Long RP Tachycardia with an Initial A-A-V Activation Sequence: What Is the Mechanism?

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Arrhythmia Rounds
Section Editor: George J. Klein, M.D.
Long RP Tachycardia with an Initial A-A-V Activation
Sequence: What Is the Mechanism?
YOSHIAKI KANEKO, M.D., Ph.D., TADASHI NAKAJIMA, M.D., Ph.D.,
TADANOBU IRIE, M.D., TOSHIMITSU KATO, M.D., TAKAFUMI IIJIMA, M.D.,
and MASAHIKO KURABAYASHI, M.D., Ph.D.
From the Department of Medicine and Biological Science, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan
Case Presentation
A 79-year-old man with a history of multiple episodes of
paroxysmal supraventricular tachycardia underwent electrophysiologic studies and a catheter ablation procedure. The
12-lead electrocardiogram during tachycardia showed a long
RP tachycardia with negative P waves in leads II, III, and
aVF. No dual anterograde atrioventricular (AV) nodal conduction was elicited by atrial extrastimulation. A narrow
QRS tachycardia documented previously was reproducibly
induced by atrial extrastimulation (Fig. 1A). During tachycardia, the HA and AH intervals measured 136 and 252 ms,
respectively, and the earliest atrial activation was recorded
at the ostium of the coronary sinus. Atrial extrastimuli delivered during the tachycardia did not reset the atrial cycle.
Atrial overdrive pacing induced a second tachycardia with a
similar atrial activation sequence and cycle length, and 2:1AV
conduction (Fig. 1B). Ventricular overdrive pacing was delivered at a slightly shorter cycle length than the tachycardia
(Fig. 2). Based upon these observations, what is the mechanism of tachycardia?
Comment
The differential diagnosis of long RP tachycardia with
2:1 AV conduction and earliest atrial activation at the ostium of the coronary sinus (Fig. 1B) includes fast–slow type
AV nodal reentrant tachycardia (AVNRT) and septal atrial
tachycardia. AV block during ongoing tachycardia excludes
the diagnosis of AV reentrant tachycardia. Presuming the
presence of dual AV nodal conduction, the electrophysiological observations shown in Figure 2 are explained as follows: (1) in the first 5 paced cycles, the ventricular wavefront
reached the atrium over a slow pathway (ventricular entrainment pacing), while another wavefront conducting through
the fast pathway collided with the orthodromic impulse; (2)
J Cardiovasc Electrophysiol, Vol. 22, pp. 945-947, August 2011.
No disclosures.
Address for correspondence: Yoshiaki Kaneko, M.D., Ph.D., Department of
Medicine and Biological Science, Gunma University Graduate School of
Medicine, 3-39-22 Showa, Maebashi, Gunma 371-8511, Japan. Fax: +8127-220-8158; E-mail: [email protected]
doi: 10.1111/j.1540-8167.2010.01997.x
the 6th paced cycle is blocked in the VA direction in the slow
pathway; (3) the absence of collision with the orthodromic
wavefront enabled 2:1 VA conduction over the fast pathway,
while the wavefront entering the slow pathway collided with
the anterograde reciprocating wavefront; (4) after cessation
of ventricular overdrive pacing (not shown), the tachycardia
was terminated. Therefore, ventricular entrainment pacing
unmasked the retrograde limb of the AV nodal reentry circuit, confirming the diagnosis of fast–slow AVNRT. It would
be very unusual to terminate an atrial tachycardia by ventricular entrainment in absence of apparent atrial capture before
termination. Since the atrial activation sequences and cycle
lengths of the first and second tachycardias were similar, both
tachycardias were diagnosed as AVNRT, the second tachycardia being associated with 2:1 anterograde block at the
level of the lower common pathway. These observations also
suggest that 2:1 block during AVNRT was functional, and
not due to structural disease of the AV conduction system.
The present case shows an important element of the differential diagnosis of supraventricular tachycardia with an
initial “A-A-V” sequence upon cessation of atrial pacing.
