Download Paroxysmal Supraventricular Tachycardia

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CIRCULATION
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28. McCammon RW: A longitudinal study of electrocardiographic intervals
in healthy children. Acta Paediatr Scand (Uppsala) (suppl) 126, 1961
29. Simonson E, Cady LD Jr, Woodbury M: The normal QT interval. Am
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30. Fraser GR, Froggatt P, James TN: Congenital deafness associated with
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31. Fraser GR, Froggatt P, Murphy T: Genetical aspects of the cardioauditory syndrome of Jervell and Lange-Nielsen (congenital deafness
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133, 1964
32. Alimurung MM, Joseph LG, Craige E, Massell BF: The QT interval in
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34. Bazett HC: An analysis of the time-relations of electrocardiograms.
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37. Schwartz PJ, Malliani A: Electrical alternation of the T-wave: Clinical
and experimental evidence of its relationship with the sympathetic nervous system and with the long Q-T syndrome. Am Heart J 89: 45, 1975
38. Jervell A, Lange-Nielsen F: Congenital deaf-mutism, functional heart
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39. James TN: Congenital deafness and cardiac arrhythmias. Am J Cardiol
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40. Olley PM, Fowler RS: The surdo-cardiac syndrome and therapeutic
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41. Garza LA, Vick RL, Nora JJ, McNamara DG: Heritable Q-T prolonga-
VOL 54, No 3, SEPTEMBER 1976
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H, Takeuchi A, Kohashi K: Heritable QT prolongation without deafness:
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Paroxysmal Supraventricular Tachycardia
Is
the Atrium
a
MARK E. JOSEPHSON, M.D.,
Necessary Link?
AND
JOHN A. KASTOR, M.D.
SUMMARY Whether or not the atrium plays an essential role in
initiating and/or sustaining atrioventricular (A-V) nodal re-entrant
tachycardia was evaluated in eight patients. In all eight patients, the
atrium could be rendered refractory to retrograde atriai echoes during the tachycardia without interrupting the arrhythmia. This was accomplished by introducing atrial premature depolarizations prior to
the time the atrium would normally be retrogradely depolarized by
atrial echoes. In one patient, two atrial premature depolarizations
could be introduced, producing A-V dissociation, without termatig
the tachycardia. In another patient, the tachycardia could be initiated
without an atrial echo.
Our data suggest that most, if not all of the atrium is unnecessary
for the initiation and maintenance of A-V nodal re-entrant supraventricular tachycardia.
MOST CASES of paroxysmal supraventricular tachycardia are initiated and sustained through re-entry within
the atrioventricular (A-V) node.' Whether or not the atria
form a portion of the re-entrant pathway remains unsettled.
The present investigation of eight patients demonstrated
that in each case no portion of the atrium recorded by our
electrode catheters was required to sustain A-V nodal re-
entrant supraventricular tachycardia and in one the atrium
did not play an essential role in initiating the arrhythmia.
From the Cardiac Clinical Electrophysiology Laboratory, Hospital of the
University of Pennsylvania; the Cardiovascular Section, Department of
Medicine, University of Pennsylvania School of Medicine, Philadelphia,
Pennsylvania.
Presented at the 25th Annual Scientific Session of the American College of
Cardiology, February 24, 1976, New Orleans, Louisiana.
Supported in part by grants from the USPHS, NIH, HL 14807, and the
American Heart Association, Southeastern Pennsylvania Affiliate.
Address for reprints: Dr. Mark E. Josephson, Director, Electrophysiology
Laboratories, 669 White Building, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, Pennsylvania 19104.
Received March 5, 1975; revision accepted March 29, 1976.
Methods, Materials, and Clinical Patient Information
Eight patients were studied in the nonsedated postabsorptive state after informed consent was obtained (table
1). All had symptomatic supraventricular tachycardia
(SVT), and none demonstrated evidence of pre-excitation.
No patient was taking antiarrhythmic drugs at the time of
the study.
