456
lACC Vol. 10, No.2
August 1987:456-61
DIAGNOSTIC STUDIES
Paroxysmal Nonreentrant Supraventricular Tachycardia Due to
Simultaneous Fast and Slow Pathway Conduction in Dual
Atrioventricular Node Pathways
SUNG SOON KIM, MD, FACC,* ROOP LAL, MD, FACC, RODOLPHE RUFFY, MD, FACC
St. Louis, Missouri
Electrophysiologic studies were performed on a 49 year
old woman who hall paroxysmal nonreentrant supraventricular tachycardia due to simultaneous anterograde
conduction through dual atrioventricular (AV) node
pathways. Slow pathway conduction was inversely related to the preceding sinus cyclelength and fast pathway
conduction was determined by the Hs-A interval (measured from the His potential due to slow pathway conduction to the onset of the subsequent atrial electrogram).
Simultaneous anterograde fast and slow pathway conduction
has been reported in patients who have dual atrioventricular
(AV) node pathways (1-3). This phenomenon was previously reported to occur primarily during rapid atrial pacing
or premature atrial stimulation, whereas sustained simultaneous anterograde fast and slow pathway conduction was
rarely observed during sinus rhythm (4-6), This report describes a case of paroxysmal nonreentrant supraventricular
tachycardia due to sustained simultaneous anterograde fast
and slow pathway conduction over dual AV node pathways,
treated successfully with flecainide, We also attempt to define the electrophysiologic determinants of sustained simultaneous anterograde fast and slow pathway conduction
during sinus rhythm.
Case Report
The patient was a 49 year old woman admitted to the
hospital for elective rectal surgery. After an uneventful operation, paroxysmal supraventricular tachycardia and interFrom the Jewish Hospital at Washington University Medical Center,
Cardiology Division, 216 S. Kingshighway, SI. Louis, Missouri 63110.
*Present address: Cardiology Division, Yonsei University College of
Medicine, c.p.a. Box 8044, Seoul, Korea.
Manuscript received August II, 1986; revised manuscript received
December 17, 1986, accepted January 9, 1987.
Address for reprints: Rodolphe Ruffy, MD, Jewish Hospital at Washington University Medical Center, Cardiology Division, 216 S. Kingshighway, SI. Louis, Missouri 63110.
© 1987 by the American College of Cardiology
Major determinants of sustained simultaneous anterograde fast and slowpathway conduction during sinus
rhythm were 1) a retrograde unidirectional block in both
fast and slow pathways, and 2) a critical conduction
delay in the slow pathway and a long enough Hs-A interval to allow sequential conduction of impulse from
both pathways. Flecainide was successful in preventing
recurrences of the tachycardia by eliminating slow path.
way conduction during long-term follow-up.
(1 Am Coil Cardiol1987;lO:456-61)
mittent 2:1 AV block were observed during her recovery.
The medical history included frequent episodes of palpitation for several years, lasting from a few minutes to V2 hour.
The patient had no known cardiac disease and was taking
no medication. Her cardiovascular examination, chest X ray
film and M-mode and two-dimensional echocardiograms
were normal. The 12 lead electrocardiogram (ECG) at rest
was normal except for occasional' 'blocked atrial premature
beats. "
Review of the patient's arrhythmias. Twenty-four hour,
ambulatory ECG monitoring after surgery showed multiple
paroxysmal episodes of both narrow and wide QRS tachycardia with one P wave for two QRS complexes (Fig. IA).
Additional rhythm strips revealed sinus rhythm with a very
prolonged PR interval (0.6 second), alternating double ventricular responses and nonconducted P waves (Fig. IB), and
sinus rhythm with occasional "blocked atrial premature beats"
(Fig. l C). These features suggested a diagnosis of simultaneous fast and slow pathway conduction in dual AV node
pathways.
