Journal of Electrocardiology Vol. 32 No. 4 1999
Paroxysmal Supraventricular Tachycardia
Caused by 1:2 Atrioventricular
Conduction in the Presence Of Dual
Atrioventricular Nodal Pathways
A u r e l i a n o Fraticelli, M D , * G a b r i e l e S a c c o m a n n o , M D , *
Carlo Pappone, MD, t and Giuseppe Oreto, MD {
Abstract: One-to-two atrioventricular conduction, ie, the double response to
a single sinus or atrial impulse, resulting in two QRS complexes for one P wave,
is a rare manifestation of dual atrioventricular (AV) nodal pathways. This
report describes the case of a 6 I-year-old w o m a n with continuous episodes of
supraventricular tachycardia caused by independent conduction to the ventricles of sinus impulses over both the fast and the slow AV nodal pathway, giving
rise to a ventricular rate that was twice the sinus rate. A wide spectrum of
electrocardiographic manifestations of 1:2 AV conduction was observed on the
surface electrocardiogram. The diagnosis was suggested by several elements
including evidence of dual AV nodal pathways during sinus rhythm and cycle
length alternans during tachycardia. The patient u n d e r w e n t successful slow
pathway ablation with complete disappearance of symptoms and electrocardiographic manifestations of 1:2 AV conduction. Key words: catheter ablation, dual atrioventricular nodal pathways, electrocardiogram, supraventricular tachycardia.
whereas radiofrequency catheter ablation of the
slow AV nodal pathway resulted in complete suppression of the arrhythmia.
A double ventricular response to a single atrial
depolarization through dual atrioventricular (AV)
nodal pathways has been described as an artificially
induced phenomenon during electrophysiologic
study (I-5) or as a spontaneous rhythm abnormality (6-13). We describe the case of a patient whose
tachyarrhythmia was caused by this mechanism.
Antiarrhythmic drugs proved to be ineffective,
Case Report
Clinical Presentation
A 61-year-old woman was referred because of
drug-resistant tachycardia. The patient had been
suffering several daily episodes of palpitations lasting from a few minutes to several hours, often
associated with flushing and dizziness, occurring
both at rest and during physical activity. Based on
From *INRCA Diparfirnento di Cardiologia, Ancona; tOspedale S.
Raffaele, Milano; and ¢Cardiologia, Universit2z di Messina, Messina,
Italy.
Reprint requests: Professor Giuseppe Oreto, Via Terranova 9,
98122 Messina, Italy.
Copyright © 1999 by Churchill Livingstone ®
0022-0736/99/3204-00065 I0.00/0
347
348
Journal of Electrocardiology Vol. 32 No. 4 October 1999
resting electrocardiogram (ECG) and Holter monitoring several different supraventricular (atrial fibrillation and flutter, AV junctional extrasystoles
and tachycardia) and ventricular arrhythmias (extrasystoles and nonsustained tachycardia) had been
suspected. Since the age of 35, she had been receiving drug t r e a t m e n t with digoxin, quinidine, verapamil, amiodarone, propafenone, sotalol, or combinations of these, with either no i m p r o v e m e n t or
only t e m p o r a r y improvement. Pertinent physical
findings were limited to irregular pulse and moderate hypertension. The echocardiogram and coronary angiogram were normal.
activity was often difficult to analyze (Fig. la) in
such a way that the pattern resembled atrial fibrillation. On other occasions the P waves were clearly
detectable (asterisks in Fig. lb) and expressed an
AV relationship that was either variable (Fig. lb) or
with a fixed 1:2 ratio (Fig. lc). Sinus r h y t h m was
frequently altered by n a r r o w p r e m a t u r e QRS complexes apparently not preceded by P waves (Fig.
