Bülent Ozin MD,* Bahar Pirat
MD,** Haldun Müderrisoglu MD,***
*Associate Professor in cardiology
**Resident in cardiology *** Professor in cardiology
Baskent University Faculty of Medicine, Department of Cardiology, Ankara,
Turkey.
Address
for correspondence: Bahar Pirat MD, Baskent University Faculty of Medicine,
Department of Cardiology, 10.sok. No:45 Bahcelievler, Ankara 06490, Turkey.
Email:
baharaloglu@hotmail.com
Abstract
Tachycardia
induced tachycardias are not common in clinical practice, and it is believed
that most cases of double tachycardia are coincidental. The existence of
two different tachycardias in the same patient almost always poses problems
in the electrophysiology laboratory. However, in rare instances, the emergence
of a second tachycardia can actually provide invaluable information about
the first one. In this report, we describe a 30-year-old woman who presented
with palpitations. Electrophysiological study revealed that atrial programmed
stimulation at baseline induced right ventricular outflow tract (RVOT) tachycardia
and supraventricular tachycardia. The study also showed that each of the tachycardias
was able to induce the other. A short run of RVOT tachycardia during supraventricular
tachycardia was able to entrain the latter. This finding provided important
information about the nature of the supraventricular tachycardia, which proved
to be atrioventricular nodal reentrant tachycardia. Both of these tachycardias
were successfully ablated, and the patient’s palpitations disappeared.
Key words: Non-sustained ventricular tachycardia, supraventricular
tachycardia, double tachycardia.
Introduction
Simultaneous
occurrence of supraventricular and ventricular tachycardia in the same
patient is very rare. Concomitance of both these forms is usually coincidental,
except in cases of digitalis toxicity and catecholaminergic tachycardias
1,2. We report a case of double tachycardia
in which right ventricular outflow tract (RVOT) tachycardia and atrioventricular
nodal reentrant tachycardia (AVNRT) were capable of initiating each other.
Case Report
A 30-year-old
woman was referred to our hospital for evaluation of non-sustained ventricular
tachycardia. She complained of palpitations lasting 20 to 30 minutes, and
said she had had this problem for 2 years. Episodes of non-sustained ventricular
tachycardia were documented during an exercise stress test. She was treated
with verapamil and metoprolol with no success. Her physical examination was
normal and an echocardiogram revealed no structural abnormalities. Electrocardiography
showed frequent monomorphic ventricular premature beats of left bundle-branch
block and inferior axis configuration.
An electrophysiological
study was performed with the patient in postabsorptive, non-sedated state.
An EP Tracer electrophysiology system (Maastricht, The Netherlands) was
used. During the study, sinus rhythm was very frequently interrupted by spontaneous
repetitive monomorphic non-sustained ventricular tachycardias (NSVT) with
left bundle-branch block and inferior axis configuration. Mapping studies
performed using an ablation catheter (Blazer II, Boston Scientific, USA)
revealed that the ectopic activity originated from the RVOT. However, attempts
to precisely map these premature depolarizations were frequently interrupted
by a supraventricular tachycardia of cycle length 280 ms, which was started
by the NSVT. The supraventricular tachycardia had a ventriculoatrial interval
of 45 ms, which suggested either AVNRT or atrial tachycardia as the pathophysiologic
mechanism.
Due to the
frequent ventricular premature beats and runs of NSVT, it was not possible
to further analyze and identify the exact nature of this supraventricular
tachycardia. In order to continue mapping for the ventricular tachycardia,
it was necessary to terminate the supraventricular tachycardia by overdrive
pacing each time. There were occasions when the supraventricular tachycardia
initiated the NSVT and vice versa (
Figure 1A and B). An episode of
NSVT during supraventricular tachycardia was observed to entrain the latter
with a pattern compatible with AVNRT (
Figure 2)
3.
Figure 1. Initiation of the two tachycardias. A. Initiation
of non – sustained ventricular tachycardia by the supraventricular tachycardia.
B. Initiation of supraventricular tachycardia by the non-sustained
ventricular tachycardia. Surface leads I, II, aVF, V1, V6 and intracardiac
recordings from the high right atrium (HRAd), His bundle (HISp) and right
ventricular outflow tract (RVOT) are shown.
Figure 2. Entrainment of the supraventricular
tachycardia by a short run of non – sustained tachycardia. Surface leads
I, II, aVF, V1, V6 and intracardiac recordings from the high right atrium
(HRAd), His bundle (HISp) and right ventricular apex (RVA) are shown.