Electrophysiologic Studies
After the patient provided written informed consent, electrophysiologic studies were performed using standard techniques with the patient in the postabsorptive, unmedicated
state, Pacing techniques included incremental atrial pacing
until the development of second degree AV node block,
0735-1097/87/$3.50
KIM ET AL.
SIMULTANEOUS FAST AND SLOW PATHWAY CONDUCTION
lACC Vol. 10. No.2
August 1987:456-61
each atrial impulse was followed by two ventricular responses. The AH interval of the first QRS response (AHf)
measured 110 to 130 ms and that of the second QRS response (AHs) measured 540 to 550 ms. A His potential was
recorded before each QRS complex with a constant HV
interval of 40 ms (Fig. 2). These findings were indicative
of sustained simultaneous fast and slow AV node pathway
conduction. The conduction pattern shifted to sustained exclusive slow pathway conduction as the Hs-A interval decreased from 250 to 220 ms (Hs-A intervals were measured
from the His potential due to slow pathway conduction to
the onset of the subsequent atrial deflection observed from
the His bundle electrogram). This decrease in Hs-A interval
was the result of a shortening of the sinus cycle length from
790 to 770 ms and a slight increase in slow pathway conduction time from 540 to 550 ms. As the sinus cycle length
decreased further to 740 ms, Wenckebach periodicity occurred in the slow pathway (Fig. 3). At sinus cycle lengths
shorter than 700 ms, alternating (2: I) simultaneous fast and
slow pathway conduction was observed. During such alternating conduction, facilitated conduction over the slow
pathway after a long cycle resulted occasionally in a critically short Hf-Hs interval (measured between the two His
potentials due to fast and slow pathway conduction of the
same atrial impulse), producing block of the impulse below
the His bundle (the seventh atrial impulse in Fig. 3). This
concealed phenomenon, however, interfered with subsequent AV conduction, producing an inappropriately nonconducted sinus P wave, or pseudo-A V block on the surface
recording (Fig. IBand 3). In addition, sustained double
ventricular responses to a single atrial impulse were on
occasion limited by His-Purkinje refractoriness.
Figure 4 depicts sustained simultaneous anterograde dual
AV node pathway conduction induced by atrial pacing at a
cycle length of 550 ms. However, only a single ventricular
response with a short PR interval was observed until the
Hf-Hs interval had lengthened beyond the effective refractory period of the His-Purkinje system as a result of deeremental conduction over the slow pathway. In this range of
cycle lengths, the His-Purkinje effective refractory period
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Figure I. Noncontinuous electrocardiographic (ECG) stnps ot
lead VI (A) and II (B,C). A, Each P wave is associated with two
QRS complexes. Note the "bigeminal" distribution of the QRS
complexes and the brief period of aberrancy in the second half of
the strip. B, Sinus rhythm with a long PR interval (0.6 second)
followed by alternating (2: I) double ventricular responses as the
sinus cycle length has shortened to 700 ms. The eleventh sinus P
wave is blocked unexpectedly. C, Frequent "blocked atrial premature beats." See text for discussion and explanation.
single atrial extrastimulation during atrial pacing at a cycle
length of 500 ms and incremental ventricular pacing.
Observations during sinus rhythm. During sinus rhythm
all the clinically recorded arrhythmias and conduction abnormalities were observed. At a cycle length of ::::790 ms,
Figure 2. Sustained simultaneous anterograde fast andslow pathway conduction shifting to sustained slow pathway conduction as
the Hs-A interval decreased to 220 ms or less (asterisks). Shown
from top to bottom are surface electrocardiographic (ECG) lead
VI, intracardiac recordings from the high right atrium (HRA),
bundle of His region (HBE) and right ventricular apex (RV) and
time lines (T). A = atrial electrogram; Hf = His potential from
fast pathway conduction; Hs = His potential from slow pathway
conduction; V = ventricular electrogram. The Hs-A interval was
measured from the H potential due to slow pathway conduction
to the onset of the next atrial electrogram (A) at the His bundle
level. On the ladder diagram, A, AV, HB, HP and V represent
the atrium, the atrioventricular (AV) node, the His bundle, the
His-Purkinje system and the ventricle, respectively. The solid and
dashed linesrepresent fastandslow AV node pathway conduction,
respectively.
