(Circulation. 1998;97:2245-2251.)
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports |
Ventriculophasic Modulation of Atrioventricular Nodal Conduction in Humans
Allan C. Skanes, MD, FRCPC;
; Anthony S. L. Tang, MD, FRCPC
From the Department of Medicine, University of Ottawa, Ontario, Canada.
Correspondence to Dr A.S.L. Tang, University of Ottawa Heart Institute, 1053 Carling Ave, Ottawa, Ontario K1Y 4E9, Canada. E-mail ttang{at}heartinst.on.ca
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Abstract
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Background—Baroreceptor-mediated
phasic changes in vagal tone have been hypothesized to cause
ventriculophasic sinus arrhythmia (VPSA). The objectives of
this study were to demonstrate ventriculophasic modulation of AV nodal
conduction and to substantiate the role of the baroreflex on
ventriculophasic AV nodal conduction (VPAVN) by pharmacological
perturbation of parasympathetic tone.
Methods and Results—Twelve patients with infra-Hisian
second-degree heart block and VPSA were studied. Incremental atrial
pacing was performed until AV nodal Wenckebach block at baseline, after
phenylephrine infusion, and after atropine. AV nodal
conduction curves were constructed for each phase and compared. At
baseline, VPAVN was present in 9 of 12 patients on the steep
portion of the AV nodal conduction curves. Phenylephrine
increased systolic blood pressure from 149±33 to 177±22
mm Hg (P<0.001) and sinus cycle length from 844±169
to 1010±190 ms (P<0.001) and shifted the AV nodal
conduction curves up and to the right. Phenylephrine
induced VPAVN in 2 of 3 patients in whom it was not present at
baseline and in 11 of 12 total. Atropine abolished both VPSA and VPAVN
in all patients.
Conclusions—VPAVN was demonstrated in patients with infra-Hisian
second-degree AV block. It was accentuated by phenylephrine
and abolished by atropine, suggesting a baroreflex mechanism for VPSA
and VPAVN.
Key Words: arrhythmia • baroreceptors • vagus nerve • atrioventricular node • phenylephrine
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Introduction
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Ventriculophasic
sinus arrhythmia describes a phenomenon in patients with heart
block in which phasic variations in sinus rate occur in relation to the
QRS complex.1 2 3 Typically, the pp intervals
encompassing a QRS complex are shorter than those without an
intervening QRS complex. Although the exact mechanism of this
phenomenon is not known, several explanations have been
proposed.2 The most likely explanation appears to
involve arterial pressure–induced phasic changes in
baroreceptor-mediated vagal input to the sinus
node.3 If indeed this is the case and
baroreceptor firing also affects AV nodal conduction, one might expect
to see the same ventriculophasic modulation of AV nodal conduction.
Ventriculophasic AV nodal conduction has never been described in
humans. The objective of this study was to document ventriculophasic
modulation of AV nodal conduction in patients with infra-Hisian
second-degree heart block. Furthermore, we sought to document the
influence of pharmacological autonomic perturbations on this
phenomenon. A model of second-degree infra-Hisian heart block was
specifically chosen because changes in AV nodal conduction could be
correlated to their relation to preceding QRS complexes on a
beat-to-beat basis.
