Majid Haghjoo,
M.D, Arash Arya, M.D, Mohammadreza Dehghani, M.D, Zahra Emkanjoo, M.D,
Amirfarjam Fazelifar, M.D, Alireza Heidari, M.D, MohammadAli
Sadr-Ameli, M.D.
Department of Pacemaker and
Electrophysiology, Shahid Rajaie Cardiovascular Medical and Research
Center, Iran University of Medical Sciences, Tehran, Iran.
Address for
correspondence:Majid Haghjoo M.D, Department of Pacemaker and
Electrophysiology, Shahid Rajaie Cardiovascular Medical and Research
Center, Mellat Park, Vali-e-Asr Avenue, Tehran 1996911151 Iran. E-mail:
majid.haghjoo@gmail.com
Abstract
Double tachycardia
is a relatively rare condition. We describe a 21 year old woman with
history of frequent palpitations. In one of these episodes, she had
wide complex tachycardia with right bundle branch and inferior axis
morphology. A typical atrioventricular nodal tachycardia was induced
during electrophysiologic study, aimed at induction of clinically
documented tachycardia. Initially no ventricular tachycardia was
inducible. After successful ablation of slow pathway, a wide complex
tachycardia was induced by programmed stimulation from right
ventricular outflow tract. Mapping localized the focus of tachycardia
in left ventricular outflow tract and successfully ablated via
retrograde aortic approach. During 7 month's follow-up, she has been
symptom free with no recurrence. This work describes successful
ablation of rare combination of typical atrioventricular nodal
tachycardia and left ventricular outflow tract tachycardia in the same
patient during one session.
Keywords: double tachycardia; left ventricular outflow tract
tachycardia; atrioventricular nodal reentrant tachycardia.
Introduction
Double
tachycardia, defined as the simultaneous occurrence of atrial and
ventricular
1,2
or junctional and ventricular tachycardia (VT)
3,
has been rarely reported and usually occurs in patients with poor left
ventricular function or in association with digitalis intoxication.
1,2,4,5
The coexistence of atrioventricular reentrant tachycardia (AVRT) and
idiopathic right ventricular outflow tract (RVOT) tachycardia
3, or atrioventricular nodal reentrant
tachycardia (AVNRT) and RVOT-tachycardia
6
has also been reported, but
coincidence of AVNRT and idiopathic left ventricular outflow tract
(LVOT) tachycardia has rarely been reported. To the best of our
knowledge, this case is the first report of successful ablation of rare
combination of AVNRT and LVOT-tachycardia in the same patient.
Case report
A 21 year old
woman with no evidence of structural heart disease referred to our
center for evaluation of palpitation and dizziness. The structural
heart disease was excluded by physical examination and transthoracic
echocardiography. Transthoracic echocardiography showed normal cardiac
chambers (including right ventricle), normal valvular function and
ejection fraction (EF) without any wall motion abnormalities. During an
episode of palpitation, the standard 12-lead electrocardiogram (ECG)
showed documented wide complex tachycardia with a heart rate of 125
beats /min. The tachycardia was refractory to two intravenous
antiarrhythmics (amiodarone, procainamide). The wide complex
tachycardia had inferior axis and right bundle branch block morphology
compatible with LVOT-tachycardia (
Figure
1). The baseline ECG showed no abnormality.
Figure1. The standard 12-lead
electrogram of wide QRS tachycardia (125 beats /min) showing right
bundle branch block and inferior axis morphology compatible with left
ventricular outflow tract tachycardia.
After
obtaining written informed consent, electrophysiologic study was done
in the postabsorptive and nonsedated state. During programmed
electrical stimulation from atrium and ventricle, dual AV nodal
physiology with nonsustained AVNRT was induced. Then programmed
ventricular stimulation was performed with standard protocol at three
cycle length (600,500,400ms) and three extrastimuli up to coupling
interval of 200 ms from two sites (RV apex , RVOT). No ventricular
tachycardia was induced with and without isoproterenol infusion. Repeat
programmed atrial stimulation resulted in induction of sustained AVNRT
under isoproterenol infusion (
Figure 2).
Radiofrequency catheter ablation of slow pathway was done at right
posteroseptal area. Postablation programmed stimulation failed to
induce any supraventricular tachycardia with and without isoproterenol
infusion but a wide complex tachycardia (cycle length=480 ms) identical
to clinically documented arrhythmia was induced by overdrive pacing
from RVOT. Mapping of RVOT failed to show any early ventricular
activation site, thus LVOT was mapped and tachycardia focus was
localized in this area with 53 ms early ventricular activation relative
to surface electrocardiogram (
Figure 3)
Radiofrequency energy delivery (50 W, 60°C) at this site resulted
in termination of tachycardia (
Figure 4).
Thirty minutes after ablation, no tachycardia was induced with and
without isoproterenol infusion. During 12 month follow-up, she has been
symptom free with no antiarrhythmic drugs.
Figure
2. Electrophysiologic tracing of narrow complex tachycardia
compatible with typical atrioventricular nodal reentrant tachycardia.
Figure
3. Demonstration of earliest activation site in left
ventricular outflow tract (A) and right ventricular outflow tract (B)
recorded during mapping by ablation catheter.
Figure
4. Termination of ventricular tachycardia by delivery of
radiofrequency energy in early site in left ventricular outflow tract.
Double
tachycardia was a relatively uncommon type of tachycardia in previous
reports.
1,3,5
In recent study by Kautzner et al
7,
this combination (RVOT-tachycardia and AVNRT) was not as uncommon (15%
of RVOT-tachycardia patients had AVNRT). In this study, three of seven
patients with coexistent idiopathic ventricular outflow tachycardia and
AVNRT had the arrhythmogenic focus localized in the uppermost part of
the septum or more epicardially near the great cardiac vein as
documented by detailed mapping but no early site was reported in LVOT
area or aortic cusps in any patients. In this study, no attempt for
ablation was made in the patients with epicardial variant.
Idiopathic VT
most commonly arises from RV than LV (70% versus 30%).
8 Idiopathic LVOT-tachycardia is one of
the three subtypes of idiopathic left ventricular tachycardia that
analogous to adenosine sensitive RVOT-tachycardia originate from deep
within the septum and exit from left side of septum, and result from
cAMP-mediated triggered activity.
9
AVNRT is a typical reentrant tachycardia originating from the AV nodal
and perinodal tissues.
10
In this
patient, clinically documented arrhythmia was ventricular tachycardia
arising from the LVOT area whereas AVNRT was the first tachycardia
induced by programmed stimulation in the electrophysiologic laboratory,
although this had not been documented clinically. Slow pathway ablation
was done because of patient request and report of future recurrence of
AVNRT in such patients.
7
Then LVOT-tachycardia was induced and ablated successfully because
catheter ablation of one arrhythmia substrate did not prevent
inducibility or clinical recurrence of the other.
7
Co existence
of AVNRT and LVOT-tachycardia may be a no more than chance association.
This suggestion appears to be supported by presence of different
mechanisms for both each type of tachycardia. On the other hand, some
debate was made for this hypothesis in Kautzner study explaining this
combination by presence of common trigger in patients with combination
of AVNRT and RVOT-tachycardia.
7
Conclusion
Our case
demonstrated: 1) Presence of rare coexistence of AVNRT and
LVOT-tachycardia
2) Feasibility of successful ablation of combination of AVNRT and
LVOT-tachycardia in the same patient during one session.
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