2a). At times, some short r h y t h m i c sequences occurred with n o r m a l rate, 1:1 AV relationship, and
very prolonged PR intervals (about 0.60 s), in such
a way that the P wave was almost simultaneous to,
and partially obscured from, the preceding QRS
complex, thereby simulating an AV junctional
rhythm. In one occasion the termination of prolonged PR interval occurred in coincidence with a
second-degree sinoatrial block, followed by sinus
r h y t h m with n o r m a l PR interval (Fig. 2b). Isolated
or repetitive wide QRS complexes were also observed (Fig. 2c). Finally, occasional episodes of
second-degree AV block were detected (Fig. 2d).
All of these ECG patterns are explained by the
presence of dual AV nodal pathways capable of
single (Fig. 2a), repetitive (Fig. la, b), or sustained
(Fig. lc and related ladder diagram) 1:2 conduction,
Holter Monitoring
A 2 4 - h o u r ambulatory recording showed an extremely variable heart rate, ranging from 45 to 200
beats/min. Normal sinus r h y t h m was limited to a
few minutes of the recording. The most c o m m o n
r h y t h m abnormality consisted of paroxysmal episodes of irregular, n a r r o w QRS complex tachycardia
at ventricular rates ranging from 100 to 200 beats/
rain (Fig. la,b). Sustained RR cycle alternans was
often observed during tachycardia (Fig. lc). Atrial
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Fig. 1. Noncontinuous ECG strips recorded during Holter monitoring (lead CM 5), showing the patient's paroxysmal
episodes of irregular, narrow QRS complex tachycardia (strips a and b). The asterisks below strip b indicate manifest sinus
P waves. Sustained RR cycle altemans can be seen in strip c. In the ladder diagram solid lines in the AV section represent
conduction over the fast pathway, and the broken lines represent conduction over the slow pathway.
1:2 Atrioventricular Conduction
•
Fraticelli et al.
349
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Fig. 2. Noncontinuous ECG strips recorded during Holter monitoring (lead CM 5), showing the variety of abnormalities
found in this patient. Strip a shows sinus rhythm altered by narrow premature QRS complexes that were apparently not
preceded by P waves. Strip b shows the termination of a prolonged PR interval occurring coincidentally with a
second-degree sinoatrial block, followed by sinus rhythm with a normal PR interval. Isolated and repetitive wide QRS
complexes are shown in strip c. One occasional episode of second-degree AV block is reported in strip d.
with occasional exclusive slow p a t h w a y conduction
(Fig. 2b). Aberrant c o n d u c t i o n (Fig. 2c), Wenckebach periodicity, and AV block (Fig. 2d) contributed to the variety of ECG manifestations.
Electrophysiologic Study
After informed written consent, an electrophysiologic study was performed, with the patient in a
fasting, u n m e d i c a t e d state. A n t i a r r h y t h m i c drugs
had been discontinued for at least 5 half-lives, and
the patient had not been taking a m i o d a r o n e in the
previous 2 years. Quadripolar 6F catheters inserted
t h r o u g h the right femoral and left subclavian veins
were placed in the right atrium, coronary sinus, His
bundle region, and right ventricular apex. A steerable 7F catheter was used for mapping and radiofrequency delivery.
During uncomplicated sinus r h y t h m (not illustrated) the intracardiac ECG was normal, except for
a slight prolongation of the HV interval to 70 ms. At
a sinus cycle length of 660 ms the AH interval was
75 ms. An example of spontaneous tachycardia is
s h o w n in Figure 3. Both the surface and the intracardiac ECG indicated sinus r h y t h m with n o r m a l
atrial activation and a stable cycle of 580 ms. There
was a regular 1:2 AV relationship. Each ventriculogram was preceded by a His deflection with a
constant HV interval. The interval b e t w e e n the
atrial wave and the first His deflection was 115 ms,
whereas the interval b e t w e e n the atrial wave and
the second His deflection was slightly variable,
ranging from 380 to 400 ms.