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Methods
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Twelve patients with documented symptomatic
second-degree heart block and a wide QRS complex suspected of having
infra-Hisian heart block were studied. Patients with complete heart
block were excluded, because influences of retrograde-concealed
penetration of the AV node from the escape focus could not be excluded
as a cause of changes in AV nodal conduction in these patients. All
patients had ventriculophasic sinus arrhythmia. After providing
written informed consent, each patient was studied in the
postabsorptive state under light sedation with diazepam. Multielectrode
catheters were inserted percutaneously via the right
femoral vein and advanced to the high right atrium and right
ventricular apex for pacing and recording. A His
catheter was advanced via the right femoral vein and placed adjacent to
the tricuspid annulus to record a His potential. Surface ECG leads
and intracardiac electrogram were recorded from the high right
atrium, His bundle, and right ventricular apex with a Gould
ES 1000 strip chart at a paper speed of 100 mm/s for
analysis. Brachial systolic and diastolic
blood pressures were recorded at 5-minute intervals throughout the
study with a noninvasive inflatable cuff. In 3 patients, femoral
arterial pressure was also recorded. After
recordings during sinus rhythm, incremental right atrial pacing
was performed until Wenckebach block occurred at the level of the AV
node. The paced atrial rate was held constant at each increment until
steady-state AV nodal conduction had been established. Of 12 patients,
9 had infra-Hisian second-degree heart block during sinus rhythm in the
electrophysiological laboratory. In the
remaining 3 patients, infra-Hisian second-degree heart block was
documented during right atrial pacing. After baseline measurements,
phenylephrine was infused beginning at a dose of 0.2
µg/kg and titrated to increase the systolic blood pressure by
25%. Measurements were repeated during sinus rhythm and during
incremental right atrial pacing until AV nodal Wenckebach block
occurred. Phenylephrine infusion was then stopped. Three
patients did not receive phenylephrine because of baseline
systolic hypertension; all had systolic blood pressure
180 mm Hg during baseline 2:1 second-degree heart block. When
blood pressure returned to baseline, atropine in sufficient doses to
abolish ventriculophasic sinus arrhythmia was given as an
intravenous bolus. Measurements during sinus rhythm and
incremental right atrial pacing were repeated. This protocol was
approved by the institutional review board. After study termination,
all patients underwent permanent pacemaker insertion.
At baseline, sinus cycle length and AH intervals were measured. All
nine patients with second-degree heart block at baseline had
ventriculophasic sinus arrhythmia with sinus cycle length
variation of 44±18 ms (Figure 1
). For
each pacing cycle length, AH intervals were measured in a standard
fashion.4 5 The local His A was measured as the
earliest reproducible rapid deflection; the local His was measured as
the earliest onset of the His deflection from baseline. As Figure 2 shows, at some paced cycle lengths, the
local A could not be measured as the earliest deflection. In these
instances, the local A was measured as the first negative deflection at
baseline. Once this was the case, all subsequent local A measurements
were made in this manner at this pacing cycle length. As such, at each
paced atrial rate, beat-to-beat variations in AH interval were measured
from a local A identified in the same manner. These measurements were
repeated after phenylephrine infusion and atropine. AV
nodal conduction curves were constructed by plotting the paced cycle
length (AA) interval on the abscissa and the corresponding AH interval
on the ordinate. AV nodal conduction curves were constructed for
intervals at baseline, after phenylephrine infusion, and
after atropine. To assess shifts in AV nodal conduction curves
resulting from phenylephrine infusion, three points on each
curve were determined and compared: Wenckebach point, AH(s), and AH(l)
as described by Page et al.6 AH(s) refers to the
AH interval at the shortest A-A pacing cycle length at which
consistent AV nodal conduction was seen at both baseline and
with phenylephrine infusion. Likewise, AH(l) refers to the
AH interval at the longest A-A pacing cycle length at which
consistent AV nodal conduction was seen at both baseline and
with phenylephrine infusion.
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Figure 1. A rhythm strip from a patient with 2:1 heart
block. The p-p intervals are indicated in milliseconds.
Ventriculophasic sinus arrhythmia is seen. Note that the
shorter p-p intervals have an intervening QRS, whereas the longer p-p
intervals are without an intervening QRS.
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Figure 2. Surface leads 1, 2, 3, V1, and
V6 and intracardiac electrogram recorded from the high
right atrium (HRA), His bundle (HBE), and right ventricular
apex (RV). Arterial pressure was also recorded. A, 2:1
infra-Hisian heart block was present during high right atrial
pacing at a paced cycle length of 840 ms. Ventriculophasic AV nodal
conduction was seen. Note that the longer AH was recorded
immediately after the arterial pressure wave and two beats
after the QRS complex. B, Pacing cycle length was decreased to 650 ms
in the same patient; 3:1 infra-Hisian block was noted. Ventriculophasic
AV nodal conduction was seen. The longest AH interval occurred
immediately after the arterial pressure wave and two beats
after the QRS complex. The AH intervals shortened progressively over
the next two beats. All values are in milliseconds.
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Statistical Analysis
All data are presented as mean±SD. Statistical
comparison between groups was performed by a two-tailed paired
Student's t test. A significant difference was accepted if
P
0.05.
