LETTER TO THE EDITORS

Supraventricular tachycardia with ‘A-A-V’ responseupon ventricular entrainment and transient 2:1 AV conductionblock

Christian Sohns • Lars Luthje • Markus Zabel •

Dirk Vollmann

Received: 31 May 2013 / Accepted: 14 August 2013 / Published online: 29 August 2013

� Springer-Verlag Berlin Heidelberg 2013

Sirs:

A 49-year-old female with recurrent paroxysmal palpi-

tations and no evidence for structural heart disease was

referred for an electrophysiological study upon ECG doc-

umentation of supraventricular tachycardia (SVT).

Vascular access was obtained through the femoral veins.

Three quadripolar catheters were positioned under fluoro-

scopic guidance into the high right atrium (HRA), the His-

position and the right ventricular apex (RVA). Normal AH

(56 ms) and HV (32 ms) times were obtained, and there

was no significant AH jump with programmed atrial ex-

trastimuli. Antegrade block cycle length (CL) was 320 ms,

and retrograde conduction was decremental with a block

CL of 250 ms. After administration of isoproterenol, a SVT

with an atrial CL of 320 ms (188 bpm) and 2:1 AV con-

duction (Fig. 1a) was induced with atrial stimulation. A

single premature ventricular stimulus caused transition

from 2:1 to 1:1 AV conduction with transient right bundle

branch block (RBBB) (Fig. 1b). This tachycardia was

entrained with overdrive stimulation from the RVA. The

response to entrainment is illustrated in Fig. 1c. What is the

SVT mechanism?

The observation of 2:1 AV conduction block during

SVT may indicate focal atrial tachycardia (AT) or atrial

macro-reentrant tachycardia as the most likely underlying

mechanism, whereas AV reentry over an accessory path-

way is excluded. AV nodal reentrant tachycardia (AVNRT)

may also exhibit 2:1 AV conduction block in B10 % of the

cases [1], and can be considered as a differential diagnosis

since VA times are constant with every second beat and P

wave morphology conforms with retrograde atrial activa-

tion (Fig. 1a). After transition to 1:1 AV conduction, the

long VA time excludes typical but not atypical AVNRT. In

this setting, entrainment with right ventricular (RV) over-

drive pacing is a powerful maneuver to discriminate AT

from AVNRT (or AVRT) [2]: An ‘A-A-V’ response upon

RV entrainment is considered as diagnostic for AT,

whereas an ‘A-V’ response indicates AVNRT or AVRT as

underlying SVT mechanism. In the present case, ‘A-A-V’

is observed upon cessation of RV pacing, which may ini-

tially be interpreted as an indicator for AT. It is of key

importance, however, to identify the last accelerated atrial

activation and to consider this as the first atrial response to

the last paced and entrained ventricular beat [3]. Failure to

do so can result in misinterpretation of a ‘pseudo A-A-V’

response (Fig. 1c) whenever retrograde conduction is

decremental with overdrive pacing and slow enough to

allow an overlap of retrograde atrial activation with the

consecutive paced ventricular activation. This may occur if

the SVT utilizes anything other than a conventional

accessory pathway or a fast AV nodal pathway for VA

conduction [4]. In the present case, the slow pathway

conducts retrograde activation to the atria, and conduction

is decremental with the increase in activation rate during

entrainment. Thus, the observed response is a typical

example for a ‘pseudo A-A-V’ and is therefore in this case

diagnostic for (atypical) AVNRT. Of note, subjects pre-

senting with atypical AVNRT commonly exhibit no sig-

nificant AH jump with programmed atrial stimulation [5].

C. Sohns (&) � L. Luthje � M. Zabel � D. Vollmann

Division of Clinical Electrophysiology, Department

of Cardiology and Pneumology, Heart Center,

Georg-August-University of Gottingen, Robert-Koch-Strasse 40,

37075 Gottingen, Germany

e-mail: sohns.christian@gmail.com

C. Sohns

Division of Imaging Sciences and Biomedical Engineering,

King’s College London, London, UK

123

Clin Res Cardiol (2013) 102:927–929

DOI 10.1007/s00392-013-0612-z

Radiofrequency application at the slow pathway with a

4-mm tipped ablation catheter caused junctional beats,

resulted in non-inducibility of any SVT, also after repeated

isoproterenol administration, and was associated with

freedom from SVT recurrence during follow-up.

Another interesting phenomenon observed in the present

case was the transition from 2:1 to 1:1 AV conduction with

a premature ventricular impulse (Fig. 1b). AV block during

AVNRT is usually localized below or within the His

bundle and functional in nature [1]. Prior studies demon-

strated that a critically timed premature ventricular acti-

vation during AVNRT with 2:1 AV conduction

consistently causes transition to 1:1 conduction by resetting

His/Purkinje refractoriness and by elimination of the

‘‘long-short sequence’’ [1]. Of note, transition to AVNRT

with 1:1 AV conduction in the present case was initially

associated with functional RBBB, which resolved sponta-

neously after 4 beats. This observation suggests a ‘‘peeling

back’’ of the refractory periods of both bundle branches

following the ventricular premature beat [6], with

improvement of the left bundle conduction properties

preceding those of the right bundle.

In summary, this case illustrates potential manifestations

of AVNRT and highlights the importance of a careful and

thorough application of pacing maneuvers for the differ-

ential diagnosis of SVT.

Acknowledgments Dr. Sohns is funded by the German Cardiac

Society (Deutsche Gesellschaft fur Kardiologie—Herz-und

Kreislaufforschung/DGK) through a grant for clinical research.

Conflict of interest There are no conflicts of interest.

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lead II, III, aVF, V2–V6, an atrial cycle length of 320 ms (188 bpm),

narrow QRS complexes and 2:1 AV conduction. b A single

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928 Clin Res Cardiol (2013) 102:927–929

123

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