Determinants of Fast- and Slow-Pathway Conduction in
Patients with Dual Atrioventricular Nodal Pathways
By Delon Wu, Pablo Denes, Ramesh Dhingra. Christopher Wyndham. and Kenneth M. Rosen
ABSTRACT
Electrophysiological studies were performed in two patients with documented paroxysmal supraventricular tachycardia and dual atrioventricular (AV) nodal pathways as
defined by the atrial extra-stimulus technique. Both patients manifested two ranges of
A-H intervals (AV nodal conduction times) at critical cycle lengths, reflecting fast- and
slow-pathway conduction. The occurrence of fast- and slow-pathway conduction at the
same cycle length depended on a long fast-pathway effective refractory period relative to
the spontaneous or driven cycle length. At critical cycle lengths with fast-pathway
conduction, a shift to slow-pathway conduction could be induced by a premature atrial
impulse falling within the effective refractory period of the fast pathway. Repetitive
retrograde concealed conduction to the fast pathway then maintained antegrade slowpathway conduction. Resumption of fast-pathway conduction was induced with premature atrial impulses falling within the effective refractory periods of both the fast and the
slow pathways, allowing recovery of the fast pathway for antegrade conduction. Atrial
echoes and AV nodal reentrant paroxysmal supraventricular tachycardia occurred when
sufficient slow-pathway delay was achieved to allow recovery of the fast pathway for
retrograde conduction.
Wolff-Parkinson-White syndrome
KEY WORDS
concealed conduction
refractory periods
paroxysmal supraventricular tachycardia
His bundle electrograms
• Recent electrophysiological studies from several laboratories have suggested that the atrioventricular (AV) node can longitudinally dissociate
into two pathways with different functional properties (1-11). In man, dual AV nodal pathways have
been described in a patient with two P-R intervals
and in several patients with AV nodal reentrant
paroxysmal supraventricular tachycardia (9-11).
In the present investigation, we studied two
patients with documented paroxysmal supraventricular tachycardia. In both of these patients, two
sets of conduction times (A-H intervals) were
demonstrated, suggesting dual AV nodal pathways. The determinants of fast- and slow-pathway
conduction and their relationship to the echo
From the Section of Cardiology, Abraham Lincoln School of
Medicine of the University of Illinois College of Medicine, and
the West Side Veterans' Administration Hospital, Chicago,
Illinois 60680.
This work was supported in part by NIH Contract 71-2478
under the Myocardial Infarction Program of the National Heart
and Lung Institute, by U. S. Public Health Service Grant
HL-05879-05S1 from the National Heart and Lung Institute,
and by basic institutional support of the West Side Veterans'
Administration Hospital, Chicago, Illinois.
Please address reprint requests to Delon Wu, M.D., Section
of Cardiology, University of Illinois Hospital, P.O. Box 6998,
Chicago, Illinois 60680.
Received January 13, 1975. Accepted for publication March
24, 1975.
782
phenomenon and reentrant paroxysmal tachycardia were analyzed.
Methods
ELECTROPHYSIOLOGICAL STUDIES
Electrophysiological studies were performed in the
postabsorptive, nonsedated state. The research protocol
had the prior approval of the University of Illinois
Committee of Associates for review of clinical research
and investigation involving human beings. Informed
consent was obtained. A tripolar electrode catheter was
percutaneously introduced into the femoral vein and
fluoroscopically positioned across the tricuspid valve for
His bundle recording (12). A second quadripolar electrode catheter was percutaneously introduced into the
other femoral vein and placed against the lateral wall of
the high right atrium for atrial stimulation and recording. Electrocardiographic leads I, II, III, and V, and high
right atrial, low right atrial, and His bundle electrograms
were simultaneously recorded on a multichannel oscilloscopic recorder (Electronics for Medicine DR-16) at