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Results
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Patient Characteristics
Twelve patients, 7 male and 5 female, with a mean age of 68±16
years were studied. Of the 12 patients, 10 had no preexisting cardiac
disease and were not taking cardiac medication at the time of
presentation or study. Two patients had preexisting cardiac
disease. One patient (patient 10; see the Table) had
known mild rheumatic mitral stenosis and paroxysmal atrial
fibrillation. For this reason, the patient was taking digoxin and
furosemide. The digoxin was discontinued after presentation
with second-degree heart block and 2 days before the
electrophysiological study. The second
patient (patient 11; the Table) was known to have congestive heart
failure on the basis of coronary artery disease and previous
myocardial infarction, type II diabetes controlled by diet, and mild
renal dysfunction with a serum creatinine of 200
µmol/L. This patient was not taking medication known to affect
autonomic tone or AV nodal conduction.
Ventriculophasic AV Nodal Conduction
Ventriculophasic AV nodal conduction referred to a
consistent pattern of fluctuation of AH intervals at a
steady-state atrial pacing rate at which the arterial
pressure wave was followed by the longer AH interval. Figure 2A
shows
an example of 2:1 infra-Hisian heart block at atrial paced cycle length
of 840 ms. Ventriculophasic AV nodal conduction was present with
alternating AH intervals of 120 and 130 ms. The beat with the longer AH
interval was preceded by the arterial pressure. The amount
of AH changes caused by ventriculophasic modulation of AV nodal
conduction was 10 ms. When higher degrees of AV block occurred, the
longest AH interval was again recorded after the
arterial pressure wave. The AH interval progressively
shortened until the next arterial pressure wave, which
initiated another cycle. Figure 2B shows an example of 3:1 infra-Hisian
heart block at a faster atrial paced cycle length of 650 ms.
Ventriculophasic AV nodal conduction was again present with the
longest AH interval (200 ms) associated with the beat immediately
following the arterial pressure wave. The AH interval of
the next two beats shortened progressively (190 to 180 ms). The amount
of AH changes caused by ventriculophasic AV nodal conduction was 20 ms.
Ventriculophasic changes in the AH interval were said to exist if this
variation in AH interval was 5 ms and consistent from cycle
to cycle.
Baseline Measurements
At baseline, the mean sinus cycle length was 844±169 ms. All
patients had ventriculophasic sinus arrhythmia of 44±18 ms. No
patient had ventriculophasic AV nodal conduction in sinus rhythm.
During incremental atrial pacing, ventriculophasic AV nodal conduction
was noted in 9 of 12 patients (patients 1 through 9; the Table). The
maximal AH interval variation caused by ventriculophasic modulation of
AV nodal conduction was between 5 and 20 ms, with a mean of 13.3±6.1
ms. The ventriculophasic changes occurred on the steep portion of the
AV nodal conduction curves (Figure 3). As
illustrated in Figure 2A and 2B, the amount of AH variation caused by
ventriculophasic AV nodal conduction increased with increasing atrial
paced rate.
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Figure 3. Representative AV nodal conduction curve from a
patient with ventriculophasic AV nodal conduction both at baseline and
with phenylephrine infusion. AV nodal conduction curves at
baseline, with phenylephrine infusion, and after atropine
infusion are indicated by circles, triangles, and squares,
respectively. Note the presence of ventriculophasic AV nodal conduction
on the steep portion of the curves. To indicate the paced AA interval
on the conduction curve at which Wenckebach was seen, we arbitrarily
chose a corresponding AH interval of 250 ms, which represents
the upper limits of our conduction curves. Wenckebach point refers to
the paced A-A cycle length at which AV nodal Wenckebach occurred. To
distinguish these points from the remainder of the AV nodal conduction
curve, Wenckebach points are illustrated as stipple-filled symbols.
Points in sinus rhythm and Wenckebach points (WBPs) are
indicated. Note that phenylephrine caused the AV nodal
conduction curve to shift up and to the right. Atropine caused the
curve to shift down and to the left. Filled symbols represent
points at which ventriculophasic AV nodal conduction was recorded;
open symbols, points at which no ventriculophasic AV nodal conduction
was recorded.
