Download Effects of Atropine on Induction and Maintenance of

Effects of Atropine on Induction and Maintenance
of Atrioventricular Nodal Reentrant Tachycardia
DELON WU, M.D., PABLO DENES, M.D., ROBERT BAUERNFEIND, M.D.,
RAMESH C. DHINGRA, M.D., CHRISTOPHER WYNDHAM, M.D., AND KENNETH M. ROSEN, M.D.
SUMMARY The electrophysiologic effects of atropine were studied in 14 patients with dual atrioventricular
(AV) nodal pathways and recurrent paroxysmal supraventricular tachycardia (PSVT). During PSVT, all
patients used a slow pathway (SP) for antegrade and fast pathway (FP) for retrograde conduction. Atropine
enhanced both SP antegrade and FP retrograde conduction, shown by a decrease in paced cycle lengths (atrial
and ventricular) producing AV and ventriculoatrial block.
Five patients had induction of sustained PSVT before and after atropine. Seven patients failed to induce or
sustain PSVT before atropine, because of retrograde FP refractoriness. All seven had induction of sustained
PSVT after atropine due to facilitation of FP retrograde conduction. Two patients had only single atrial
echoes before atropine, reflecting SP antegrade refractoriness. After atropine, sustained PSVT was inducible
in one, and nonsustained in the other. PSVT cycle length could be compared in seven patients before and after
atropine and decreased from 383 + 25 to 336 ± 17 (p < 0.05).
Thus, in patients with dual AV nodal pathways, atropine facilitated SP antegrade and FP retrograde conduction, shortened cycle length of PSVT and potentiated ability to sustain PSVT.
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Methods
DUAL ATRIOVENTRICULAR (AV) nodal pathways can be demonstrated in most patients with AV
nodal reentrant paroxysmal supraventricular tachycardia (PSVT).' 6 In these patients, the most common
type of sustained AV nodal reentrance involves using a
slow pathway for antegrade conduction and a fast
pathway for retrograde conduction.' 6 Recent pharmacologic studies have demonstrated that digitalis,
propranolol and verapamil may prevent induction of
sustained AV nodal reentrant PSVT by increasing
antegrade slow pathway refractoriness.34'4 7- Procainamide may prevent PSVT induction in patients
with dual AV nodal pathways, by increasing retrograde fast pathway refractoriness.10
Limited data are available describing the effect of
agents that facilitate conduction on AV nodal reentry.
Akhtar and co-workers reported induction of AV
nodal reentrant PSVT only after atropine in five
patients with no previous history of PSVT, suggesting
that vagolysis facilitated the development of AV nodal
reentrant circus movements." In this study, we report
the effects of atropine in patients with previously
documented PSVT and electrophysiologically demonstrable dual AV nodal pathways. The effects of
atropine on fast and slow pathways are quantitated,
and the effects of this agent on PSVT induction noted.
Patient Selection
Criteria for inclusion in this study included: 1) a
history of electrocardiographically documented
recurrent PSVT; 2) absence of preexcitation on all
available ECGs; 3) electrophysiological demonstration of dual AV nodal pathways with demonstration
of discontinuous A1-A2, H,-H2 curves during atrial
extrastimulus testing (10 patients) or demonstration of
two sets of A-H intervals at identical atrial paced cycle lengths (four patients)." 12-16 The latter demonstrations were during the same trial of incremental
atrial pacing, the two sets of A-H reflecting fatigue
(block) in the fast pathway with resultant slow pathway conduction, and 4) demonstration of AV nodal
reentrant PSVT (see Results).", 2, 17-19
Fourteen patients, nine females and five males, ages
24-81 years (mean ± SD 59 ± 16 years) were studied.
Electrophysiological Studies
Electrophysiological study was performed with the
patient in the nonsedated supine state. Cardiac drugs
were discontinued at least 72 hours before study. Informed written consent was obtained in each patient.
A #7 quadripolar electrode catheter was placed across
the tricuspid valve percutaneously via the right
femoral vein. The proximal two electrodes were used
for His bundle recording, while the distal two electrodes were used for ventricular pacing.20 A second #6
hexapolar electrode catheter was positioned in the distal coronary sinus via an antecubital vein. The distal
two electrodes were used for recording of left atrial
electrograms, the middle two electrodes for recording
of high right atrial electrogram, and the proximal two
electrodes for high right atrial pacing. Multiple surface and intracardiac electrograms were recorded
simultaneously via a multichannel oscilloscopic
recorder (Electronics for Medicine DR-16, White
From the Cardiology Section, Department of Medicine,
Abraham Lincoln School of Medicine, University of Illinois
College of Medicine, and West Side Veterans Administration
Hospital, Chicago, Illinois.