VI
457
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HV_---L._
p --+=--+'-"'---+o'=-----\,.=--+'-"'--+=-----1-'-'''-------l,.,..,..-----+-'''''-----+'-'''-----+'"'''-_L.-_...J......_--L-_----L_ _...L--J...
.L-....JL....J--_
458
JACC Vol. 10, No, 2
KIM ET AL.
SIMULTANEOUS FAST AND SLOW PATHWAY CONDUCTION
August 1987:456-61
VI -v----"""'v,..------..r----"""'v~----""""\v
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HP
V -----T-'-''---------r-'"-----\-=--------'P----'P-----\-~-=--------P'----r'''
-L'---'----'"_ _---J'----'
---'-_ _- - L -
Figure 3. Wenckebach periodicity in the slow pathway and 2: I
simultaneousfast and slow pathway conduction. As the sinus cycle
length decreased from 740 to 670 ms, Wenckebach periodicity
occurred in the slow pathway, followed by 2: I simultaneous dual
AV node pathway conduction. The seventh atrial impulse produced
two His bundle responses due to simultaneous fast and slow pathway conduction but the second ventricular response did not follow
the slow pathway conduction because of a short Hf-Hs interval
(410 ms). Note that the eighth sinus beat was blocked because of
refractorinessof both pathways secondary to concealed conduction
of the preceding slow pathway conduction. Abbreviations as in
Figure 2.
could be precisely measured to be 410 ms. On a surface
ECG, this concealed phenomenon would have appeared as
sustained exclusive fast pathway conduction. Sustained simultaneous fast and slow pathway conduction could also
appear as exclusive slow pathway conduction with a long
PR interval on the surface ECG because of His-Purkinje
block after each fast AV node pathway conduction (Fig. 5).
Finally, Figure 6 shows that the' 'blocked atrial premature
beats" illustrated in Figure lC were, in fact, single AV
node (slow-fast) echoes with an HA interval of 80 ms and
a low to high atrial sequence occurring with or without a
ventricular response. Sustained AV node reentrance, however, was not observed.
Observations during programmed electrical stimulation. Incremental atrial pacing demonstrated alternating
(2: 1) simultaneous fast and slow pathway conduction at
pacing cycle lengths of 600,550 and 500 ms. Shorter pacing
cycle lengths were associated with 1:1 exclusive fast AV
node pathway conduction; at a cycle length of 350 ms, AV
node Wenckebach periodicity occurred. Standard single atrial
extrastimulation testing was impossible during sinus rhythm
as well as during atrial pacing at cycle lengths of 600 and
500 ms because of intermittent anterograde slow pathway
conduction. Modified single atrial extrastimulation was performed during atrial pacing at a cycle length of 500 ms. At
this cycle length, alternating simultaneous anterograde fast
and slow pathway conduction was associated with an AH J
interval of 100 ms and an AHs interval of 550 ms with the
H,-Hs interval being 450 ms (Fig. 7). Atrial extrastimuli
were delivered after fast pathway conduction. At A 1-A2
intervals :::::450 ms an H 2 response could not be elicited
because the impulse (A J) carried over the slow pathway
always preempted the His bundle (Hs) (Fig. 7). At A,-A 2
Figure 4. Apparentexclusive fast pathway conduction. Atrial pacing at a cycle length of 550 ms was associated with alternating
(2: I) simultaneous fast and slow pathway conduction. Termination
of pacing was followed by sustained simultaneous dual AV node
pathway conduction. However, the impulse carried over the slow
pathway could not reach the ventricles because of His-Purkinje
refractoriness until the Hf-Hs interval lengthened to 420 ms (asterisks). Note the intermittent rate-dependent left bundle branch
block on the surface electrocardiogram (the second, fourth and last
two QRS complexes). S = stimulation artifact; other abbreviations
as in Figure 2.