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Effect of Phenylephrine Infusion
Phenylephrine was infused at a mean dose of 1.3±0.4
mg/kg in nine patients, which increased systolic blood pressure
by 27.6% from 149±33 to 177±22 mm Hg (P<0.001).
Sinus cycle length increased by 19.7% from 860±162 to 1010±190 ms
(P<0.001). Of the nine patients who had 2:1 distal heart
block during sinus rhythm at baseline study, three did not receive
phenylephrine because of systolic hypertension as
stated above. Of the remaining six who received
phenylephrine, two developed 1:1 conduction during
phenylephrine infusion. Hence, only four patients had 2:1
heart block at baseline and during phenylephrine infusion
while in sinus rhythm and before atrial pacing. In these four patients,
ventriculophasic sinus arrhythmia increased from a mean of
31±10 to 73±42 ms (P=0.12).
The paced atrial cycle length at which AV nodal Wenckebach occurred
increased by 14.4% from 386±93 to 441±119 ms (P=0.03).
Ventriculophasic AV nodal conduction was noted in 8 of 9 patients who
received phenylephrine and in 11 of 12 of the total group.
The maximal AH interval variation caused by ventriculophasic modulation
of AV nodal conduction in the patients who received
phenylephrine was 13.8±4.4 ms (range, 10 to 20 ms). Six
patients who had ventriculophasic AV nodal conduction (VPAVN) at
baseline also received phenylephrine. In this group, the
magnitude of VPAVN at baseline was 10.0±5.5 ms; after
phenylephrine, a similar magnitude was seen (11.7±5.2 ms).
As noted above, 3 patients did not receive phenylephrine
infusion because of hypertension. Phenylephrine infusion
brought out ventriculophasic AV nodal conduction in 2 of 3 patients
(patients 10 and 11; the Table) in whom it was not present at
baseline (Figure 4). Ventriculophasic
changes were seen on the steep portion of the AV nodal conduction
curve. Furthermore, phenylephrine caused AV nodal
conduction curves to shift up and to the right as evidenced by the
increase in AV nodal Wenckebach point from 385.6±93.3 to 443.3±117.3
ms (P=0.05), AH(l) from 63.9±200.0 to 82.2±36.2 ms
(P=0.03), and AH(s) from 138.9±40.4 to 171.7±34.8 ms
(P<0.01).
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Figure 4. Representative AV nodal conduction
curve from a patient who had ventriculophasic AV nodal conduction
induced by phenylephrine infusion. No ventriculophasic AV
nodal conduction was seen at baseline. Phenylephrine
infusion shifted the curve up and to the right and induced
ventriculophasic AV nodal conduction on the steep portion of the curve.
Atropine was not given to this patient. Symbols as in Figure 3.
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In one patient (patient 12; the Table) who had no ventriculophasic AV
nodal conduction at baseline, phenylephrine at a dose of
1.2 mg/kg did not induce ventriculophasic AV nodal conduction. Yet
sinus cycle length increased from 910 to 1160 ms, and systolic
blood pressure increased from 148 to 190 mm Hg. There was only a
minimal corresponding shift in the AV nodal conduction curve as
evidenced by minimal changes in AH(s), AH(l), or Wenckebach point
(patient 12; the Table and Figure 5).
This is in contrast to the two patients (patients 10 and 11) who had
ventriculophasic AV nodal conduction provoked by
phenylephrine infusion. These two patients had substantial
shifts in their AV nodal conduction curves. This is consistent
with a disparate effect of baroreflex-mediated vagal influence on the
sinus node and AV node. The single patient without ventriculophasic AV
nodal conduction was 69 years old, had no known cardiac disease, was on
no medication that would alter the autonomic tone, and had no history
of hypertension.
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Figure 5. AV nodal conduction curve from the patient who did
not have ventriculophasic AV nodal conduction recorded. Symbols as
in Figure 3. Phenylephrine infusion caused an increase in
sinus cycle length but had minimal effect on the AV nodal conduction
curve, because the baseline curve and the curve after
phenylephrine infusion is virtually superimposable. WBP
indicates Wenckebach points.