A quadripolar electrode catheter was introduced percutaneously into an antecubital and/or femoral vein and
positioned under fluoroscopic control against the lateral wall
of the high right atrium and/or the coronary sinus. The
proximal pair of electrodes was used to record a high right
atrial or coronary sinus electrogram, while the distal pair
was used for atrial stimulation. A bipolar electrode catheter
431
SUPRAVENTRICULAR TACHYCARDIA/Josephson, Kastor
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was similarly introduced into another antecubital vein and
positioned in the right ventricular apex for stimulation. A
His bundle electrogram was obtained using a tripolar electrode catheter introduced percutaneously into the right
femoral vein.4 The intracardiac electrograms were filtered at
40 and 500 Hz and were simultaneously displayed with at
least three surface ECG leads and timelines generated at 10
and 100 msec on a multichannel oscilloscope (Electronics
for Medicine DR-16). Rectangular impulses of I msec duration and at approximately twice diastolic threshold were
delivered by a specially designed programmed digital
stimulator (Murray Bloom, Narberth, Pa.). All data were
stored on magnetic tape (Honeywell 14 channel recorder)
and later retrieved on photographic paper at speeds of 150 to
200 mm/sec.
In each patient, after initiation of A-V nodal re-entrant
tachycardia, atrial premature depolarizations were introduced to activate the atria prior to the time they would
have been retrogradely activated by atrial echoes during the
tachycardia. In addition, refractory periods were determined
by the extrastimulus method.
Results
All patients were in sinus rhythm at the beginning of the
study and no abnormalities of conduction were present
(table 1). In each patient, single atrial premature beats at
coupling intervals ranging from 255-380 msec initiated the
tachycardia. The echo zones1 2 were 10 to 120 msec in duration. The critical A-H interval required for the initiation of
the tachycardia ranged between 140 and 400 msec.3 The
tachycardia could also be started in each patient during
Wenckebach cycles produced by rapid atrial pacing,3 and in
two patients (E.H. and H.H.), by one or more ventricular
premature beats.
In all patients, atrial premature depolarizations could be
introduced at intervals resulting in atrial depolarizations 10
to 130 msec prior to the time of spontaneous retrograde
atrial activation without interrupting the tachycardia or
altering its cycle length. In three patients, both right and left
atrial (coronary sinus) sites were prematurely depolarized
without influencing the tachycardia. Examples are shown in
TABLE 1. Clinical Data
PR* QRS* AH*
HV*
A-H required
to initiate
SVT*
125
140
75
90
70
95
50
35
400
170
165
160
135
ASHD 155
None 148
ASHD 160
65
82
86
88
90
90
90
78
50
85
80
92
40
45
50
48
45
45
145
140
295
195
250
290
Pt/Age/Sex
Dx
K.M./27/F
H.H./66/M
MVP
ASHD
IMI
MVP
ASHD
MVP
M.B./17/F
W.P./56/M
E.H./37/F
M.U./55/M
L.R./18/F
C.N./72/F
*All values are given in msec.
Abbreviations: ASHD = atherosclerotic heart disease; MVP = mitral
valve prolapse; IMI = inferior myocardial infarction.
figures 1-3. Note in particular that the low right atrium is
depolarized: a) 30 and 20 msec early in beats 2 and 4 of
figure 1; b) 25 msec early in beat 3 of figure 2; c) 70 msec
early in beat 3 of figure 3A and 100 msec early in beat 3 of
figure 3B. Furthermore, the coronary sinus is depolarized
120 msec early in figure 3A and 55 msec early in figure 3B.
The configuration of the high and low atrial electrograms
were different in the atrial premature depolarizations (Ap)
when compared to the atrial echoes (Ae). In addition, the
atrial electrograms of the premature depolarizations introduced from the right or left atrium were recorded before
the onset of the His bundle deflection in the patient illustrated in figure 3. Thus in each of these three cases, that
part of the atria giving rise to the high right atrial electrogram, low right atrial electrogram (in the His bundle recording), and in one case the coronary sinus electrogram, could
be prematurely depolarized without interrupting the tachycardia. Since the atrial refractory periods of our patients
were 210-300 msec, the atria would have been refractory for
at least 200 msec after Ap, during which time Ae would have
appeared (10 to 130 msec after the atrium was prematurely
depolarized).
