted to the ventricles because the P9R8 interval of 0.20 s is too short to be followed by QRS complexes of the same configuration as mentioned above. Figure 4 shows that another form of escape rhythm occurs as shown in R5, R6, R7, and R8, which originate from another escape pacemaker represented by solid circles (E2). Those escape QRS complexes are somewhat different in configuration and in length of the escape cycle from the escape

QRS complexes originating from the escape pacemaker represented by solid squares. Namely, in the escape complexes R5 to R8, the escape cycle is 1.06 s, which is significantly shorter than 1.28 s in the escape complexes originating from pacemaker E1. The configuration of R5 to R8 shows borderline left axis deviation, which is the same as that of the fifth QRS complex in Figure 2A. These findings suggest that these escape pacemaker E2 is located at a site higher than the escape pacemaker E1. In Figure 4, R3 is an escape originating from pacemaker E1; and R4 is intermediate in configuration between R2 and R5, suggesting that R4 might be a fusion of the sinus beat and the escape beat E2.

Fig. 4. Part of a long recording in which escape QRS complexes, R5, R6, R7, and R8, with borderline left axis deviation occur in succession. The escape complexes originate from another escape pacemaker E2, represented by solid circles. P5 is conducted retrogradely through the slow pathway ␥. R3 originates from escape pacemaker E1. Abbreviations are the same as in Figure 2.

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Fig. 5. Schemata to represent conduction of impulses through triple atrioventricular nodal pathways. Conduction in the fast pathway ␣, the slow pathway ␤, and the slowest pathway ␥ is represented by solid lines, dashed lines, and dot lines, respectively. Schema A shows that a sinus impulse passing through pathway ␣ is conducted to the ventricles with borderline left axis deviation because the impulse travels through the lower portion of the atrioventricular junction in the transverse direction and then reaches the left anterior fascicle after some delay. Schemata B and C show that a sinus impulse passing through pathway ␤ or ␥ is conducted to the ventricles without left axis deviation.

Discussion It was shown in the present case that atypical AV Wenckebach periodicity of variant IIb occurred showing longitudinal dissociation in the AV junction (13). The above eletrocardiographic findings, however, cannot be explained by only using the presence of dual AV nodal pathways. In the present case, invasive electrocardiographic studies were not performed. It seems that to disclose the mechanism exactly, transesophageal electrocardiogram recording, programmed electrical pacing, or pervenous electrophysiological studies must be performed; however, the above findings in the present case suggest that atypical AV Wenckebach periodicity was caused by the presence of triple AV nodal pathways. Attempts will be made to explain atypical AV Wenckebach periodicity in the present case by using the concept of triple AV nodal pathways as a probable mechanism. It seems that this may be the first report suggesting triple atrioventricular nodal pathways associated with longitudinal dissociation in the His bundle. Triple AV Nodal Pathways In usual cases of longitudinal dissociation caused by dual AV nodal pathways, it is shown that in the discontinuous distribution in AV conduction time, it can be divided into 2 groups; namely, that there is a period of at least 50 ms, usually 70-100 ms in conduction time between the 2 groups (14). In the same way, triple AV nodal pathways are diagnosed

with 2 discrete discontinuities of AV conduction (6). In the present case, the distribution of the PR intervals was clearly divided into 3 groups, ie, 0.21-0.23 s, 0.35 s, and 0.41-0.64 s. These findings strongly suggest the presence of triple AV conduction pathways, although electrophysiological study was not performed in this case. Figure 5 shows schemata to explain conduction of impulses through the triple AV nodal pathways. The schemata show that the sinus impulse is always blocked in the RBB. In the schemata, there are 2 pathways, ␣ and ␤, ␣ being faster conducting and ␤ being slower conducting. The effective refractory period of pathway ␣ is longer than that of pathway ␤. The conduction velocity in pathway ␣ is faster than that in pathway ␤. In the slowest pathway ␥, the effective refractory period is considerably shorter and the conduction velocity is much slower than in the other 2 pathways. Schema A shows that when a sinus impulse falls after the effective refractory period of the fast pathway ␣, it is conducted to the ventricles through pathway ␣ with only a slight delay, in which the PR interval measures 0.21 s or 0.22 s. The effective refractory period of pathway ␣ is the longest in the triple pathways. In the other 2 pathways, ␤ and ␥, the sinus impulse travels more slowly, and interferes with the impulse conducted retrogradely from pathway ␣. Pathway ␣ is connected with the posterior fascicle P of the left bundle branch (LBB). After the sinus impulse reaches the fascicle P, it travels through the lower portion of the AV junction. Thus, after some delay, it reaches the anterior

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Fig. 6. Schemata to represent the sites of escape pacemakers E1 and E2. Escape pacemaker E1 is located in the lower portion of pathway ␤. Escape pacemaker E2 is located in the upper portion of pathway ␣. The impulse originating from escape pacemaker E2 is conducted to the ventricles with borderline left axis deviation, whereas the impulse originating from pacemaker E1 is conducted without left axis deviation.