VI -,r----. ,----,,.----- ,---,,.-----""""Ir-----'r----'/'-------..r--,
T
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JACC VoL 10, NO.2
August 1987:456-61
KIM ET AL.
SIMULTANEOUS FAST AND SLOW PATHWAY CONDUCTION
459
HRA
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V_.L..:!:>!.!L---l..~~--:::l~---L_~"'----_----l..-_~~_-L-_~"'----_-L-----'~~_L.-_~~__''____'''.:ll<..._~
Figure5. Apparent exclusive slow pathway conduction. After two
sinus beats with double ventricular responses, each subsequent
sinus beat was followed by a single ventricular response despite
sustained simultaneous dual AV node conduction. This was initiated by a short Hs-Hf interval of 350 ms (asterisk) and perpetuated by a long-short sequence. Abbreviations as in Figure 2.
ultimately treated with oral flecainide, 50 mg every 12 hours.
This treatment resulted in apparent exclusive fast pathway
conduction at rest and during exercise testing. There was
no recurrence of nonreentrant paroxysmal supraventricular
tachycardia or apparent slow pathway conduction for the
next 16 months. At the last measurement, the ftecainide
plasma level was 210 ng/m!.
Determinants of fast and slow pathway conduction.
Slow pathway conduction was inversely related to the preceding sinus cycle length (Fig. 8). The slow pathway developed Wenckebach periodicity at the unusually long cycle
length of 740 ms indicative of very prolonged refractoriness.
At sinus cycle lengths between 750 and 850 ms, stable slow
pathway conduction was present with AHs intervals ranging
from 500 to 570 ms (Hf-Hs interval 2:420 ms). At longer
sinus cycle lengths (between 860 and 950 ms), the slow AV
node pathway was capable of conducting impulses with
shorter AHs intervals, ranging from 460 to 480 ms, resulting
in critically short Hf-Hs intervals «420 ms) associated with
block below the His bundle. At cycle lengths >950 ms,
slow pathway conduction was no longer observed, probably
because the conduction delay in the slow pathway was not
sufficient to allow recovery of the distal common pathway
intervals between 430 and 340 ms H)-H2 intervals gradually
shortened from 430 to 370 ms. At A)-A2 intervals from 330
to 220 ms the H 1-H2 (H1-Hs) interval suddenly lengthened
to 450 ms and remained constant, indicating the reappearance of slow pathway conduction of A) and block of A2 in
the fast pathway. No ventriculoatrial conduction was observed at any ventricular paced cycle lengths.
Drug intervention. The intravenous administration of
2 mg of atropine sulfate decreased the sinus cycle length to
600 ms. Frequent single AV node reentrant echoes, with or
without simultaneous ventricular responses, were observed.
Alternating, but not sustained, simultaneous fast and slow
pathway conduction was observed intermittently after atropine was given. Intravenous administration of digoxin (0.75
mg) and propranolol (0.15 mg/kg body weight) had no apparent effect on the phenomena described. The patient was
HRA
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Hs-Ae --,-=::--r--;::-:;;-~r-~;:;;::;----'---;::-;;-;;~---;:;-;:;:;:::--'-----'=:--lr-;::-;:;;:;::-:::':-A~..,.-~~-k-~~I.,-~~---4""""":=::--J.,..,----~~4-'-'=-"'---J\o;-:-"'=".:'-:::-J-
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-~----'~~-----\r--=r-----r"'-----p'-----""r­
-~::---+=::--+=,.-----t-:;,;o;---+-----+--~r----\'­
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---'-1-_ _- - - ' - _ - - ' - _
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Figure 6. Single AV node reentrant (slowfast) echoes with or without ventricular responses. The atrial sequence of the echo
beat (Ae) was low to high and the H-Ae
interval of 80 ms was fixed, whether associated with a ventricular response or not.