paper speeds of 100 and 200 mm/sec. Recordings were
also simultaneously recorded on an eight-channel tape
system for further analysis. Stimuli were provided by a
programmable digital pulse generator (manufactured by
M. Bloom, Philadelphia. Pa.). Stimuli were approximately twice diastolic threshold and 2 msec in duration.
The atria were paced at rates slightly faster than the
sinus rhythm. Paced rates were increased in 10-beat/min
increments until type 1 block proximal to the His bundle
was observed. Refractory periods and echo zones were
determined with the atrial extra-stimulus technique (13,
Circulation Research, Vol. 36, June 1975
DUAL ATRIOVENTRICULAR NODAL PATHWAYS
14). The extra stimulus was coupled to sinus rhythm and
decreased in 5-10-msec steps.
ELECTROPHYSIOLOGICAL DEFINITIONS
HRA,, A,, H,, and V, were, respectively, the high right
atrial, the low right atrial, the His bundle, and the
ventricular electrograms of sinus beats. HRA2, A2, H2,
and V2 were, respectively, the high right atrial, the low
right atrial, the His bundle, and the ventricular responses to the extra stimulus (S2) or to spontaneous
premature atrial beats. Conduction intervals and refractory periods were measured as previously defined (13,
14). A,-A2, H,-H2 and A,-A2, A2-H2 curves were constructed (9, 10, 13, 14).
AV nodal reentrance and echo zones were defined as
previously described (10, 11, 15-17). Dual AV nodal
pathways were diagnosed when two sets of conduction
times and refractory periods were demonstrated during
atrial premature stimulation (9-11). Fast-pathway and
slow-pathway conduction times and refractory periods
were defined as previously described (9-11).
Results
PATIENT 1
This patient was a 59-year-old woman with
documented recurrent paroxysmal supraventricular tachycardia. Electrophysiological studies during sinus rhythm revealed an A-H interval of 90
msec (normal 54-130 msec) and an H-V interval of
45 msec (normal 31-55 msec).
Atrial extra stimuli were coupled to sinus
rhythm at a cycle length of 830 msec (Fig. 1). As
A r A 2 intervals were decreased from 690 to 370
msec, H,-H 2 intervals shortened from 700 to 470
msec. At an A r A 2 interval of 365 msec, the H r H 2
interval suddenly increased to 655 msec, reflecting
a marked increase in the A2-H2 interval. With
A,-A2 intervals between 365 and 300 msec, H,-H2
CL»83O
msec
500
msec
600
400
700
:
, 300
600
4
E
200
500
100
400
30O
500 600
A, (msec)
100
500
600
A, A2 (msec)
FIGURE 1
Atriouentricular conduction curves from patient I, showing dual
AV nodal pathways. A: H,-H7 responses are plotted against
AfA, coupling intervals. B: A7-H7 responses are plotted
against A,-At coupling intervals. The fast-pathway effective refractory period was 365 msec. The atrial functional refractory
period of 300 msec limited slow-pathway conduction.CL = cycle
length.
Circulation Research, Vol. 36, June 1975
783
intervals were 655 to 620 msec and A2-H2 intervals
were 360 to 440 msec. Atrial echoes and paroxysmal
tachycardia were not induced. AV conduction was
atrially limited with an atrial functional refractory
period of 300 msec. Examination of the A^Aj,
H,-H2 (Fig. 1A) and A,-A2, A2-H2 (Fig. IB) curves
suggested dual AV nodal pathways with a fastpathway effective refractory period of 365 msec.
During constant atrial pacing, intact AV conduction was noted at paced rates up to 140/min. At
paced rates between 70 and 100/min, A-H intervals
were 90-100 msec (Fig. 2A). At paced rates between
110 and 140/min, A-H intervals were either 125-185
msec (fast-pathway conduction) (Figs. 2B and 3A)
or 360-420 msec (slow-pathway conduction) (Figs.