In patient K.M., two premature atrial depolarizations
(Ap) could be introduced which depolarized both the high
and low right atrium without terminating the tachycardia
(fig. 4). In addition, after the two stimulated atrial
FIGURE 1. A trial stimulation during supraventricular tachycardia in patient K.M. This figure
and all subsequent intracardiac recordings are
similarly organized. From top to bottom are ECG
leads I, II, III, V1; high right atrial electrogram
(HRA), His bundle electrogram (HBE), and
timelines (T) generated at 10 and 100 msec. During supraventricular tachycardia (SVT), which
has a stable cycle length of 340 msec, each QRS is
associated with atrial echoes (Ae) reflecting retrograde depolarization of the atria. Note that the
atrial electrogram of the A e in the HBE precedes
that in the HRA. A trial premature beats (Ap) are
introduced at a coupling interval of 22S msec after
thefirst and third QRS complexes. In the Ap, the
HRA precedes the atrial electrogram in the HBE
and both occur earlier than they would during the
tachycardia. Despite the fact that the atrium is
depolarized prior to the time the Ae would normally occur. the tachycardia continues its cycle
length unaffected by the stimulated atrial beats. S
represents the stimulus artifact.
CIRCULATION
432
alanallif
ki idfillII II J
FIGURE 2. A trial stimulation during supraventricular tachycardia in patient M.B. The panel
is organized as in figure 1. Supraventricular
tachycardia is present at a cycle length of 470
msec. After the third QRS an atrial premature
beat (Ap) is introduced at a coupling interval of
400 msec. In the Ap, the HRA precedes the atrial
depolarization in the His bundle electrogram
(JIBE), a reversal of the sequence of the atrial
echo (A e). Despite this, the tachycardia is unaffected. Also note the change in the atrial electrograms produced by Ap.
finilli
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tiated in the absence of an atrial echo (Ae) (fig. 5). On other
occasions, an atrial echo was seen following the stimulated
atrial premature depolarization (A2) if the resulting A2H interval exceeded 200 msec. This was the only patient we
observed in whom no atrial echo followed the atrial
premature depolarizations initiating the tachycardia. In two
of the eight patients, A-V nodal refractory curves were consistent with "dual pathways."5
premature depolarizations, there is a pause in atrial activity
followed by what appears to be a sinus P wave (A.). A8 does
not conduct because the A.H interval of 40 msec is too short
(AH during sinus rhythm was 70 msec). Thus a period of
A-V dissociation resulted without termirnating the tachycardia. That A8 arises in the area of the sinus is supported
by: a) the sequence of atrial activation (high right atrium activated prior to low right atrium), and b) the normal
appearance of the P wave seen in the surface ECG (heavy
arrow, fig. 4). The pause and transient change in ventricular
cycle length developed because the first Ap penetrated the
A-V node and depolarized the ventricles while the second Ap
did not penetrate the A-V node. The tachycardia continued
even though no atrial echoes (Ae) were seen following the
fifth and sixth QRS complexes.
In patient W.P., supraventricular tachycardia was ini-
A
VOL 54, No 3, SEPTEMBER 1976
Discussion
The purpose of these studies was to determine whether the
atria form part of the re-entrant circuit in patients with A-V
nodal re-entrant tachycardia.1 3 In an attempt to answer this
question, premature atrial depolarizations were introduced
during the tachycardia prior to the time the atria would have
been retrogradely activated during the tachycardia. Per-
i
____________
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FIGURE 3. A trial stimulation during supraventricular tachycardia in patient E.H. Panels A
and B are organized from top to bottom leads I,
aVF, V1, high right atrial electrogram (HRA), coronary sinus electrogram (CS), His bundle electrogram (HBE) and timelines (T). Supraventricular
tachycardia (SVT) is present at a cycle length of
370 msec in each panel. Note that during supraventricular tachycardia, the atrial electrograms in
the JBE, HRA and CS follow the onset of the
His deflection. In panel A, an atrial premature
beat (Ap) is stimulated from a catheter in the
distal coronary sinus 250 msec after the prior CS
electrogram. This results in depolarization of both
the high and low atrium, as well as that part of the
left atrium recorded by the CS electrogram prior
to the inscription of the His bundle, without altering the H-H interval or cycle length of the supraventricular tachycardia. Thus both atria were
depolarized 70-120 msec prior to the time Ae
would have occurred without altering the SVT. In
panel B, an Ap from the high right atrium is introduced 240 msec after the prior high right atrial
electrogram. The high and low right atrial and
coronary sinus electrograms appear 130, 100, and
55 msec premature respectively without altering
the SVT.