Supported in part by NIH training grant HL 07387-OlAl and
NIH grant HL 18794-04, and Basic Institutional Support, MRIS
1828, West Side Veterans Administration Hospital, Chicago,
Illinois.
Address for reprints: Kenneth M. Rosen, M.D., Cardiology Section, University of Illinois Hospital, P.O. Box 6998, Chicago,
Illinois 60680.
Received June 21, 1978; revision accepted November 8, 1978.
Circulation 59, No. 4, 1979.
779
780
CIRCULATION
Plains, New York) at a paper speed of 100 and 200
mm/sec. Stimuli were provided via a programmable
digital stimulator (manufactured by M. Bloom, Narbeth, Pennsylvania) with a strength of approximately
twice diastolic threshold and 2 msec long.
Antegrade and retrograde conduction properties,
refractory periods and echo zones were studied with
atrial and ventricular incremental pacing and extrastimulus technique.1' 10, 14 Retrograde His bundle
potentials could not be reliably recorded at all coupling intervals during ventricular extrastimulus testing
in most of the patients. After control recording,
studies were initiated 15 minutes after administration
of 0.5-1 mg atropine intravenously.
Electrophysiological Definitions
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HRA1, A1, H1, and V1 were the high right atrial, low
septal right atrial, His bundle, and ventricular
responses to driven stimuli (S1), respectively. HRA2,
A2, H2, and V2 were the high right atrial, low septal
right atrial, His bundle and ventricular responses to
test stimuli (S2), respectively. Ae, He and Ve were the
atrial, His bundle and ventricular responses of AV
nodal reentrant echo beats, respectively. Conduction
intervals, refractory periods, echo zones, and critical
A-H and V-A intervals (for induction of AV nodal
reentrant echoes and PSVT) were measured and
defined as previously described." 10, 14
Antegrade dual AV nodal pathways were diagnosed
when discontinuous A-A2, H,-H2 curves were demonstrated, or when two sets of A-H intervals were demonstrated at identical atrial paced cycle lengths." 12-16
Both antegrade and retrograde effective refractory
periods of the fast and slow pathway were defined as
previously described." 10, 14
The diagnosis of AV nodal reentrant PSVT was
made with combinations of the following diagnostic
criteria: 1) induction of PSVT related to achievement
of a critical A-H delay, with both incremental atrial
pacing and with atrial extrastimulus testing;" 2, 21-23 2)
demonstration of discontinuous A1-A2, H,-H2 curves,
suggesting dual AV nodal pathways, with induction of
PSVT relating to antegrade block in the fast
pathway;"' 2, 13-1' 3) demonstration of atrial activation
before or simultaneous with onset of ventricular activation during PSVT, suggesting that the ventricles
were not part of an AV reentrant circus movement;" 2, 17 4) normal retrograde atrial activation sequence during PSVT, with low septal right atrium being activated earlier than all other atrial recording
sites;24' 25 5) increase of ventriculoatrial (VA) interval
with incremental ventricular pacing with type I VA
block at critical rate, suggesting retrograde AV nodal
conduction;"' 17 6) demonstration of His bundle activation (H2) preceding the atrial activation (A2) with ventricular extrastimulus testing during ventricular pacing and/or PSVT, suggesting retrograde AV nodal
conduction;"' 17 7) absence of previously described
criteria for diagnosis of concealed extranodal
pathways, or sinoatrial reentry.1 2, 26-3 All patients
manifested criteria 4 and either 3 or 6.
VOL 59, No 4, APRIL 1979
Sustained PSVT was defined as induced PSVT that
lasted longer than 2 minutes. Sustained PSVT was
always terminated with single, double or multiple
atrial extrastimuli. Nonsustained PSVT was defined
as induced PSVT terminated spontaneously (within 2
minutes). In almost all instances, nonsustained PSVT
terminated spontaneously within 10-20 seconds of
PSVT induction. In patients with nonsustained PSVT,
the site of block (weak-link) in the circuit was determined by noting whether PSVT was terminated with
an atrial response (block in antegrade limb) or with a
QRS complex (block in retrograde limb).10
The determinants of reentrance (antegrade slow
pathway and retrograde fast pathway) were evaluated
as previously described.34 The evaluation of antegrade
slow pathway primarily depended on noting the paced
atrial cycle length producing AV nodal block. Since in
the patient with dual pathways, the antegrade fast
pathway has a longer refractory period than the
antegrade slow pathway, this paced cycle length
reflects slow pathway refractoriness.