This appeared as "blockedatrial premature
beats" on the surface electrocardiogram
(ECG) (arrow). The top tracing on this
figure is surface ECG lead II. Hs-Ae =
interval between Hs and Ae; other abbreviations as in Figure 2.
460
KIM ET AL.
SIMULTANEOUS FAST AND SLOW PATHWAY CONDUCTION
500
Cycle Length' 500
.....
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JACC Vol. 10, No.2
August 1987:456--61
The shortest Hf-Hs interval that allowed double ventricular
responses was 420 ms (Fig. 4). Therefore, paroxysmal nonreentrant supraventricular tachycardia due to sustained simultaneous fast and slow pathway conduction during sinus
rhythm was observed at sinus cycle lengths between 780
ms (Hs-A :::::240 ms, AHf 120 ms and Hf-Hs :::::420 ms) and
850 ms.
300
I
Discussion
I
I
I
300
400
500
A I-A2 (rns )
Figure 7. Single atrial extrastimulation during atrial pacing at a
cycle length of 500 ms. AI and HI are the right atrial and His
bundle responses to the driven beats and Hs is the His bundle
electrogram due to slow pathway conduction. A z and Hz are the
right atrial and His bundle responses to atrial extrastimulation. The
conduction curve suggests dual AV node pathways. See text for
discussion.
from prior activation through fast pathway. In contrast to
slow pathway conduction, fast pathway conduction was determined by the Hs-A interval. This interval was a function
of the preceding sinus cycle length and the slow pathway
conduction time of the preceding atrial impulse (Fig. 2).
Simultaneous anterograde fast and slow pathway conduction
was present when the Hs-A interval was >220 ms. When
the Hs-A interval measured ::;220 ms, the fast pathway was
refractory.
To have double ventricular responses to a single atrial
impulse, the difference in conduction times between the fast
and the slow pathways (Hf-Hs) had to be longer than the
effective refractory period of the distal conducting system,
including distal common pathway and His-Purkinje system.
Figure 8. Effect of the preceding sinus cycle length (A-A) on
slowpathwayconduction. A-Hs = slow pathwayconduction time;
A-Hf = fast pathway conduction time; H-P = His-Purkinje. See
text for discussion.
600
500
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1000 1100
PRECEDING A-A (rns)
Determinants of sustained simultaneous fast and slow
pathway conduction. Simultaneous anterograde fast and
slow pathway conduction has been observed during rapid
atrial pacing or atrial extrastimulation in patients with AV
node reentrant paroxysmal supraventricular tachycardia (1-3).
In these patients simultaneous fast and slow pathway conduction was usually followed by a slow-fast reentrant echo
or a reentrant tachycardia. A critical conduction delay as
well as unidirectional retrograde block in the slow pathway
have been postulated as major determining factors for this
phenomenon (3). Csapo (4) and Sutton and Lee (5,6) reported four cases of dual AV node pathways in which sustained simultaneous anterograde fast and slow pathway conduction during sinus rhythm manifested itself as nonreentrant
paroxysmal supraventricular tachycardia. It was suggested
that nonreentrant supraventricular tachycardia was possible
only when the refractory period of the distal conducting
system was shorter than the shortest cardiac cycle length
and unidirectional retrograde block was present in both fast
and slow pathways (5).