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Effect of Atropine
Atropine in a mean dose of 1.3±0.4 mg was given as an
intravenous bolus to 10 of 12 patients. Two patients did
not receive atropine because of glaucoma. Atropine shortened sinus
cycle length by 33% from 1010±190 to 658±109 ms
(P<0.001) and reduced the Wenckebach point by 25% from
443±125 to 334±65 ms (P<0.005). Atropine abolished
ventriculophasic sinus arrhythmia and ventriculophasic changes
in AV nodal conduction in all patients.
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Discussion
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The major finding of this study is the demonstration of
ventriculophasic AV nodal conduction in patients with second-degree
infra-Hisian heart block. This ventriculophasic modulation of AV nodal
conduction was seen at baseline in 9 of 12 patients with second-degree
infra-Hisian heart block and ventriculophasic sinus arrhythmia.
When not seen at baseline, it could be induced by
phenylephrine infusion in 2 of the 3 remaining patients.
Thus, all patients except 1 exhibited this phenomenon. This is the
first description of phasic modulation of AV nodal conduction in a
model of intact baroreflex.
Previous Animal Studies
The phasic effects of baroreceptor-mediated fluctuations in vagal
tone on the SA and AV nodes have been studied in animal models. In
these studies, brief burst stimulation of the vagal efferent were meant
to simulate those caused by stimulation of the baroreflex in response
to beat-to-beat fluctuations in arterial
pressure.7 8 Burst vagal stimulation was found to
cause sinus node slowing in a phase-dependent
manner.9 10 11 At the level of the AV node, most
studies found that dromotropic effects were balanced by effects on the
sinus node so that 1:1 conduction was maintained over a wide spectrum
of stimulation frequencies.12 13 When the input
to the AV node was fixed by atrial pacing, however, a direct negative
dromotropic response was seen in AV nodal
conduction.14 This response of the AV node to
postganglionic vagal stimulation during atrial pacing was also found to
be phase-dependent.12 Hence, these studies would
predict that in the intact reflex, phasic fluctuations in blood
pressure would cause phase-dependent changes in AV nodal conduction.
Animal studies have used direct fluctuations in blood pressure to cause
baroreflex-mediated changes in vagal tone.15 16 17
Despite measurements on a beat-to-beat basis of AV nodal conduction in
these studies, phasic changes in AV nodal conduction were limited by
the development of high-degree heart block. Therefore, beat-to-beat
fluctuations in AV intervals secondary to the baroreflex were
superimposed on typical Wenckebach changes in the AV interval.
Furthermore, AH intervals, which better reflect AV nodal conduction,
were not measured. Hence, phasic fluctuations in the AH interval on a
beat-to-beat basis in isolation of other effects have not been studied
previously.
Previous Human Studies
Baroreceptor-mediated effects on AV nodal function have been
studied in humans. Mancia et al,18 using
intravenous nitroglycerin and
phenylephrine boluses to cause fluctuations in blood
pressure, studied the effect of the baroreflex on the AH and HV
intervals both during sinus rhythm and during atrial pacing. As in
animal studies, increases in blood pressure were accompanied by sinus
slowing. There was little change in AH or HV intervals during sinus
rhythm. During atrial pacing, which fixed the input to the AV node, the
AH interval changed in direct relation to the blood pressure. Hence,
tonic increases in baroreceptor-mediated vagal tone influenced AV nodal
conduction in humans. Page et al6 studied the
effects of tonic increases in vagal output via a baroreceptor-mediated
mechanism on the AV nodal conduction curve in 10 patients being
investigated for syncope or presyncope. Phenylephrine
caused an increase in sinus cycle length in all patients and was noted
to shift the AV nodal conduction curve up and to the right in 8 of 10
patients. Hence, phenylephrine was found to induce a
vagal-mediated effect on AV nodal conduction in these patients. Neither
of these studies in humans described the effects of phasic changes in
baroreflex-mediated vagal tone on AV nodal conduction.