For the retrograde fast pathway, this evaluation
primarily depended on noting the paced ventricular
cycle length producing VA block. This procedure is
based on the assumption that the shortest VA
retrograde refractory period in these patients is that of
the retrograde fast pathway, rather than the
retrograde slow pathway. This assumption is based on
the following observations: 1) Retrograde conduction
curves (H1-H2, A,-A2) are smooth and suggest one
retrograde pathway; 2) VA conduction times are short
(there are not two populations of retrograde conduction times) and are consistent with observed antegrade
fast pathway conduction times; 3) retrograde conduction is via AV node (normal retrograde activation sequence, and H2 and A2 are both driven out of the QRS
with closely coupled ventricular extrastimuli).
Retrograde fast pathway effective refractory period
cannot be directly measured in most patients with dual
AV nodal pathways because of either limiting ventricular refractoriness or limiting refractoriness
between the ventricle and His bundle.
Results
PSVT Induction (table 1)
In seven of the 14 patients, sustained AV nodal
reentrant PSVT could not be induced before atropine
administration, despite achievement of sole conduction in the antegrade slow pathway (antegrade failure
of the fast pathway) with atrial extrastimulus testing
and/or rapid incremental atrial pacing (cases 1-7). In
three of these patients (cases 1-3), nonsustained AV
nodal reentry was induced before atropine, with spontaneous termination of PSVT due to block in the
retrograde fast pathway (inadequate retrograde fast
pathway conduction) (fig. IA). In four of the patients
(cases 4-7), no AV nodal reentrant atrial echoes were
noted because of inadequate retrograde fast pathway
conduction (fig. 2B). After atropine, all seven patients
had induction of sustained AV-nodal PSVT due to
enhanced retrograde fast pathway conduction (figs.
ATROPINE AND AV NODAL REENTRY/Wu et al.
781
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TABLE 1. Effects of Atropine on Induction and Maintenance of Atrioventricular Nodal Reentrant Tachycardia
PSVT
Ability
to
Weak CL
Antegrade (msec)
Retrograde (msec)
Case Induction sustain link (msec) FP-ERP SP-ERP Echo zone CL-AVB FP-ERP SP-ERP Echo zone CL-VAB
1 C Echo
330
0
(-)
No
340
Ret
320
0
300
280
400
A Yes
0
Yes
No
300
300
0
300
260
250
316
(-)
2 C Yes
0
No
Ret
300
<230
<353
270
370
300-230
375
(-)
A Yes
Yes
No
315
270
0
<250 270-250 <300
<250
(-)
<316
3 C Yes
No
Ret
320
<240 330-240
333
<355
435
0
(-)
500
A Yes
Yes
No
350
280
<230
0
261
<325
0
316
(-)
4 C No
(-)
Ret
0
(-)
0
550
(-)
650
375
<315
667
A Yes
Yes
No
350
< 320
0
316
<310
0
(-)
333
(-)
5 C No
(-)
0
()
Ret
320
> 500
0
400
370
429
(-)
A Yes
Yes
No
340
300
<290 330-290
375
<230
0
(-)
<353
6 C No
(-)
(-)
0
(-)
Ret
410
353
430
<270
333
0
A Yes
Yes
No
305
<260
0
0
284
(-)
325
()
300
7 C No
(-)
0
(-)
Ret
462
420
350
0
390
<290
375
A Yes
Yes
No
<260
365
0
0
261
<240
()
(-)
284
8 C Echo
No
Ant (-)
370-340
375
390
()
<340
360 400-365
500
A Yes
Yes
No
<310
0
500
(-)
0
333
< 340
()
<300
9 C Echo
0
300
No
Ant (-)
(-)
<350
390
<260 370-260
429
A Echo
No
Ant (-)
<310
0
353
<350
(-)
0
()
<300
10 C Yes
Yes
0
No
<333
305
()
270
<210 270-210
<230
300
A Yes
Yes
No
300
<270
(-)
0
284
<230
0
()
<300
11 C Yes
Yes
No
0
355
295
<300
<280 290-280
()
< 175
333
A Yes
0
(-)
Yes
<300
No
300
()
<200
< 175
0
<273
12 C Yes
< 353
Yes
No
0
480
()
410
280 380-280
462
<370
A Yes
<353
0
Yes
No
()
390
<280
t-)
0
<273
<370
13 C Yes
()
Yes
No
420
(-)
<310
470-260 <316
0
<333
250
A Yes
(-)
Yes
No
400-290 <375
400
()
<290
<300
0
280
14 A Yes
<316
Yes
No
315
(-)
295
0
<255 295-255
333
<340
C Yes
Yes
No
300
260
<300
<255 260-250 <316
0
<316
()
Abbreviations: PSVT = paroxysmal supraventricular tachyeardia; CL = cycle length; FP-ERP effective refractory period
of the fast pathway; SP-ERP = effective refractory period of the slow pathway; CL-AVB iongest atrial paced cycle length
producing atrioventricular block; CLVAB - longest ventricular paced cycle length producing ventriculoatrial (VA) block;
C = control; A = atropine; Ant = antegrade; Ret = retrograde.