fascicle A of the LBB, and is conducted to the ventricles. Schema B in Figure 5 shows that when a sinus impulse falls in the effective refractory period of the fast pathway ␣, and before that of the fast pathway ␤, it is conducted to the ventricles through pathway ␤. Conduction velocity in pathway ␤ is considerably slower than that of pathway ␣. Thus, the PR interval measures 0.35 s, which is considerably longer than the PR interval of 0.21 s or 0.22 s in schema A. In the slowest pathway ␥, the sinus impulse is travels markedly slowly and interferes with the impulse conducted retrogradely from pathway ␤. The impulse passing through pathway ␤ is conducted to the ventricles with normal conduction in the LBB except for RBBB. Schema C in Figure 5 shows that when a sinus impulse falls in the effective refractory periods of pathways ␣ and ␤, and before that of slowest pathway ␥, it is conducted only through pathway ␥ with marked delay. The PR intervals range between 0.41 s and 0.64 s. The impulse passing through pathway ␥ is also conducted to the ventricles with normal conduction in the LBB except for RBBB, in the same way as that in the impulse passing through pathway ␤. The diagram below strip C in Figure 2 shows conduction of impulses in triple AV nodal pathways. In the ladder diagram, solid lines, dashed lines and dot lines represent conduction of impulses through the fast pathway ␣, the slow pathway ␤, and the slowest pathway ␥, respectively. In the diagram, impulse P9 falls after the effective refractory periods of all the triple pathways, and passing through the fastest pathway ␣, is conducted to the

ventricles. On the other hand, impulse P5 falls in the effective refractory period of pathway ␣, and passing through pathway ␤, is then conducted to the ventricles.

Sites of Longitudinal Dissociation As mentioned above, it seems that the QRS complex of the shortest PR interval of 0.21 s was produced by the impulse passing through the fast pathway ␣. If the sites of longitudinal dissociation in the AV junction are localized only within the AV node, this QRS complex will not show left axis deviation. This suggests that in the lower portion of the AV junction, the impulse travels in the transverse direction with considerable delay and then reaches the left anterior fascicle (15). Thus, it seems that longitudinal dissociation extends into the His bundle (16).

Sites of Escape Pacemakers In the present case, two forms of escape QRS rhythm are found: one (originating from escape pacemaker E1) shows the same morphology as that of the basic QRS complex and the slower escape rate (the escape cycle of 1.28 s); and the other (originating from escape pacemaker E2) shows borderline left axis deviation and the faster escape rate (the escape cycle of 1.04 s). Figure 6 shows schemata to represent the sites of escape pacemakers E1 and E2. The above findings suggest that escape pacemaker E1 is located in the lower portion of

Triple AV Junctional Pathways •

pathway ␤, and that the escape impulse originating from pacemaker E1 is conducted to the ventricles without left axis deviation. On the other hand, escape pacemaker E2 is located in the upper portion of pathway ␣, and that the impulse originating from pacemaker E2 is conducted to the ventricles with borderline left axis deviation. The occurrence of such 2 forms of escape rhythm strengthen the above suggestion that longitudinal dissociation in this case extends to the His bundle. Diagrams below the strips in Figures 3 and 4 show conduction of escape impulses originating from escape pacemakers E1 and E2.

Possible Alternative Mechanisms for Aberrant Conduction Showing Borderline Left Axis Deviation In the present case, as mentioned above, when the RP interval containing a blocked P wave was comparatively long, the next P wave was followed by a QRS complex of somewhat different configuration showing borderline left axis deviation, with a shorter PR interval of 0.21 s or 0.23 s. It is suggested that such borderline axis deviation occurred as a result of dissociation in the His bundle. As a possible alternative mechanism, the occurrence of such borderline left axis deviation might could be explained without dissociation in the His bundle. Namely, such axis deviation could be explained by a combination of constant conduction delay in the left anterior fascicle and periodic improvement in the conduction delay in the left posterior fascicle. In this mechanism, the conduction delay in the left posterior fascicle may normalize only after sufficient lengthening of the RP interval beyond 0.95 s. However, in the escape rhythm with a longer escape cycle of 1.28 s in Figure 3, the escape QRS complexes are the same in configuration as the basic QRS complex with normal axis deviation. Thus, it seems to us that this alternative mechanism is unlikely. As another possible alternative mechanism, the change to such borderline left axis deviation in the QRS configuration might be explained by deceleration aberrancy. As shown in Figure 2A, however, in the simultaneous recordings in leads I, II, and V1, the configuration and width of QRS complex in lead V1 are not changed. Thus, it seems to us that the change in configuration cannot be simply explained by deceleration aberrancy.

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