Figure 4 shows sustained exclusive anterograde
conduction over the slow p a t h w a y : a 1:1 AV relationship is shown, with constant AH intervals of
380 ms. Figure 5 shows a p r e m a t u r e atrial beat that
resets the modality of AV conduction: a sequence of
1:1 conduction over the slow p a t h w a y was interrupted by an atrial extrasystole (arrow) that
"switches" to n o r m a l exclusive conduction over the
fast pathway. A standard study of AV nodal function with p r e m a t u r e atrial extrastimuli could not be
performed because of disturbing double responses.
350
Journal of Electrocardiology Vol. 32 No. 4 October 1999
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(I, III, aVF, and V]) and intracardiac electrograms f r o m the
high fight atrium, distal (HRAd)
and proximal (HRAp), the His
bundle r e , o n , proximal (HBEp)
and distal (HBEd), the coronary sinus, p r o x i m a l (CSp)
and distal (CSd), and the right
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Ventricular pacing resulted in complete retrograde
VA block (not illustrated).
After obtaining intracardiac recordings, radiofreq u e n c y a b l a t i o n of t h e s l o w p a t h w a y w a s p e r f o r m e d . T w o r a d i o f r e q u e n c y p u l s e s (55 °, 60 s e a c h )
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d e l i v e r e d i n t h e r i g h t p o s t e r o s e p t a ] r e g i o n n e x t to
t h e c o r o n a r y s i n u s os, i n c o r r e s p o n d e n c e w i t h a
typical "slow pathway potential," resulted in block
of c o n d u c t i o n o v e r t h e s l o w p a t h w a y . A f t e r a b l a tion, neither spontaneous nor induced arrhythmias
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as in Fig. 3.
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351
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Fig. 5. Simultaneous recording of four surface ECG leads
(I, III, aVF, and V1) and intracardiac electrograms. Symbols
as in Fig. 3. The arrow indicates an atrial extrasystole.
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could be observed during electrophysiologic study.
Figure 6 compares the 24-hour heart rate profiles
recorded before and after the procedure, in the
absence of antiarrhythmic treatment, showing
complete suppression of tachycardia.
Discussion
Simultaneous fast and slow pathway conduction
to the ventricles over dual AV nodal pathways may
occur spontaneously for single (13) or consecutive
(5-12) atrial impulses, in the latter case resulting in
a tachycardia with ventricular rate twice the atrial
rate. Very few cases of such arrhythmia, often
called "paroxysmal non-reentrant supraventricular
tachycardia," have been described (6-12). In our
patient the Holter recording revealed a spectrum of
ECG patterns that could be misinterpreted as AV
junctional accelerated rhythm, atrial fibrillation,
ventricular extrasystoles, or runs of ventricular
tachycardia. The marked PR interval change (from
less than 0.20 s to more than 0.40 s) during sinus
rhythm was a key for the interpretation of this case.
AV Conduction and Dual AV Pathways
In the presence of dual AV nodal pathways,
conduction of sinus impulses to the ventricles may
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occur in three different modalities: (1) over the fast
pathway; (2) over the slow pathway; (3) simultaneously over both fast and slow pathways (1:2
response, illustrated in the ladder diagram of Fig. 1).
The sinus impulse approaches simultaneously the
proximal edge of both pathways, but in the majority of subjects conduction to the ventricles occurs
through one single pathway, and 1:2 response does
not occur because of (1) concealed retrograde conduction into the "nondominant" pathway (the slow
pathway during anterograde fast pathway conduction and vice versa) (3,7), and (2) refractory state of
the distal common pathway, occurring whenever
its recovery time exceeds the difference between
slow and fast pathway conduction time.
The determinants of conduction over dual AV
nodal pathways include sinus rate changes
(6,8,9,14), atrial or ventricular premature beats
(7,8,13-15), and electrophysiologic properties of
both the pathways and the distal conduction system
(conduction velocity, refractoriness, retrograde
conduction) (3,6,8,9). Autonomic nervous system
(7,14) and drugs (2,6-10) can modify these properties and, consequently, the modality of AV conduction. In the present case, slow pathway conduction time ranged from 0.40 to 0.80 s, with longer
intervals recorded during the night, suggesting a
strong vagal influence on slow pathway conduction
velocity.