IC and 2C). PSVT was induced with either rapid
atrial pacing (all seven patients) or with double atrial
extrastimuli (cases 1-3, 6, 7). In only two patients was
PSVT inducible with single atrial extrastimulus
testing after atropine (cases 2 and 5).
In two of the 14 patients, sustained PSVT was not
induced before atropine due to inadequate antegrade
slow pathway conduction (cases 8 and 9). In both
patients only single AV nodal reentrant atrial echoes
were induced after achievement of sole antegrade slow
pathway conduction (fig. 3A). After atropine, one of
these patients had induction of sustained PSVT due to
enhanced antegrade slow pathway conduction (case 8)
(fig. 3B), while the other continued to have induction
of only single AV nodal reentrant atrial echoes
(case 9).
Five of the 14 patients had induction of sustained
PSVT before atropine (cases 10-14) (fig. 4A). In all
five patients, PSVT was inducible with rapid atrial
pacing and in four with single atrial extrastimulus
testing (cases 10-12 and 14). After atropine administration, all five patients had induction of
sustained PSVT with either rapid atrial pacing (at
faster paced rates than those necessary for induction
prior to atropine) or with double atrial extrastimuli
(A1, A2, A3, testing) (figs. 4B and 4C). In only one
patient was PSVT inducible with single atrial extrastimulus testing after atropine (case 14).
Conduction Curves and Echo Zones (table 1)
Discontinuous A1-A2, H,-H2 curves suggesting dual
AV nodal pathways were demonstrated in 10 of the 14
patients before atropine (cases 1-3, 7-12 and 14) (figs.
2A, 2B and 5). In eight of these 10 patients, an echo
zone could be defined which coincided with either the
whole slow pathway curve or the leftward portion of
the slow pathway curve. In two patients, an echo zone
was not defined, despite demonstration of the discontinuous curve (cases 1 and 7) (fig. 5, left panel). After
atropine, discontinuous A1-A2, H1-H2 curves were
demonstrated in four of these 10 patients (cases 1-3
and 14). Three of these four had echo zones before
atropine, and two of four had echo zones (and PSVT
; @;^*^|1l;^A|L~ ~ ~
CIRCULATION
782
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VOL 59, No 4, APRIL 1979
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RA
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HBE
FIGURE 1. Recordings from case 2, showing induction of sustained atrioventricular (A V) nodal reentrant paroxysmal
supraventricular tachycardia (PSVT) after atropine and the effects of atropine on antegrade and retrograde conduction. Shown
are lead II, the right atrial electrogram (RA) and His bundle electrogramr (HBE). S, A, and H are stimulus artifact, atrial and
His bundle responses, respectively, during atrial pacing. Ae and He are atrial and His bundle responses of the A V nodal reentrant beats. Time lines are at I second and paper speed is 100 mm/sec. Paced cycle length (CL) is listed on top of each panel,
and the critical A-H interval is listed on bottom of the panel. Panel A demonstrates induction of nonsustained PSVT after
cessation of rapid atrial pacing at a paced CL of 353 msec before atropine (antegrade slow-pathway conduction). CL of PS VT
was 370 msec. The heavy vertical black line represents a 4-second discontinuity in recordings. PSVT was terminated when He
was not followed by an atrial response, suggesting retrograde block in the fast pathway. Panel B demonstrates second degree
ventriculoatrial (VA) block at a ventricular paced CL of375 msec before atropine. Panel C demonstrates induction ofsustained
PSVT after atropine following cessation of rapid atrial pacing at a paced CL of 300 msec. CL of PSVT was 315 msec. Panel D
demonstrates one-to-one V-A conduction after atropine at a shorter ventricular paced CL of 316 msec.