2C and 3C). The determinants of antegrade AV
conduction were studied during sinus rhythm by
randomly initiating atrial stimulation at rates of
90-140/min. At critical pacing rates, the coupling
interval of the first paced beat determined whether
that beat and all subsequent beats utilized the fast
or the slow pathway for antegrade conduction. At
paced rates equal to or less than 100/min, with an
initial coupling interval of less than 365 msec, the
first paced beat was conducted via the slow pathway (Fig. 2A), but all subsequent beats were
conducted via the fast pathway (Fig. 2A). At a
paced rate of 110/min, with an initial coupling
interval of longer than 365 msec, the first paced
beat and all subsequent beats were conducted via
the fast pathway (Fig. 2B). At a paced rate of
110/min, with the initial coupling interval equal to
or shorter than 365 msec, the first paced beat and
all subsequent beats were conducted via the slow
pathway (Fig. 2C).
At paced rates of 140/min, prolonged periods of
both fast-pathway conduction (Fig. 3A) and slowpathway conduction (Fig. 3C) were noted. A shift
from fast-pathway to slow-pathway conduction
occurred via a Wenckebach mechanism of the fast
pathway (Fig. 3B). A gradual increase in the
fast-pathway A-H interval was terminated by prolonged periods of slow-pathway conduction (Fig.
3B).
At a paced rate of 130/min, an unexpected
shortening of the A-H interval during fast-pathway
conduction was observed (Fig. 4), which appeared
to reflect simultaneous fast- and slow-pathway
conduction (from the preceding paced P wave).
There was a tendency for beats postulated to be
conducted via the slow pathway to show minor
notching or plateauing of the QRS complexes in
lead II, as opposed to the QRS complexes con-
784
WU. DENES. DHINGRA. WYNDHAM, ROSEN
Pacing HR = 90/min
Coupling interval =365
AH = IOO
| 3 6 5 | 667 | 667 I
01-i—375 W !6oCi—IOo\
Pacing HR = IIO/min
Coupling interval=375
AH = I25
At
Pacing HR=IIO/min
Coupling interval = 365
I
830
I375 I
545
830
1365 1 545 I 545 I 545 I
I
5 4 5
I
545
AH = 360
H ^
TV
At I
•.
, V'
'.A
H
t1
,
AVN
V
H
90H
I
\ v y v \
90V
1
395S
1
375%— 360V- 3«>\
1
'
1
FIGURE 2
Recordings from patientl, showing dual AV nodal conduction times during constant atrial pacing. Shown are electrocardiographic lead
II, the high right atrial electrogram (HRA), and the His bundle electrogram (HBE). A and H are, respectively, low right atrial and His
bundle electrograms. Time lines are at 1-second intervals, and paper speed is 100 min/sec in this and subsequent illustrations. Conduction intervals are listed in msec. Electrocardiographic leads I, II, and V, are deleted. In each section, the first two beats are sinus beats
with a cycle length of 830 msec and an A-H interval of 90 msec. The third and subsequent beats are paced beats. A: Pacing rate (HR)
was 90/min. The first paced beat had a coupling interval of 365 msec (equal to the fast-pathway effective refractory period) and was
conducted via the slow pathway with an A-H interval of 375 msec. The second and subsequent paced beats were conducted via the fast
pathway with an A-H interval of 100 msec. B and C show pacing rates of 110/min. B: Coupling interval of the initial paced beat was 375
msec (fast-pathway effective refractory period), and the beat was conducted via the fast pathway with an A-H interval of 180 msec. The
subsequent beats were also conducted via the fast pathway with an A-H interval of 125 msec. C: Coupling interval of the first paced
beat was 365 msec (equal to the fast-pathway effective refractory period), and the beat was conducted via the slow pathway with an
A-H interval of 395 msec. The second and subsequent paced beats were also conducted via the slow pathway with an A-H interval of
360 msec. Proposed mechanisms are present in the ladder diagrams on the right, which depict the atrium (AT), the AV node (AVN)
and the His bundle (H). Solid lines reflect fast-pathway conduction, and broken lines reflect slow-pathway conduction. Ladder diagrams in all subsequent figures follow this format.
ducted via the fast pathway which tended to be of
greater amplitude. Examples of this phenomenon
are shown in Figures 2A and C, 3A and C, and 4.