Our study is unique in that it is the first clear delineation of a
phasic modulation of AV nodal conduction in a model of intact
baroreflex. Patients with distal infra-Hisian second-degree heart block
serve as a unique model in which to study beat-to-beat variations in
the AH interval with and without the influence of
ventricular systole and therefore the baroreflex. A
consistent relationship was found between the AH interval and
the preceding QRS complex and arterial pulse. During 2:1
infra-Hisian heart block, the longer AH interval followed the
arterial pressure wave and was typically re-corded two
beats after a QRS complex. This latency consisted of a delay from
electrical activation (QRS) to mechanical cardiac output
(arterial pulse) and baroreflex latency. This baroreflex
latency has previously been shown in animal studies to be approximately
500 ms.19 20 In higher degrees of infra-Hisian AV
block, the longest AH interval was recorded after the
arterial pressure wave; it progressively shortened until
the next arterial pulse. This is in keeping with animal
studies that demonstrated that the effects of postganglionic brief
vagal bursts were maximal in the first beat and dissipated over 5 to 10
beats.14
Of 12 patients, 9 had ventriculophasic AV nodal conduction at baseline.
Of 3 patients who did not have ventriculophasic AV nodal conduction at
baseline, phenylephrine was able to induce it in 2. One
patient never exhibited ventriculophasic changes at the AV node,
despite the fact that the reflex was intact and operative in this
patient. This patient had ventriculophasic sinus arrhythmia at
baseline when she presented in 2:1 infra-Hisian heart block.
Furthermore, phenylephrine was able to cause a
vagal-mediated increase in sinus cycle length. Despite this, no
ventriculophasic AV nodal conduction was seen, and the AV nodal
conduction curves before and after phenylephrine were
virtually superimposable, suggesting that the reflex vagal stimulation
had minimal effect on the AV node. Atropine shifted the AV nodal
conduction curve down and to the left, suggesting that the AV node was
functioning under the influence of some degree of vagal tone. Page et
al,6 using a similar method of autonomic
perturbation, found a similar result in 2 of their patients who had
sinus slowing with phenylephrine-induced increases in
blood pressure. However, AV nodal conduction curves in these patients
also remained unchanged. This is consistent with a disparate
effect on the SA and AV node, which is known to exist in response to
fluctuations in baroreflex-mediated vagal tone in
animals7 and humans.6
In all cases in which ventriculophasic AV nodal conduction was seen, it
was noted on the steep portion of the AV nodal conduction curve and
increased in an absolute amount as the paced atrial rate was increased
until Wenckebach occurred. This phenomenon has been noted in models
using brief vagal stimuli in dogs. Salata et al21
found that the phase-dependent changes in AV nodal conduction were also
cycle length dependent; the variation in the AH interval was increased
as the paced cycle length decreased. The study by Page et
al6 found that phenylephrine caused a
shift in the AV nodal conduction curve from baseline that was greatest
at shorter paced cycle lengths; hence, the vagal-mediated effects of
phenylephrine were greatest on the steep portion of the
curve. It is therefore not surprising to find a greater vagal-mediated
effect inducing ventriculophasic AV nodal conduction on the steep
portion of the curve. Atropine abolished both ventriculophasic sinus
arrhythmia and ventriculophasic changes in AV nodal conduction
in all patients. The ability to accentuate or provoke ventriculophasic
changes with phenylephrine and to abolish the effects with
atropine strongly suggests a baroreflex-mediated mechanism. Other
interacting factors may contribute to the vagal-mediated modulation of
the AV node. Vagal stimulation has been shown to cause a shift in the
site of sinus nodal pacemakers22 23 24 and a change
in the spread of conduction from the SA node to AV
node.25 Furthermore, AV nodal conduction has been
shown to be modulated by a change in the relative contributions of the
crista terminalis and interatrial septal
inputs.26 27 28 In our study, AH measurements were
recorded during atrial pacing from the high right atrium; thus, the
site of earliest atrial activation was fixed, and the inputs to the AV
node were unlikely to shift significantly. Therefore these factors were
unlikely to make a significant contribution to our results.