induction) after atropine (cases 2 and 14). In six
patients (cases 7-12), discontinuous A1-A2, H1-H2
curves became continuous after atropine due to
facilitation of fast pathway conduction (see below)
and echo zones were not defined (fig. 5, middle panel).
Antegrade block in the fast pathway with antegrade
slow pathway conduction (with echoes and PSVT) in
these six patients was achieved with rapid atrial pacing
and/or double atrial extrastimuli after atropine (figs.
2C, 3B, 4B, 4C and 5, right panel).
Continuous A,-A2, H1-H2 curves were demonstrated in four of the 14 patients before atropine
(cases 4-6 and 12). In three of these four patients,
atrial functional refractory period was longer than the
effective refractory period of the fast pathway (cases 4,
6 and 13), and in the other (case 5) only the slow
pathway was used for antegrade conduction at the
tested driven cycle length. Echo zones were not
demonstrated in these four patients, although in one
patient (case 13) sustained PSVT was inducible with
rapid atrial pacing. After atropine, continuous curves
without definition of an echo zone were demonstrated
in three of the four patients (cases 4, 6 and 13). In all
three patients, sustained PSVT could be induced after
atropine with rapid atrial pacing and/or double atrial
extrastimuli. In the remaining patient (case 5, the
patient with only slow pathway conduction with extrastimulus testing), A1-A2, H1-H2 curve became discontinuous after atropine due to shortening of antegrade
fast pathway refractory period. An echo zone was
~ ~ ~-N ;I7
ATROPINE AND AV NODAL REENTRY/Wu et al.
Control
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FIGURE 2. Recording from case 7, demonstrating induction of sustained paroxysmal supraventricular tachycardia (PS VT)
after atropine. Left atrial electrogram recordedfrom coronary sinus (CSA) is also shown. S1, A1, and H1 are stimulus artifact,
atrial and His bundle responses to the basis driven beat, respectively; S2, A2, and H2 are stimulus artifact, atrial and His bundle
responses to the test beat, respectively; S3, A3, and H3 are stimulus artifact, atrial and His bundle responses to a second test
beat. Paced cycle length (CL), A1-A2, and A2-A3 intervals are listed on top ofeach panel, and A2-A2 or A3-H3 are listed on bottom of each panel. The basic driven CL was 400 msec before and after atropine. RA = right atrial electrogram; HBE = His
bundle electrogram. Panel A demonstrates antegrade fast-pathway conduction of A2 at A 1-A2 of 360 msec before atropine.
Panel B demonstrates antegrade block of the fast pathway with conduction via the slow pathway at A1-A2 of 350 msec before
atropine. Note lack of atrioventricular nodal reentrant atrial echo despite achieving a slow-pathway A2-H2 of400 msec. Panel C
demonstrates induction of sustained PSVT after atropine with A1A2A testing. At A1-A 2 of270 msec, A2 was still conducted via
the fast pathway. However, A3 was blocked in the fast pathway and conducted via the slow pathway at A2-A3 of 250 msec.
Sustained PSVT was induced at A3-H3 of 425 msec.
3
defined, and coincided with the whole slow pathway
Antegrade Slow Pathway Properties (table 1)
curve.
Refractoriness of the antegrade slow pathway could
be evaluated in 12 patients before and after atropine
by noting the longest atrial paced cycle length producing AV nodal block (cases 1, 3-12 and 14). The atrial
paced cycle length producing AV block was 373 18
msec (range 300-500 msec) before atropine, and
decreased to <301 ± 11 msec (range <273-375) after
atropine (p < 0.01).
