Europace Advance Access originally published online on November 15, 2007
Europace 2008 10(1):110-111; doi:10.1093/europace/eum240
Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007.For permissions please email: journals.permissions@oxfordjournals.org
ELECTROCARDIOGRAPHY
Wide QRS-complex tachycardia with variable VA-conduction: what is the mechanism?
Hildegard Tanner,
Takao Sakata and
Etienne Delacrétaz*
Swiss Cardiovascular Center Bern, University Hospital, CH-3010 Bern, Switzerland
Manuscript submitted 3 September 2007. Accepted after revision 8 October 2007.
* Corresponding author: Tel: +41 31 632 2111; fax: +41 31 632 1414. E-mail address: etienne.delacretaz{at}insel.ch
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Abstract
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We describe the case of a 16-year-old woman with a surgically
corrected tetralogy of Fallot presenting with recurrent wide-QRS-complex
tachycardia. The tachycardia could be induced and terminated
with ventricular stimulation only. QRS morphology during sinus
rhythm and tachycardia was identical and variable VA-conduction
was observed. Mapping of the tachycardia showed that variations
of HH intervals preceded VV intervals. Therefore, a mechanism
involving re-entry within the bundle branches was suggested.
However, detailed mapping showed cranial to caudal depolarization
of the His bundle, leading to the diagnosis of atrioventricular
node re-entrant tachycardia. The tachycardia was abolished by
radiofrequency catheter ablation of the slow AV nodal pathway.
We conclude that variable VA conduction can occur in patients
with atrioventricular node re-entrant tachycardia. The atrial
tissue is not always an integral part of the re-entrant circuit.
Key Words: Wide-QRS-complex tachycardia, Tetralogy of Fallot, Catheter ablation, AV nodal reentry tachycardia
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Case presentation
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A 16-year-old woman with a surgically corrected tetralogy of
Fallot at the age of 4 years was referred for electrophysiological
study because of paroxysmal wide-QRS-complex tachycardia.
Programmed atrial stimulation did not induce any tachycardia, whereas wide-QRS-complex tachycardia with a cycle length of 430 ms was reproducibly induced with programmed ventricular stimulation. Spontaneous terminations of the tachycardia with ventricular premature beats occurred repeatedly (Figure 1). QRS-complex morphology during tachycardia is practically identical to QRS morphology during sinus rhythm. A close look at Figure 1 shows variable VA conduction—best visible in lead III—that was confirmed by intra-cardiac recordings. Furthermore, His-bundle recording showed H deflections preceding each QRS by 60 ms (Figure 2). During the cycle-length oscillations following tachycardia induction, variations of HH intervals preceded variations of VV intervals (data not shown). HV interval during sinus rhythm measured 50 ms.
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Figure 1 Twelve-lead ECG showing a wide-QRS-complex tachycardia at a cycle length of 430 ms with spontaneous termination following a ventricular premature beat. The QRS morphology during sinus rhythm appears identical to the QRS morphology during tachycardia. Variable VA conduction is seen in lead III.
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Figure 2 Wide-QRS-complex tachycardia with right bundle branch morphology at a cycle length of 430 ms. Shown are surface ECG leads I, aVF and V1, and intracardiac recordings from His-bundle electrogram (HBE 1,2 to HBE 5,6), and right ventricular apex (RVA).
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Commentary
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The morphology of QRS complex was similar in tachycardia and
sinus rhythm, suggesting supraventricular tachycardia. However,
variable VA conduction during tachycardia and the finding that
the tachycardia was only inducible by ventricular stimulation
in a patient with structural heart disease suggest ventricular
tachycardia. Moreover, the recording of H deflections before
each QRS with HH intervals variations preceding VV interval
variations, and QRS morphology during tachycardia identical
to bundle branch block during sinus rhythm suggest a mechanism
involving reentry within the bundle branches. In the presence
of a right bundle branch morphology during tachycardia, left
intra-fascicular or inter-fascicular reentry was suspected.
However, the mapping of the right and left side of the septum
during sinus rhythm and tachycardia showed cranial to caudal
depolarization of the His bundle (
Figure 3) and bundle
branches (not shown), ruling out intra-ventricular reentry and
therefore the important differential diagnosis of bundle branch
reentry tachycardia. Thus, the only possible mechanism was atrioventricular
(AV) node reentrant tachycardia with variable VA block. The
observation of further tachycardia episodes revealed variations
in cycle lengths, and episodes of 1:1 VA conduction during tachycardia
with a longer cycle length of 470 ms. Administration of intravenous
adenosine caused prolongation of VA intervals followed by the
termination of tachycardia with VA block. Atypical, slow–slow
AV nodal reentry tachycardia was diagnosed. The tachycardia
was abolished by radiofrequency catheter ablation of the slow
AV nodal pathway.
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Figure 3 His bundle activation during sinus rhythm (top) and during tachycardia (bottom) showing cranial to caudal depolarization of the His bundle. Shown are surface ECG leads I, aVF and V3, and intracardiac recordings from His-bundle electrogram (HBE 1,2 to HBE 3,4).
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This example demonstrates that variable VA conduction or even
high-degree VA block can occur in patients with AV nodal reentrant
tachycardia, and that the atrial tissue is not always an integral
part of the reentrant circuit. Furthermore, the case illustrates
that some of the features characterizing bundle branch reentry
or inter-fascicular reentry are not specific and can be found
in supraventricular tachycardias.
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Abstract
Case presentation