The phenomenon was not always present, however; exceptions are demonstrated in Figures 2B
and 3B.
In this patient, the postulated determinants of
fast- and slow-pathway conduction are demonstrated in the ladder diagrams on the right of
Figure 2. In Figure 2A, at a paced rate of 90/min,
the first paced beat encountered the effective
refractory period of the fast pathway and conducted via the slow pathway; the paced cycle
length was long enough to allow recovery of the fast
pathway for antegrade conduction of all of the
subsequent beats. In Figure 2B and C, the paced
rate was 110/min. In 2B, the first paced beat fell
beyond the fast-pathway effective refractory period, so that that beat as well as all subsequent
beats were conducted via the fast pathway. In 2C,
the first paced beat encountered the effective
refractory period of the fast pathway and conducted via the slow pathway. Repetitive retrograde
concealed conduction (or possibly repetitive antegrade concealed conduction or a combination of the
two) maintained fast-pathway refractoriness, so
that all subsequent beats were conducted via the
slow pathway.
The shift from fast- to slow-pathway conduction
at a paced rate of 140/min appeared to reflect type
1 block in the fast pathway (Fig. 3). Once the fast
pathway failed, the slow pathway was available for
conduction. Repetitive concealed conduction
would then maintain slow-pathway conduction.
The postulated mechanism for those beats with
unexpected shortening of the A-H interval at a
paced rate of 130/min is shown in the ladder
diagram in Figure 4. Pacing-induced lengthening of
the conduction time involving both pathways can
put these pathways out of phase, so that the
Circulation Research, Vol. 36. June 1975
DUAL ATRIOVENTRICULAR NODAL PATHWAYS
Pacing HR = l 4 0 / m i n
785
AH = I85
JL
HRAH
u
l
k
l
lA
U
LJ
A
i
jA
^
\
HBE
I.
I
I'
IP
'
Pacing HR = l40/min.
11
I
\l
I
,
II,
L
I
AH=420
—R,H—fri—i\
FIGURE 3
^WAH^^b;
Recordings from patient 1, showing two A-H intervals at a paced heart rate of 140/min. A: A-H interval was 185 msec, consistent with
fast-pathway conduction. B: Progressive lengthening of the A-H interval from 100 to 190 msec was followed by a sudden jump of the
A-H interval to 400 msec, suggesting type 1 block in the fast pathway with shift of conduction to the slow pathway. C: A-H interval 420
msec, consistent with slow-pathway conduction. Abbreviations are the same as they are in Figure 2.
ventricles can respond twice to a single atrial
impulse. The fourth QRS complex in Figure 4 was
the first ventricular response to the fourth atrial
paced beat conducted via the fast pathway. The
fifth QRS complex, which shows minor notching, is
postulated to be the second ventricular response to
the fourth atrial paced beat conducted via the slow
pathway. The fifth atrial paced beat was blocked in
both pathways. Superimposition of this and the
fifth QRS complex resulted in an apparent short-
Pacing HR= 30/min.
At
FIGURE 4
Recordings from patient 1, showing pseudoshortening of the A-H interval and shift of conduction from the fast to the slow pathway. The
paced heart rate was 130/min. The fifth paced beat had an unexpected shortening of the A-H interval {65 msec), which occurred during
a pacing-induced Wenckebach sequence. The sixth paced beat was blocked in the AV node. The seventh and subsequent paced beats
showed a progressive lengthening of the A-H intervals, followed by a sudden jump of the A-H interval to 385 msec; the interval
then stabilized, suggesting type 1 block in the fast pathway with shifting of conduction to the slow pathway. Interpretations are shown
in the ladder diagram. See text for further discussion. Abbreviations are the same as they are in Figure 2.