352
Journal of Electrocardiology Vol. 32 No. 4 October 1999
6. Twenty-four hour
heart rate profiles (A) before
and (B) after radiofrequency
ablation.
Fig.
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Second-Degree AV Block in Dual AV
Nodal Pathways
One of the ECG manifestations of dual AV nodal
p a t h w a y s is "atypical" second-degree W e n c k e b a c h
type AV block (I4). In our patient second-degree
AV block was frequent, usually occurring after one
or m o r e double responses (Fig. 2d). Completely
blocked sinus impulses always follow a QRS complex resulting f r o m conduction over the slow pathway: the block occurs w h e n e v e r the ensuing sinus
impulse, w h i c h is very "early" in the cardiac cycle,
traverses the fast p a t h w a y but finds the final comm o n p a t h w a y refractory and cannot reach the
ventricles. On the other hand, if the s a m e impulse
also undergoes a block in the slow p a t h w a y , a total
absence of conduction to the ventricles ensues. In
this situation, AV block is not an expression of AV
nodal i m p a i r m e n t , but rather a manifestation of
dual AV nodal pathways. It is w o r t h noting that in
our patient AV block was totally absent in two
2 4 - h o u r recordings following slow p a t h w a y ablation.
In the presence of dual AV nodal p a t h w a y , per-
sistence of exclusive slow p a t h w a y conduction is
not, in itself, an expression of p o o r fast p a t h w a y
conduction, but usually results from concealed retrograde conduction into the fast p a t h w a y ; following
a sinus impulse conducted over the slow p a t h w a y
only, the fast p a t h w a y is invaded retrogradely, and
becomes refractory to the ensuing supraventricular
impulse, w h i c h is again conducted to the ventricles
over the slow p a t h w a y , with retrograde concealed
conduction into the fast p a t h w a y , and so on. Such
a m e c h a n i s m , h o w e v e r , was not operating in our
patient, since it was impossible to assume retrograde invasion of the n o n d o m i n a n t p a t h w a y , a
p h e n o m e n o n that w o u l d h a v e p r e v e n t e d I:2 conduction. It is m o r e likely that exclusive anterograde
conduction over the slow p a t h w a y was occurring,
because the impulse conducted over the fast pathw a y was blocked in the final c o m m o n p a t h w a y .
This block was favored by the very long slow
p a t h w a y conduction time; as a consequence, the
c o m m o n p a t h w a y was still refractory w h e n it was
reached by the ensuing sinus impulse conducted
over the fast p a t h w a y .
Accordingly, the finding of exclusive slow path-
1:2 Atrioventricular C o n d u c t i o n
w a y conduction in the reported case did not cause
a n y concern for potential p o o r fast p a t h w a y conduction; this is also p r o v e d by the postablation
follow-up, d e m o n s t r a t i n g n o r m a l a n t e r o g r a d e fast
p a t h w a y conduction.
•
Fraticelli et al.
353
RR
PR
Incidence of Paroxysmal Tachycardia
Caused by 1:2 Conduction
RR
The prevalence of p a r o x y s m a l tachycardia resulting f r o m double response to sinus impulses is pres u m a b l y v e r y low. We are a w a r e of only seven
reported cases (6-12). O n e - t o - t w o AV conduction
is probably rare e v e n a m o n g patients with electrocardiographic evidence of dual AV nodal pathways.
In a series of l0 such patients identified f r o m
analysis of 3,200 Holter recordings, 1:2 AV conduction was not m e n t i o n e d e v e n t h o u g h the majority
of patients had their longest PR interval ranging
f r o m 0.40 to 0.64 s (15). M o r e recently, Fisch et al.
(13) reported on 21 patients with ECG evidence of
dual AV n o d e physiology during sinus r h y t h m .
Only 1 of these subjects s h o w e d episodic 1:2 conduction of single impulses. Although supraventricular tachycardia due to 1:2 AV conduction is rare, it
is likely that its prevalence is u n d e r e s t i m a t e d because of the difficulties in differentiating this arr h y t h m i a f r o m other m o r e c o m m o n ones.