In our patient we were able to identify the electrophysiologic determinants of sustained simultaneous fast and slow
pathway conduction. This conduction abnormality was
maintained in a range of sinus cycle lengths associated with
a critical conduction delay in the slow pathway and long
enough Hs-A intervals to allow sequential conduction of
impulse from both pathways. Although a discontinuous AV
node conduction curve could not be demonstrated because
standard programmed atrial extrastimulation could not be
performed, the presence of two distinct AV node pathways
was strongly suggested when modified extrastimulation testing was performed during atrial pacing at a cycle length of
500 ms. Also suggestive of dual AV node pathways was
the observation of single AV node (slow-fast) echoes with
or without a ventricular response. Despite the absence of
ventriculoatrial conduction during ventricular pacing, the
fast pathway was occasionally capable of retrograde conduction in our patient. This indicates that the reentrant circuit
was confined to the AV node and that ventricular tissue was
not necessary to produce reentrant echoes, in accordance
with the observation of Wellens et al. (7).
Because of the unreliable retrograde conduction properties of the fast pathway, our patient presented mainly with
paroxysmal nonreentrant supraventricular tachycardia and
JACC Vol. 10, NO.2
August 1987:456-61
had only rare single AV node reentrant echoes. Although
such single echoes were possible, sustained AV node reentrance was not because of the unusually long refractory
period of the slow pathway. The cycle length of the AV
node echo was 640 ms (AH interval 560 ms, HA interval
80 ms), far shorter than the slow pathway block cycle length
of 740 ms.
Effects of antiarrhythmic agents. Previous investigators (4-6) have noted the unusual response to atropine sulfate and type I antiarrhythmic drugs such as ajmaline, procainamide and quinidine in patients who had nonreentrant
paroxysmal supraventricular tachycardia due to sustained
simultaneous conduction through dual AV node pathways.
This response is probably related to the effect of such drugs
on retrograde fast pathway conduction. Our patient had more
frequent single AV node reentrant echoes and no sustained
simultaneous anterograde fast and slow pathway conduction
after the administration of atropine, probably because the
drug had improved retrograde fast pathway conduction to
facilitate AV node reentrance (8). Flecainide, on the other
hand, appeared to have prevented sustained simultaneous
fast and slow pathway conduction by total elimination of
slow pathway conduction. In patients who have a dual AV
node pathway it is known that flecainide has a weak depressant effect on anterograde slow pathway conduction in
addition to a marked depressant effect on the conductive
properties of the retrograde limb (9,10). Because we did
not repeat electrophysiologic studies during flecainide treatment' we have not confirmed that the effect of flecainide
was limited to the AV node. It seems equally likely that
normalization of the surface ECG may have occurred as a
result of a flecainide effect on the His-Purkinje system.
Because the conductive properties of the His-Purkinje system were demonstrably abnormal before flecainide administration, it is reasonable to hypothesize that flecainide, even
in small amounts, may have further disabled the infra-Hisian
propagation of impulses occurring at relatively short coupling intervals, namely those carried over the slow pathway.
Clinical implications. Simultaneous anterograde fast and
slow pathway conduction may not be simply a rare electrophysiologic observation of academic interest only. In our
case moderate changes in sinus rate and in fast or slow
pathway conduction times resulted in a variety of ECG
manifestations, simulating supraventricular and ventricular
bigeminy, junctional premature beats and junctional tachycardia, ventricular tachycardia and unexplained sudden PR
KIM ET AL
SIMULTANEOUS FAST AND SLOW PATHWAY CONDUCTION
461
prolongation or unexpected (pseudo) AV block (4,II). These
complex ECG manifestations could all be explained on the
basis of intermittent or sustained simultaneous anterograde
dual AV node pathway conduction, aberrant intraventricular
conduction and concealed fast and slow pathway conduction. This recognition may also have important therapeutic
implications, because the response of this type of arrhythmia
to traditional type I drugs differs from the response of more
common varieties of supraventricular tachycardia. In our
patient, flecainide, a class IC drug, was successful in preventing recurrences of nonreentrant paroxysmal supraventricular tachycardia by maintaining apparent sustained fast
pathway conduction during long-term follow-up.
We thank Margie Galkowski for expert secretarial assistance and Roberta
Rich and Mary Sorrells for preparation of illustrations.
References
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