Circulation Research, Vol. 36, June 1975
786
ening of the A-H interval. The sixth to ninth atrial
paced beats were conducted via the fast pathway
with type 1 block. The tenth and subsequent beats
were conducted via the slow pathway.
PATIENT 2
This patient was a 61-year-old man with arteriosclerotic heart disease and documented recurrent
paroxysmal supraventricular tachycardia. Electrocardiograms taken over 2 years revealed two
ranges of P-R intervals (0.18 and 0.28 seconds,
respectively) without intermediate values.
Electrophysiological studies during sinus rhythm
at a cycle length of 520 msec revealed A-H intervals
of either 160 msec (fast pathway) or 260 msec (slow
pathway), suggesting dual AV nodal pathways
(Figs. 5 and 6). The response to coupled stimulation was studied by analyzing the responses to both
spontaneous atrial premature contractions and test
extra stimuli.
During sinus rhythm with fast-pathway conduction (Fig. 5), extra stimuli and premature atrial
contractions, as well as subsequent sinus beats,
were conducted via the fast pathway at coupling
intervals of 500 to 410 msec (with the A2-H2
interval ranging from 160 to 205 msec) (Fig. 5A).
Extra stimuli and premature atrial contractions
and all subsequent sinus beats were conducted via
the slow pathway at coupling intervals of 400 to 375
msec (with the A2-H2 interval ranging from 280 to
310 msec) (Fig. 5B). AV nodal reentrant atrial
echoes with paroxysmal supraventricular tachycardia occurred at coupling intervals of 365 to 300
msec, with a critical A2-H2 interval (slow pathway)
of 320 msec or greater (Fig. 5C). The AV nodal
effective refractory period of 290 msec limited AV
conduction (Fig. 5D).
During sinus rhythm with slow-pathway conduction (Fig. 6), extra stimuli and premature atrial
contractions were conducted via the slow pathway
(A2-H2 interval of 260 to 340 msec) at all coupling
intervals (Fig. 6A and B). AV nodal reentrant atrial
echoes with paroxysmal supraventricular tachycardia occurred at A,-A2 coupling intervals of 365
to 300 msec, with the A2-H2 interval equal to or
greater than 320 msec (Fig. 6B). A shift to fastpathway conduction occurred following extra stimuli which were blocked in the AV node (coupling
intervals of 290 to 260 msec) (Fig. 6C). The atrial
effective refractory period was 250 msec. A shift of
AV conduction from the slow to the fast pathway
also occurred following spontaneous ventricular
premature beats (Fig. 6D).
The postulated mechanisms of shifting conduction and the relationship to paroxysmal supraven-
WU. DENES. DHINGRA. WYNDHAM. ROSEN
tricular tachycardia are presented in the ladder
diagrams in Figure 7. Figure 7A-C reflects fastpathway conduction. In 7A, the extra stimulus and
all subsequent sinus beats were conducted via the
fast pathway. In 7B, the extra stimulus encountered the effective refractory period of the fast
pathway (400 msec) and conducted via the slow
pathway. Repetitive retrograde concealed conduction kept the fast pathway refractory, and, therefore, antegrade conduction shifted to the slow
pathway. In 7C, the extra stimulus achieved a
critical delay (A2-H2 interval of 320 msec or
greater) in the slow pathway, allowing recovery of
the fast pathway for total retrograde conduction;
therefore, paroxysmal supraventricular tachycardia occurred. Figure 7D-E reflects slow-pathway conduction. In 7D, the extra stimulus achieved
a critical A2-H2 delay of 320 msec with occurrence
of atrial echoes and paroxysmal supraventricular
tachycardia, as in 7C. In 7E, the extra stimulus
encountered the effective refractory period of the
slow pathway (290 msec) and was blocked. Retrograde concealed conduction to the fast pathway
therefore could not occur, and conduction shifted
back to the fast pathway. In 7F, the premature
ventricular beat interfered with the slow pathway
(retrograde concealed conduction), allowing the
fast pathway to recover. Therefore, conduction
resumed in the fast pathway.