SUPRAVENTRICULAR TACHYCARDIA/Josephson, Kastor
433
4
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A
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FIGURE 4. A trial premature beats causing A- Vdissociation during supraventricular tachycardia in patient K.M. During
SVT, two Ap's are introduced depolarizing both the high and low atrium prematurely without terminating the tachycardia. The next spontaneous atrial depolarization (As) has the appearance of a sinus beat both by its surface ECG
appearance (heavy arrow) and the sequence of atrial activation. Clearly the HRA precedes the atrial electrogram in the
HBE as it does in sinus beats. A period of A-V dissociation is present since As occurs almost simultaneously with the His
deflection and could therefore not be responsible for it. Thus, no Ae is seen after the fifth and sixth QRS complexes, and in
spite of transient A-V dissociation, the SVT continues.
sistence of the tachycardia without change of cycle length in
the face of atrial capture was considered presumptive
evidence that the recorded atrium did not form part of the
re-entrant circuit. This technique of atrial "pre-excitation"
has been previously utilized in an effort to determine the role
of the atrium in the production of ventricular echoes.6' The
role of the atrium in the initiation and maintenance of A-V
nodal re-entrant tachycardia has not yet been evaluated in
arrhythmia. If any atrial tissue is necessary, it may be a very
small rim immediately adjacent to the A-V node that was
not recorded by our catheters. Resolution of this question
must come from appropriate intra-atrial mapping and
stimulation during open heart surgery in patients with A-V
nodal re-entrant tachycardia.
man.
One could postulate that each premature atrial
depolarization was conducted down the antegrade limb of
the re-entrant circuit and fortuitously failed to alter the cycle
length of the tachycardia due to an exact "compensatory"
delay of conduction down that limb. However, premature
atrial depolarizations could be delivered over a range of
20-50 msec without changing the tachycardia. Some
irregularity of cycle length should have been noted during
the scanning interval. Furthermore, in the presence of
premature capture of the low right atrium by as much as 100
msec (fig. 3B), it seems very unlikely that the impulse would
not have altered the cycle length of the tachycardia.
Fortuitous atrial participation certainly could not explain
the findings noted in figure 4 in which two successive
premature depolarizations capture the atrium without interrupting the tachycardia. Although the first Ap could have
and probably did capture the ventricle, the second could not
possibly have penetrated the re-entrant circuit since it had
just been depolarized by the first Ap and would have been
refractory. The persistence of the tachycardia after two
Ap's, despite the altered cycle length, the absence of echoes,
and subsequent period of A-V dissociation, argues strongly
against fortuitous atrial participation.
In one patient, W.P., the tachycardia was initiated in the
absence of an atrial echo following the premature beat (fig.
5). This phenomenon, not previously described, strongly implies that the atrium was not necessary to initiate the
tachycardia. Superficial examination of the record might
lead one to suggest that retrograde atrial depolarization did
The Route of A-V Nodal Re-entry
The physiologic basis of A-V nodal re-entry depends on
the presence of longitudinal dissociation of the A-V node
into two pathways: one with fast conduction and a long
refractory period (beta pathway), and the other with slower
conduction but shorter refractoriness (alpha pathway).
Sustained tachycardias develop when atrial premature
depolarizations are blocked in the beta pathway but conduct
sufficiently slowly down the alpha pathway so that the impulse can retrogradely activate the previously refractory
beta pathway returning through atrial tissue back to the
alpha pathway to complete the circuit. This concept
proposed by Moe and Mendez8 I included the atrium as a
necessary link in the re-entrant circuit.