Diagnosis of Paroxysmal Tachycardia
Caused by 1:2 Conduction
The possibility of dual AV nodal pathways with
simukaneous fast and slow conduction should be
suspected in the presence of irregular paroxysmal
supraventricular tachycardia associated with marked
PR changes during sinus rhythm. Sustained cycle
length altemans during tachycardia could be a further
indicator of this arrhythmia. In fact, initiation of stable
1:2 conduction over dual AV nodal pathways results
in RR cycle alternans regardless of slow p a t h w a y
conduction velocity, with the single exception in
which the difference between slow and fast conduction times is half of the sinus cycle length (Fig. 7).
Cycle length alternans also occurs in m o r e c o m m o n
supraventricular arrhythmias such as atrial flutter or
tachycardia, AV nodal reentrant tachycardia, and AV
reentrant tachycardia. Sustained cycle length alternans, however, is unusual both in AV nodal and in
AV reentrant tachycardia, but is relatively c o m m o n in
atrial tachycardia associated with 3:2 AV conduction
ratio and Wenckebach periodicity. On the other hand,
cycle length alternans appears as the rule in the case
of tachycardia due to 1:2 AV conduction; all published
PR
Fig. 7. Schematic ECGs showing cycle length alternans
during tachycardia due to 1:2 atrioventricular conduction. Numbers below the tracings express PR intervals,
and numbers above the tracings correspond to RR intervals, in hundredths of a second. The sinus cycle is
constant, and measures .80 s. Each sinus impulse is
followed by a double ventricular response. The upper
tracing shows ventricular cycle length alternans, whereas
in the lower tracing the RR cycles are constant because
the difference between the PR intervals of the two beats
related to any given sinus impulse is half the sinus cycle
length (52 - 12 = 40).
reports show ECGs with RR alternans during tachycardia (6-9,11,12), although this finding is not m e n tioned. Thus, detection of sustained cycle length alterhans
during
supraventricular
tachycardia
of
undetermined origin should raise the suspidon of
dual AV nodal pathways and dictate the need for
accurate and detailed P wave sequence analysis in
multiple ECG leads. A n u m b e r of P waves half that of
QRS complexes will establish the diagnosis of 1:2
conduction.
The electrophysiologic study m a y provide further
but not conclusive clues, such as the constancy of
HV interval of " n o r m a l " and " p r e m a t u r e " beats, a
response to p r o g r a m m e d atrial stimulation consisting in l e n g t h e n i n g coupling of the a p p a r e n t l y "ectopic" beat with increasing p r e m a t u r i t y of extrastimuli (11), and evidence of dual AV nodal
physiology (6,9). Nevertheless, it is theoretically
impossible to exclude an AV junctional ectopic
focus giving rise to p r e m a t u r e interpolated beats
often occurring in bigeminy, or an accelerated AV
junctional r h y t h m .
A n t i a r r h y t h m i c drugs h a v e b e e n either ineffective or detrimental in m o s t reported cases (6-11 ), as
in our patient. Clinical i m p r o v e m e n t has b e e n
obtained with flecainide (9) or a m i o d a r o n e (10),
which was ineffective in o u r case. In contrast,
354
Journal of Electrocardiology Vol. 32 No. 4 October 1999
r a d i o f r e q u e n c y a b l a t i o n of t h e slow AV n o d a l p a t h w a y r e p r e s e n t s a safe a n d d e f i n i t i v e cure for this
u n u s u a l a r r h y t h m i a (11,12). D i s a p p e a r a n c e of the
m u l t i p l e ECG m a n i f e s t a t i o n s of 1:2 AV c o n d u c t i o n
f o l l o w i n g successful r a d i o f r e q u e n c y a p p l i c a t i o n is
p r o b a b l y t h e s t r o n g e s t e l e m e n t s u p p o r t i n g t h e diagnosis.
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