Discussion
Electrophysiological studies in both animal and
human hearts suggest that the AV node can undergo longitudinal dissociation into two pathways
with different functional properties (1-11). Rosen
et al. (9), utilizing His bundle recording and the
atrial extra stimulus technique in a patient with
two P R and A-H intervals, have reported discontinuity in the A,-A2, H r H 2 curve, suggesting dual
AV nodal pathways. Denes et al. (10) have demonstrated similar curves in two patients with AV
nodal reentrant paroxysmal tachycardia. Wu et al.
(11) have demonstrated conduction curves suggesting dual pathways in 7 of 12 patients with AV nodal
reentrant paroxysmal tachycardia. The present
study suggests that two ranges of P-R intervals
during sinus rhythm or two ranges of A-H intervals
at critical paced atrial rates can occur in patients
with AV nodal reentrant paroxysmal supraventricular tachycardia. Presumably, dual conduction
times and AV nodal reentrant paroxysmal supraventricular tachycardia are both manifestations
of dual AV nodal pathways.
The occurrence of two P-R or A-H intervals
Circulation Research, Vol. 36, June 1975
DUAL ATRIOVENTRICULAR NODAL PATHWAYS
787
'iA
B
A,
A2 =400
H, H 2 =520
FIGURE 5
Recordings from patient 2, showing a shift of conduction to the slow pathway and an induction of paroxysmal supraventricular
tachycardia during fast-pathway conduction. Shown are electrocardiographic leads III, V,, HRA, and HBE. A, and H, are atrial and
His bundle electrograms of the last sinus beat. A, and H, are atrial and His bundle responses to a test stimulus (S,) or to a spontaneous
premature atrial beat (PAB). E represents echo. ArAt, H,-Ht, and A-H intervals (in msec) are listed. The sinus cycle length was 520
msec, and the A-H interval was 160 msec (fast pathway). A: A,-At interval was 430 msec. A7-H, interval was 200 msec. Subsequent
beats were conducted via the fast pathway with an A-H interval of 160 msec. B: A,-A, interval was 400 msec, A,-Ht interval was 280
msec. Subsequent beats were conducted via the slow pathway with an A-H interval of 260 msec. C: A,-A, interval was 320 msec. A,-H2
interval was 325 msec. Echoes and paroxysmal supraventricular tachycardia occurred. D: A,-Aj interval was 290 msec. A, was blocked
in the A V node. Subsequent beats were conducted via the fast pathway with an A-H interval of 160 msec.
Circulation Research, Vol. 36, June 1975
788
WU. DENES. DHINGRA. WYNDHAM. ROSEN
A
CL=52O
HBE-v
A. A2=385
Hi H 2 =425
V
26b ,
', 260
300
A, A , =365
i-i
'260
H
\
\-
H
,'>
260
\
H, H, =425
D
FIGURE 6
Recordings from patient 2, showing slow-pathway conduction and paroxysmal supraventricular tachycardia. Sinus cycle length was 520
msec, and the A-H interval was 260 msec (slow pathway). A: A,-A, interval was 385 msec. A,-H, interval was 330 msec. Echoes and
paroxysmal supraventricular tachycardia were not seen. Subsequent beats were conducted via the slow pathway with anA-H interval of
260 msec. B: A^-A, interval was 365 msec. At-Ht interval was 320 msec. Echoes and paroxysmal supraventricular tachycardia were
induced. C: A ,-A 2 interval was 290 msec. A 2 was blocked in the A V node. Subsequent beats were conducted via the fast pathway with
an A-H interval of 160 msec. D: Sinus beats following a premature ventricular beat (PVC) were conducted via the fast pathway with an
A-H interval of 160 msec. Abbreviations are the same as they are in Figure 5.