The data obtained in this study suggest that most, if not
all, of the atria are uninvolved in the re-entrant circuit. In
each case, both the high and low right atrium could be
depolarized without altering the tachycardia. In addition,
the left atrium could be "captured" without influencing the
tachycardia in three cases, suggesting that the demonstration of atrial "capture" without altering the tachycardia was
unrelated to the direction of the wavefront of the premature
atrial depolarization. Furthermore, A-V dissociation during
the tachycardia was produced in one patient (fig. 4), and an
atrial echo was not required to initiate the tachycardia in
another (fig. 5). These findings suggest that none of the
recorded atrial tissue was required to sustain the
Alternative Explanations
VOL 54, No 3, SEPTEMBER 1976
CIRCULATION
434
1
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2 ____
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HPS
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occur but that the atrial electrogram was "buried" in the
ventricular electrogram. This conclusion is unlikely for three
reasons. First, during the tachycardia the atrial electrogram
clearly appears before each QRS, and would therefore certainly be present in that position for the initiation. Second, if
atrial depolarization did occur and was buried within the
ventricular electrogram, one would have to assume
simultaneous intra-atrial block preventing it from
propagating to the high right atrium since there is no
evidence of activity at that site. No intra-atrial block or
latency was seen at similar coupling intervals during
premature stimulation and these phenomena are less likely
to occur in this situation since the introduction of A2 would
shorten atrial refractoriness for the subsequent beat. Third,
with a greater increase in the A2H interval, the atria had
time to recover and an Ae was demonstrated at the onset of
the tachycardia. Thus evidence for "hidden" atrial
depolarization after A2 is lacking.
V
V
FIGURE 5. Initiation of supraventricular tachycardia without a
critical atrial echo. The panels are organized as in figure 1, but in
addition, the top panel has a ladder diagram underneath depicting
the mechanism of the arrhythmia. In the ladder diagram and top
panel, A, is eighth of a series ofpaced atrial beats at a cycle length
of 700 msec. A, represents the premature beat. In the ladder
diagram, A is atrium, A VN is A - V node, HPS is His-Purkinje, and
V is ventricle. A, is introduced at a coupling interval of 300 msec
and SVT is initiated. However, no atrial echo is seen during or after
the stimulated beat, but is present in subsequent beats of the SVT.
As depicted in the ladder diagram, re-entry occurs within the A - V
node; the atrium is not depolarized initially because it is still refractory. The lack of an initial Ae strongly suggests that the Ae is not
necessary to initiate SVT. In panel opposite, A2 is delivered at a
coupling interval of 300 msec after the eighth paced beat at a cycle
length of 600 msec. The resulting A2H of 220 msec is long enough to
allow atrial refractoriness to recover and atrial echo to resume.
Therapeutic Implications
Clinical practice has established that drugs and
maneuvers which prolong A-V nodal conduction can interrupt and prevent episodes of supraventricular tachycardia. Electrophysiologic studies have demonstrated that
digitalis,10 propranolol,'1 Valsalva maneuver,'2 and carotid
sinus pressure2' 13 prolong A-V nodal conduction and refractoriness, thereby altering the temporal relationships within
the A-V node that must be established to initiate and sustain
supraventricular tachycardia. Quinidine and procainamide,
which are less useful in the treatment of supraventricular
tachycardia, have minimal effects on A-V nodal conduction
and tend to shorten A-V nodal refractoriness by their
vagolytic properties.'4' '5 Similarly, because of its lack of
effect on the A-V node, lidocaine is of little value in the
management of supraventricular tachycardia. However,
quinidine and procainamide are useful in preventing supraventricular tachycardia by suppressing the atrial or ventric-
SUPRAVENTRICULAR TACHYCARDIA/Josephson, Kastor
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ular premature beats that initiate the arrhythmia.