The ventricular
tachycardia was eliminated after 14 radiofrequency applications (EPT, USA)
were delivered to the RVOT. Ventricular programmed stimulation after the
ablation revealed no inducible ventricular tachycardias and demonstrated that
the ventriculoatrial conduction was decremental. Atrial programmed stimulation
showed dual atrioventricular nodal physiology and inducible AVNRT. A single
radiofrequency application to the right posterior septum eliminated the dual
nodal physiology and AVNRT. At a follow-up check 1 month after the procedure,
the patient was free of palpitations.
Discussion
Tachycardia
induced tachycardia is a rare phenomenon that is only discussed in a few
case reports in the literature. Wagshal and colleagues described one patient
with idiopathic left ventricular tachycardia and AVNRT
4.
In that case, each of the tachycardias transformed into the other spontaneously.
Washizuka and co-workers reported another patient who had RVOT tachycardia
and atrioventricular reciprocating tachycardia
5.
Similar to what we observed in our case, the ventricular tachycardia in this
patient was able to entrain the supraventricular tachycardia.
Cooklin and
McComb recently reported a case in which AVNRT was induced by RVOT tachycardia
during infusion of isoprenaline in an electrophysiological study
6. Our patient also exhibited both AVNRT and RVOT tachycardia;
however, in contrast to the case reported by Cooklin and McComb, both these
tachycardias were capable of inducing each other. In addition, there are
a few other discrepancies between that case and ours. First, our patient
exhibited excellent ventriculoatrial conduction, which could easily explain
the mechanism of induction of AVNRT during RVOT tachycardia. Second, neither
isoprenaline nor any other beta-mimetic agents were used during our electrophysiological
study, and induction of RVOT tachycardia by AVNRT took place at the basal
state. It is well-known that triggered activity is the mechanism behind
RVOT tachycardia, and rapid atrial pacing in a patient with good atrioventricular
conduction might induce this form of tachycardia. In our case, we believe
that RVOT tachycardia was induced by the rapid atrial depolarizations conducted
to the ventricle during AVNRT.
The consecutive
occurrence of two different tachycardias during electrophysiological testing
always presents a major challenge for the electrophysiologist. During our
electrophysiological study, we aimed to ablate the RVOT tachycardia first
since it was responsible for the patient’s main symptoms. However, our attempts
to locate the earliest ventricular activating sites during RVOT tachycardia
were frequently interrupted by intervening AVNRT. To address this, we changed
our strategy and decided to ablate the supraventricular tachycardia first,
but the frequent premature beats and ventricular tachycardias arising from
the RVOT prevented analysis of the mechanism of the supraventricular tachycardia.
Thus, we had to change our plan again, and finally ablated the RVOT tachycardia
after 14 radiofrequency applications.
Apart from
the problems mentioned above, we observed that double tachycardias actually
helped establish the diagnosis during electrophysiological study. In our
case, a three-beat run of RVOT tachycardia during the supraventricular tachycardia
entrained the latter with an ‘atrial-ventricular’ pattern, and helped us
diagnose AVNRT (
Figure 2).
In conclusion,
this case is of particular interest because of the unusual finding of double
tachycardia, with each form capable of inducing the other. The case is
also noteworthy in that it highlights the advantages and disadvantages
of dealing with two different tachycardias in the electrophysiology laboratory.
References
1. Chowdhry IH, Hariman RJ, Gomes
JA El-Sherif N. Transient digitoxic double tachycardia. Chest 1983;83(4):686-7.
2. Benson DW Jr, Gallagher JJ, Sterba R, Klein GJ,
Armstrong BE. Catecholamine induced double tachycardia: case report in a
child. Pacing Clin Electrophysiol 1980;3(1):96-103.
3. Knight BP, Zivin A, Souza J,
Flemming M, Pelosi F, Goyal R, et al. A technique for the rapid diagnosis
of atrial tachycardia in the electrophysiology laboratory. J Am Coll Cardiol
1999;33:775-81.
4. Wagshal AB, Mittleman RS, Schuger
CD Huang SK. Coincident idiopathic left ventricular tachycardia and atrioventricular
nodal reentrant tachycardia: control by radiofrequency catheter ablation
of the slow atrioventricular nodal pathway. Pacing Clin Electrophysiol 1994;17(3
Pt 1):386-96.
5. Washizuka
T, Niwano S, Tsuchida K Aizawa Y. AV reentrant and idiopathic ventricular
double tachycardias; complicated interactions between two tachycardias.
Heart 1999;81(3):318-20.
6. Cooklin M, McComb JM. Tachycardia
induced tachycardia: case report of right ventricular outflow tract tachycardia
and AV nodal reentrant tachycardia. Heart 1999;81(3):321-2.