Circulation Research, Vol. 36, June 1975
789
DUAL ATRIOVENTRICULAR NODAL PATHWAYS
*l
At
| 520 I 430 | 560 | 520
| 520
AVN
H
B At
A|
A2
| 520 / 400/
560 I 520 I 520~l
260\— 260p
II
A|
At
A2
I 520
At
AVN
H
I 520 I 520 I:
520 | 520 | 520
ZB
26'
'\- °rr
260'i
PVC
FIGURE 7
Ladder diagrams for Figures 5 and 6, showing determinants of fast and slow pathway conduction and the relationships to induction of
paroxysmal suprauentricular tachycardia. See text for discussion. Abbreviations are the same as they are in Figure 2.
depends on a long fast-pathway effective refractory
period relative to cycle length. At critical heart
rates, a premature impulse can encounter the
effective refractory period of the fast pathway and
conduct via the slow pathway. Subsequent repetitive retrograde concealed conduction (and possibly
antegrade concealed conduction) to the fast pathway can keep the fast pathway refractory for
subsequent antegrade conduction and maintain
slow-pathway conduction. With slower rates, the
fast pathway can recover for subsequent antegrade
conduction despite concealed conduction. Thus,
the shift to persistent slow-pathway conduction
can be induced by a critically timed premature
atrial beat only at critical heart rates. The difference between the cycle length of the critical heart
rate and the effective refractory period of the fast
pathway could reflect the conduction time of the
retrograde concealed impulse to the fast pathway.
A shift of conduction to the slow pathway can occur
at a heart rate which induces type 1 block in the
fast pathway. A shift of conduction from the slow to
the fast pathway occurs when the premature atrial
impulse is blocked in both pathways, allowing
recovery of the fast pathway for subsequent antegrade conduction.
The occurrence of echoes and paroxysmal supraventricular tachycardia due to AV nodal reentrance depends on a slow conduction delay sufficient to allow recovery of the fast pathway for
retrograde conduction (10, 11, 17). Echoes and
paroxysmal supraventricular tachycardia were always induced in patient 2 at coupling intervals
Circulation Research, Vol.
36, June
1975
which achieved a slow pathway A2-H2 interval of
320 msec or more. Inability to induce atrial echoes
and paroxysmal supraventricular tachycardia in
patient 1 probably reflected increased retrograde
refractoriness of the fast pathway on the day of
study.
A dual AV nodal pathway can result in double
ventricular responses to a single P wave if the
slow-pathway conduction time (relative to the
fast-pathway conduction time) is sufficient for
recovery of the distal His-Purkinje system and
ventricle for reexcitation. Bailey et al. (18), working with depressed canine Purkinje fibers, have
suggested that a single impulse can excite distal
tissue twice due to longitudinal dissociation of
conduction. In man, double ventricular responses
to a single P wave have recently been demonstrated
by Puech and Grolleau (19) in a patient with
preexcitation, in whom single atrial extra stimuli
are conducted via both anomalous (first QRS) and
normal (second QRS) pathways. In patient 1,
double ventricular responses occurred during pacing-induced type 1 block in both pathways. Superimposition of the second ventricular response with
the subsequent atrial paced beat resulted in pseudoshortening of the A-H interval.
The mechanism of minor notching of the QRS
complex without a change in the H-V interval
during antegrade slow-pathway conduction in patient 1 is unclear. In other patients with dual AV
nodal pathways reported on previously, the ventricles responded with similar QRS complexes
whether the fast or the slow pathway was utilized
WU. DENES. DHINGRA. WYNDHAM. ROSEN
790
for antegrade conduction (10-12). Sherf and James
(20) have postulated longitudinal dissociation and
preferential conduction in the His-Purkinje system, dependent on atrial input. The QRS complex
during slow-pathway conduction may be explained
by this concept.
In conclusion, the occurrence of both fast- and
slow-pathway conduction at identical cycle lengths
depends on a long fast-pathway effective refractory
period relative to cycle length. Repetitive retrograde concealed conduction to the fast pathway is
responsible for the maintenance of slow-pathway
conduction. Atrial echoes and paroxysmal supraventricular tachycardia occur when sufficient slowpathway conduction delay is achieved, allowing
recovery of the fast pathway for retrograde conduction. Shift from the fast to the slow pathway can
result in changes in ventricular activation by an
unknown mechanism.