Antegrade effective refractory period of the slow
pathway could be compared with extrastimulus tech-
Antegrade Fast Pathway Properties (table 1)
Antegrade fast pathway effective refractory periods
measured in 11 patients before and after atropine
(cases 1-3, 5, 7-12 and 14) (fig. 5, left and right panels). Antegrade fast-pathway effective refractory
period was <340 ± 21 msec (mean ± SEM, range 270
to <500) before atropine, and decreased to <276 ± 9
msec (range <200 to 300) after atropine (p < 0.01).
were
VOL 59, No 4, APRIL 1979
CIRCULATION
784
Control
Atropine
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CL =333
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FIGURE 3. Recordings from case 8 demonstrating induction of sustained paroxysmal supraventricular tachycardia (PSVT)
after atropine. RA = right atrial electrogram; HBE = His bundle electrogram. Panel A demonstrates induction of only a
single atrioventricular nodal reentrant atrial echo after cessation ofrapid atrialpacing at a paced cycle length (CL) of 500 msec
before atropine. The critical A-H (slow-pathway conduction) was 610 msec. The atrial echo (Ae) was not followed by His bundle and verltricular responses, suggesting antegrade block in the slow pathway. Panel B demonstrates induction of sustained
PSVT after atropine following cessation ofrapid atrial pacing at a paced CL of333 msec, which achieved a slow-pathway A-H
of 400 msec. CL of PS VT was 500 msec.
nique before and after atropine in only two patients,
and was decreased in both patients after atropine
(cases 1 and 5).
shorter than that of the slow pathway or shorter than
the ventricular functional refractory period (continuous V1-V2, A,-A, curves).
Retrograde Fast Pathway Properties (table 1)
Cycle Lengths of PSVT (table 1)
Retrograde fast pathway conduction could be
evaluated in nine patients before and after atropine by
noting the longest ventricular paced cycle length
producing VA block34 (cases 1-9) (figs. lB and ID).
VA conduction was via fast pathway at short paced
cycle lengths in most patients before atropine, and in
all patients after atropine (see below).34 The ventricular paced cycle length producing VA block was
429 ± 36 msec (range 375-667 msec) before atropine,
and decreased to <313 ± 7 msec (range 284-333)
after atropine (p < 0.01).
The retrograde effective refractory period of the fast
pathway could be compared before and after atropine
in seven patients (cases 1, 2, 4-7 and 13) and decreased
from 390 ± 51 msec (range 250-650 msec) to
<271 ± 14 msec (range <230-325 msec) after
atropine (p < 0.05). The retrograde effective refractory period decreased in six of these seven patients. In
seven patients (3, 8-12 and 14), retrograde fast
pathway effective refractory periods could not be
measured because of limiting ventricular refractoriness.
Cycle lengths of PSVT could be compared in seven
patients before and after atropine (cases 2, 3, 10-14)
(figs. 1 A and C and 4A and C). Cycle lengths of PSVT
ranged from 305-480 msec (mean ± SEM 383 ± 25
msec) before atropine, and ranged from 300-400 msec
(mean ± SEM 334 ± 17 msec) after atropine. The cycle lengths of PSVT shortened significantly after
atropine (p < 0.05). This shortening reflected decrease
in both antegrade slow pathway conduction time
(mean ± SEM). The A-H interval during PSVT
decreased from 294 ± 18 to 226 ± 12 msec after
atropine (p < 0.05), and retrograde fast pathway conduction time H-A during PSVT decreased from 89 ±
16 to 71 ± 12 msec after atropine (p < 0.05). A-H and
H-A are only approximate measures of antegrade
slow and retrograde fast pathway conduction time (H
is distal to the final common pathway).
Retrograde Slow Pathway Properties (table 1)
Although retrograde effective refractory period of
the slow pathway was achieved in four patients before
atropine (1, 4, 6 and 7), it was not achieved in any of
the 14 patients after atropine because retrograde effective refractory period of the fast pathway was either
Discussion
AV Nodal Reentrant PSVT
Dual AV nodal pathways are demonstrable in most
patients with AV nodal reentrant PSVT. In these
patients, critically timed atrial premature stimuli
block in a fast AV nodal pathway resulting in sudden
increase in A-H interval (sole antegrade slow pathway
conduction). If the blocked fast pathway is available
for retrograde conduction, PSVT induction may
result. The usual circus movement in these patients
ATROPINE AND AV NODAL REENTRY/Wu et al.
Control A
785
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FIGURE 4. Recordings from case 1I demonstrating induction ofsustained paroxysmal supraventricular tachycardia (PSVT)
before and after atropine. RA = right atrial electrogram; CSA = coronary sinus electrogram; HBE = His bundle electrogram.