It has been recently demonstrated that extra-nodal bypass
tracts exist and can function as part of the retrograde limb of
the re-entrant circuit, even in the absence of their utilization
in an antegrade fashion.'6"'i Demonstration that the atrium
is not required to sustain supraventricular tachycardia
argues against the presence of functional bypass tracts during the tachycardia. From a pharmacologic standpoint, if
such retrograde bypass tracts and atrial tissue formed part
of the re-entrant pathway, drugs affecting atrial and bypass
conduction and refractoriness, i.e., quinidine and
procainamide, would be useful.", "I
Occasionally, permanent atrial or ventricular pacing is
employed to treat patients whose supraventricular tachycardia is refractory to drug therapy.2" 22 The success of
pacemaker therapy in supraventricular tachycardia depends
on the ability of the induced atrial or ventricular beat to
penetrate the re-entrant circuit and interrupt the
arrhythmia. Infrequently, the use of single atrial beats is ineffective; the atrium may be depolarized without terminating
the arrhythmia. In such cases, lack of atrial requirement
during supraventricular tachycardia may explain the lack of
success.
Evidence from Animal Experiments
Whether or not the atrium forms a requisite link in
sustaining atrial echoes, supraventricular tachycardia, or
ventricular echoes has not been resolved in the animal
laboratory. The original mechanism of supraventricular
tachycardia described by Moe and Mendez", I included the
atrium and a longitudinally dissociated A-V node to form
the re-entrant circuit. More recently, Wit et al.23 showed
that in the isolated rabbit heart, a small but significant portion of the right atrium was required to sustain supraventricular tachycardia. However, Janse and co-workers,2'
using a similar preparation with a plaque electrode over the
A-V node, came to the opposite conclusion, i.e., that reentry was entirely subatrial, located entirely in the A-V
node. Both these latter studies demonstrated that infranodal
structures were unnecessary to sustain supraventricular
tachycardia. Findings in studies attempting to evaluate the
role of the atrium in the production of ventricular echoes
have contributed to the controversy. Using the technique of
"atrial pre-excitation," Mignone and Wallace25 found that
ventricular echoes resulted from re-entry within the A-V
node and did not require the atrium. Mendez and Moe'
came to the opposite conclusion in the isolated rabbit heart.
Thus, several carefully designed animal studies have failed
to resolve the question of atrial requirement in these reentrant arrhythmias.
Conclusion
Our data strongly suggest that in certain patients with
A-V nodal re-entrant supraventricular tachycardia, no part
of the recorded atrium is required to sustain or initiate A-V
nodal re-entrant tachycardia. The demonstration of lack of
the atrial requirement could be shown in the absence of
A-V nodal refractory curves demonstrating "sdual
pathways."5 It therefore seems likely that, in these cases, the
basic re-entrant circuit is limited to the A-V node and that
the atrial and ventricular responses during supraventricular
435
tachycardia are "secondary" phenomena. The finding of
lack of atrial requirement in a patient with paroxysmal
supraventricular tachycardia suggests the absence of a functional extranodal bypass tract and directs pharmacologic
therapy toward those drugs which have a major action on
A-V nodal conduction and/or refractoriness. Since the atria
can be captured without terminating the tachycardia, an explanation is now available for the occasional inability to terminate supraventricular tachycardia with induced atrial
premature beats.
References
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2. Goldreyer BN, Bigger JT Jr: Site of re-entry in paroxysmal supraventricular tachycardia. Circulation 43: 15, 1971
3. Goldreyer BN, Damato AN: The essential role of atrioventricular conduction delay in the initiation of paroxysmal supraventricular tachycardia. Circulation 43: 679, 1971
4. Scherlag BJ, Lau SH, Helfant RH, Berkowitz WD, Stein E, Damato
AN: Catheter technique for recording His bundle activity in man. Circulation 39: 13, 1969
5. Denes P, Wu D, Dhingra R, Chuguimia R, Rosen KM: Demonstration
of dual A-V nodal pathways in patients with paroxysmal supraventricular tachycardia. Circulation 48: 549, 1973
6. Schuilenburg RM, Durrer D: Further observations on the ventricular
echo phenomenon elicited in the human heart. Circulation 45: 629, 1972
7. Narula OS: Ventricular echoes without atrial participation. (abstr) Am J
Cardiol 35: 160, 1975
8. Moe GK, Mendez C: The physiologic basis of reciprocal rhythms. Prog
Cardiovasc Dis 8: 461, 1966
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M E Josephson and J A Kastor
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Circulation. 1976;54:430-435
doi: 10.1161/01.CIR.54.3.430
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