AV node: A model for reentry. Am Heart J 70:505-514,
1965
7. SCHUILENBURC RM, DURRER D: Ventricular echo beats in the
human heart elicited by induced ventricular premature
beats. Circulation 40:337-347, 1969
8. JANSE MJ, VAN CAPELLE GJL, FREUD GE, DURRER D: Circus
movement within the AV node as a basis for supraventricular tachycardia as shown by multiple microelectrode
recording in the isolated rabbit heart. Circ Res
28:403-414, 1971
9. ROSEN KM, METHA A, MILLER RA: Demonstration of dual
atrioventricular nodal pathways in man. Am J Cardiol
33:291-294, 1974
10. DENES P, WU D, DHINGRA RC, CHUQUIMIA R, ROSEN KM:
Demonstration of dual A-V nodal pathway in patients
with paroxysmal supraventricular tachycardia. Circulation 48:549-555, 1973
11. Wu D, DENES P, DHINGRA RC, KHAN A, ROSEN KM: Effects
of propranolol on induction of A-V nodal reentrant
paroxysmal tachycardia. Circulation 50:665-677, 1974
12. SCHERLAG BJ, LAU S, HELFANT RH, STEIN E, BERKOWITZ WD,
DAMATO AN: Catheter technique for recording His bundle
activity in man. Circulation 39:13-18, 1969
13. WIT AL, WEISS MB, BERKOWITZ WD, ROSEN KM, STEINER C,
Acknowledgment
The authors wish to express their appreciation for the
secretarial help of Ms. Valerie Woods and Ms. Therese Calderon.
DAMATO AN: Patterns of atrioventricular conduction in
the human heart. Circ Res 27:345-359, 1970
14. DENES P, WU D, DHINGRA R, PIETRAS RJ, ROSEN KM: Effects
of cycle length on cardiac refractory periods in man.
Circulation 49:32-41, 1974
15. BIGGER JT JR, GOLDREYER BN: Mechanism of supraventric-
References
1. MOE GK, PRESTON JB, BURLINGTON H: Physiologic evidence
for a dual AV transmission system. Circ Res 4:357-375,
1956
2. MENDEZ C, HAN J, GARCIA DE JALON PD, MOE GK: Some
characteristics of ventricular echoes. Circ Res 16:562-580,
1965
3. MENDEZ C, MOE GK: Demonstration of a dual AV nodal
conduction system in the isolated rabbit heart. Circ Res
19:378-393, 1966
4. ROSENBLUTH A, RUBIO R: Ventricular echoes. Am J Physiol
195:53-60, 1958
5. KISTIN AD: Multiple pathways of conduction and reciprocal
rhythm with interpolated ventricular premature systoles.
Am Heart J 65:162-179, 1963
6. WATANABE Y, DREIFUS LS: Inhomogeneous conduction in the
ular tachycardia. Circulation 42:673-688, 1970
16. GOLDREYER BN, BIGGER JT JR: Site of reentry in paroxysmal
supraventricular tachycardia in man. Circulation
43:15-26, 1971
17. GOLDREYER BN, DAMATO AN: Essential role of atrioventricular conduction delay in the initiation of paroxysmal
supraventricular tachycardia. Circulation 43:679-687,
1971
18. BAILEY JC, ANDERSON GJ, FISCH C: Digitalis-induced longi-
tudinal dissociation in canine cardiac Purkinje fibers. Am
J Cardiol 32:202-208, 1973
19. PUECH P, GROLLEAU R: L'activite du faisceau de His
normale et pathologique. Sandoz Editions, 1972, pp
182-183
20. SHERF L, JAMES TN: New electrocardiographic concept:
Synchronized sinoventricular conduction. Dis Chest
55:127-140, 1969
Circulation Research, Vol. 36. June 1975