Panel A demonstrates induction of sustained PSVTbefore atropine after cessation of rapid atrialpacing at a atrial paced cycle
length (CL) of 333 msec, which achieved a slow-pathway A-H of 450 msec. CL of PSVT was 355 msec. Panel B demonstrates
no induction of PSVT after atropine at a shorter atrial paced CL of 273 msec with an A-H (fast-pathway conduction) of 130
msec. Panel C demonstrates induction ofsustained PSVT after atropine with atrial extrastimulus testing. The basic driven CL
was 400 msec. A ,-A2 was 220 msec, and A2 was still conducted via the fast-pathway. PSVT was induced by a premature atrial
beat (PA B) (A3) after A2. The A3 achieved slow-pathway conduction with an A3-H3 of 340 msec. CL of PS VT was 300 msec.
consists of a slow AV nodal pathway (antegrade), a
fast AV nodal pathway (retrograde), a proximal
common pathway, and a distal common pathway.1-
8
10, 12-16, 33-39
The occurrence of sustained AV nodal reentry requires the capability of repetitive antegrade slow
pathway conduction and the capability for repetitive
retrograde fast pathway conduction.'0' 33, 34 The cycle
length of PSVT must be longer than the effective
refractory period of any component of the circus
pathway. '0 34 In patients with dual AV nodal
pathways, inability to sustain PSVT reflects either
depressed antegrade slow pathway or depressed
retrograde fast pathway conduction.
In patients with depressed slow pathway conduction, only single AV nodal reentrant atrial echoes or
nonsustained PSVT can be induced with atrial
stimulation.34 Termination of PSVT in these patients
occurs when atrial responses are not followed by His
bundle or ventricular responses, suggesting block in
the antegrade limb of the circuit. In patients with
depressed retrograde fast pathway conduction, induction of AV nodal reentrant atrial echoes may not be
possible, or only nonsustained PSVT may be induced
with atrial stimulation.34 Termination of PSVT in
these patients occurs when QRS complexes are not
followed by atrial responses, suggesting block in the
retrograde limb of the circuit.'0
CIRCULATION
786
Control
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Antiarrhythmic Agent and AV Nodal Reentrance
Previous electrophysiological studies have demonstrated that antegrade and retrograde properties of
both fast and slow pathway can be modified by antiarrhythmic agents, and the ability to induce or sustain
PSVT may be suppressed or enhanced after drug administration.3 4 7-10 Propranolol, digitalis and
verapamil increase antegrade slow pathway refractoriness.3' 4 7-8 There is little information regarding
the effects of propranolol and verapamil on retrograde
fast pathway conduction. Digitalis appears to have little effect on retrograde fast pathway refractoriness.3
All of these drugs inhibit the ability to sustain PSVT
in some patients with AV nodal reentrance, by increasing refractoriness in the antegrade limb of the
circus movement. Procainamide depresses retrograde
fast pathway conduction and inhibits the ability to induce or sustain PSVT in the majority of the patients
with AV nodal reentrant PSVT.10 However, procainamide may enhance antegrade slow pathway conduction due to vagolytic effect and potentiates the ability
to sustain PSVT in a minority of patients with AV
nodal reentrance.
Effects of Atropine
In this study, we demonstrated that atropine
enhanced retrograde fast pathway and antegrade slow
pathway conduction, and thus potentiated the ability
to induce sustained PSVT. In seven patients with
either no induction of AV nodal reentrant atrial
echoes or induction of nonsustained PSVT due to
depressed retrograde fast pathway conduction, improvement of retrograde fast pathway conduction was
sufficient to allow induction of sustained PSVT after
|-
VOL 59, No 4, APRIL 1979
FIGURE 5. Atrioventricular (AV) conduction curves before and after atropine in case
7. The basic driven cycle length {CL) was
400 msec. Solid circles represent responses
without echoes, while open circles represent
responses with echoes. Left panel demonstrates discontinuous A1-A2, A2-H2 and A1A2, H1-H2 curves, suggesting dual A V nodal
pathways before atropine. The effective
refractory periods of the fast and slow
pathway were 420 msec and < 290 msec,
respectively. An echo zone was not defined.