The atrial response (A-A-V or A-V) following cessation of
entrainment of the tachycardia by ventricular pacing provides useful information to differentiate atrial tachycardia
from AVNRT.1 An “A-A-V” sequence is typically indicative
of atrial tachycardia, whereas an “A-V” response excludes
this diagnosis. This suggests that AV nodal reentry is unlikely to explain the second “A” of “A-A-V,” which occurs
immediately after the first “A,” caused by retrograde AV
nodal conduction. However, the diagnostic significance of
an “A-A-V” sequence after cessation of atrial pacing has not
been previously published. The differential diagnosis of the
origin of the second “A” of an initial “A-A-V” activation generally includes a repetitive atrial response and the first cycle
of atrial tachycardia or of AV nodal reentry induced by the
first “A.” The activation sequence of the second “A” was the
same as the subsequent atrial cycles during AVNRT, supporting the diagnosis of AV nodal reentry instead of repetitive
atrial response and atrial tachycardia. Furthermore, the interval between the first “A” and the second “A” of the initial
“A-A-V” activation was nearly the same as the subsequent
atrial cycle length during AVNRT with 2:1 AV conduction,
supporting the immediate development of 2:1 anterograde
block at the level of the lower common pathway after the
first “A” during ongoing AVNRT. Thus, an “A-A-V” response observed upon cessation of atrial pacing is not an
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Journal of Cardiovascular Electrophysiology Vol. 22, No. 8, August 2011
Figure 1. A: Atrial extrastimulation at the high right atrium (HRA) with an S1–S2 coupling interval of 370 ms at an S1–S1 cycle length of 600 ms, induced
long RP tachycardia with stable 1:1 AV conduction. B: After cessation of atrial overdrive pacing at an S–S cycle length of 330 ms delivered transiently during
ongoing AVNRT, another tachycardia with stable 2:1 AV conduction was observed, following an initial “A-A-V” electrogram sequence. The atrial cycle
length and site of earliest atrial activation at the ostium of the coronary sinus were similar to the tachycardia shown in A. Note the visible His electrogram
associated with the cycles blocked in the AV direction, consistent with intra- or infrahisian block. The numbers indicate the cycle lengths in ms. I, II, and V 1
= surface electrocardiogram; HBE 1–2 and 3–4 = distal to proximal His bundle region; CS 9–10 = proximal CS recording; RVA = right ventricular apex;
H = His bundle electrogram.
Figure 2. RV overdrive pacing at a cycle length of 380 ms during AVNRT with an atrial cycle length of 400 ms. The first 5 paced cycles capture the atria
with a long VA interval and earliest site of atrial activation at the ostium of the coronary sinus (CS 9–10), consistent with retrograde conduction over a slow
pathway. After a gradual rate-dependent increase in VA conduction time over the slow pathway between the 3rd and 5th paced cycle, the 6th cycle is blocked.
The 7th paced cycle captured the atrium with a short VA interval and earliest site of atrial activation in the His bundle (HBE 1–2) region, consistent with
retrograde conduction over a fast pathway, followed by 2:1 VA conduction over that pathway. The numbers between atrial electrograms at the HRA indicate
the cycle lengths in ms. The other abbreviations are as in Figure 1.
Kaneko et al. Long RP Tachycardia with an Initial A-A-V Activation Sequence
electrophysiological proof of diagnosis of atrial tachycardia.
In contrast to ventricular entrainment pacing, atrial pacing
readily induced anterograde block in the lower common pathway during atypical AVNRT,2,3 perhaps associated with the
development of an initial “A-A-V” activation sequence after
atrial pacing.
Slow pathway ablation, performed in the posteroseptal
right atrium, near the ostium of the coronary sinus, at the site
of earliest retrograde atrial activation, was associated with a
junctional rhythm during delivery of radiofrequency energy
and eliminated the inducible tachycardia.
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References
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1990;15:385-392.
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