Middle panel demonstrates continuous A1A2, A1-H1 and A,-A2, H1-H2 curves after
atropine. The curves became continuous
because of shortening in antegrade fastpathway effective refractory period (< 260
msec). Right panel demonstrates discontinuous A2-A3, A4-H3 and A2-A3, H2-H3
curves after atropine, suggesting dual A V
nodal pathways. The driven CL (A1-A1) was
400 msec, and A1-A2 was 270 msec. The
effective refractory periods of the fast and
slow-pathway were 290 msec and < 255
msec. The echo zotie coincided with the
whole slow-pathway curve.
atropine. In one of the two patients with induction of
only single AV nodal reentrant atrial echoes due to
depressed antegrade slow pathway conduction, the improvement of antegrade slow pathway conduction
after atropine was sufficient to allow induction of
sustained PSVT.
Although atropine facilitated the induction of
sustained AV nodal reentrant PSVT in patients with
dual pathways with either inadequate antegrade slow
pathway, or inadequate retrograde fast pathway conduction, PSVT induction in the laboratory was frequently more difficult after atropine administration.
This reflected the effects of atropine on fast and slow
pathways. Facilitation of fast pathway conduction
frequently changed discontinuous to continuous conduction curves (decrease of fast pathway effective
refractory period so that it was less than atrial functional refractory period). This prevented achievement
of antegrade slow pathway conduction with the atrial
extrastimulus technique. Despite the continuous conduction curves in these patients, failure of the fast
pathway (with resultant antegrade slow pathway conduction and PSVT induction) could be achieved after
atropine using either rapid incremental atrial pacing
(repetitive rapid conduction may produce block in the
fast pathway) or S1S2S3 stimulation. Even when discontinuous conduction curves were present after
atropine administration, echo zones might not be
delineated because of facilitation of antegrade slow
pathway conduction, making achievement of the slow
critical pathway A-H necessary for reentry difficult.
Critical slow-pathway A-H could be achieved after
atropine using other forms of atrial stimulation (rapid
incremental atrial pacing and/or S1S2SS technique).
In patients who had PSVT before and after
ATROPINE AND AV NODAL REENTRY/Wu et al.
atropine, atropine shortened the cycle length of
PSVT, primarily due to shortening antegrade slow
pathway conduction time (A-H). Although retrograde
fast pathway conduction time (H-A) was also
shortened after atropine, the amount of shortening
was relatively small compared with shortening of
antegrade slow pathway conduction time. Since induction of sustained PSVT requires the cycle length of
PSVT to be longer than the effective refractory
periods of any component of the reentrant circuit, it is
theoretically possible (although not noted in our
study) that atropine could also abolish the ability to
sustain PSVT if shortening of PSVT cycle length exceeded shortening of refractory period of a portion of
the reentrant circuit.
Electrophysiological Applications
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This study has increased our knowledge of the
nature of the fast AV nodal pathway. In a recent
study, we demonstrated that procainamide selectively
depressed retrograde and not antegrade fast pathway
conduction, an unexpected response.10 We could not
distinguish whether the retrograde fast pathway was
an intranodal, atrionodal or extranodal structure. We
also did not know whether the retrograde fast pathway
was anatomically identical to the antegrade fast
pathway. The present demonstration of marked
facilitation of both antegrade and retrograde fast
pathway conduction with atropine strongly suggests
that the fast pathway is partially or totally within the
AV node.
In conclusion, atropine enhances antegrade slow
pathway conduction, antegrade and retrograde fast
pathway conduction, and allows induction of
sustained PSVT. Facilitation of both antegrade and
retrograde fast pathway conduction by atropine is
consistent with the hypothesis that the fast pathway is
partially or totally within the AV node. Induction of
PSVT after atropine usually requires faster atrial
paced rates (than before atropine) and/or double
atrial extrastimuli. Inability to induce sustained PSVT
in the catheterization laboratory in some patients with
known PSVT due to AV nodal reentry probably
reflects inadequate antegrade slow pathway or
retrograde fast pathway conduction on the day of
study (autonomically mediated). Administration of
atropine in these patients may be useful in potentiating PSVT induction, thus helping to delineate the
mechanism of tachycardia.
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787
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CIRCULATION
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Effects of atropine on induction and maintenance of atrioventricular nodal reentrant
tachycardia.
D Wu, P Denes, R Bauernfeind, R C Dhingra, C Wyndham and K M Rosen
Downloaded from http://circ.ahajournals.org/ by guest on June 17, 2017
Circulation. 1979;59:779-788
doi: 10.1161/01.CIR.59.4.779
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1979 American Heart Association, Inc. All rights reserved.
Print ISSN: 0009-7322. Online ISSN: 1524-4539
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