Clinical Significance
Ventriculophasic modulation of AV nodal conduction may be
important during atrial fibrillation. As in this study,
ventriculophasic effects on the AV node have been difficult to
demonstrate in sinus rhythm because vagal-mediated sinus slowing
reduces the subsequent cycle length of the input to the AV node,
thereby attenuating any direct vagal-mediated slowing in AV nodal
conduction.12 13 During atrial fibrillation,
however, the irregular ventricular rate and resultant
fluctuations in cardiac output are expected to produce similarly
irregular fluctuations in baroreflex-mediated vagal tone. Two recently
published studies have demonstrated that rapid fluctuations of vagal
tone can contribute to the irregularity of the ventricular
response during atrial fibrillation.29 30
Although the baroreflex was not investigated directly, it is reasonable
to expect that ventriculophasic modulation of AV nodal conduction
contributes to the complex dynamics of AV nodal function during atrial
fibrillation.
Received November 21, 1997;
revision received January 13, 1998;
accepted January 30, 1998.
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References
|
|---|
1.
Parsonnet AE, Miller R. Heart block: the influence
of ventricular systole upon the auricular rhythm in
complete and incomplete heart block. Am Heart J. 1944;27:676–687.
2.
Rosenbaum MB, Lepeschkin E. The effect of
ventricular systole on auricular rhythm in
auriculoventricular block. Circulation. 1955;11:240–261.[Medline]
[Order article via Infotrieve]
3.
Levy MN, Edelstein J. The mechanism of synchronization
in isorhythmic A-V dissociation, II: clinical studies.
Circulation. 1970;42:689–699.[Abstract/Free Full Text]
4.
Josephson ME. Clinical Cardiac
Electrophysiology: Techniques and Interpretation. 2nd ed.
Philadelphia, Pa: Lea & Febiger; 1993:26.
5.
Josephson ME. Clinical Cardiac
Electrophysiology: Techniques and Interpretation. 2nd ed.
Philadelphia, Pa: Lea & Febiger; 1993:22.
6.
Page RL, Tang ASL, Prystowsky EN. Effect of continuous
enhanced vagal tone on atrioventricular nodal and
sinoatrial nodal function in humans. Circ Res. 1991;68:1614–1620.[Abstract/Free Full Text]
7.
Jewett DL. Activity of single efferent fibers in the
cervical vagus nerve of the dog with reference to possible
cardioinhibitory fibers. J Physiol (Lond). 1965;175:321–357.
8.
Randall WC, Ardell JL, O'Toole MF, Wurster RD.
Differential autonomic control of SAN and AVN regions of the canine
heart: structure and function. In: Mazgalev T, Dreifus, LS, Michelson
EL, eds. Electrophysiology of the Sinoatrial and
Atrioventricular Nodes. New York, NY: Alan R.
Liss; 1988:15–31.
9.
Brown GL, Eccles JC. The action of a single vagal
volley on the rhythm of the heart beat. J Physiol
(Lond). 1934;82:211–241.
10.
Jalife J, Moe GK. Phasic effects of vagal stimulation
on pacemaker activity of the isolated sinus node of the young cat.
Circ Res. 1979;45:595–608.[Free Full Text]
11.
Jalife J, Slenter VAJ, Salata JJ, Michaels DC. Dynamic
control of pacemaker activity in the mammalian sinoatrial node.
Circ Res. 1983;52:642–656.[Abstract/Free Full Text]
12.
Spear JF, Kronhaus KD, Moore EN, Kline RP. The effect
of brief vagal stimulation on the isolated rabbit sinus node.
Circ Res. 1979;44:75–88.[Abstract/Free Full Text]
13.
Martin P. The influence of the parasympathetic nervous
system on atrioventricular conduction. Circ
Res. 1977;41:593–599.[Free Full Text]
14.
Mazgalev TL, Dreifus S, Michelson EL, Pelleg A, Price
R. Phasic effects of postganglionic vagal stimulation on
atrioventricular nodal conduction. Am J
Physiol. 1986;251:H619–H630.
15.
O'Toole MF, Wurster RD, Randall WC. Parallel
baroreceptor control of sinoatrial rate and
atrioventricular conduction. Am J
Physiol. 1984;246:H149–H153.
16.
Warner MR, DeTarnowsky JM, Whitson CC, Loeb JM.
Beat-by-beat modulation of AV conduction, II: autonomic neural
mechanisms. Am J Physiol. 1986;251:H1134–H1142.
17.
Warner MR, Loeb JM. Reflex regulation of
atrioventricular conduction. Am J
Physiol. 1987;252:H1077–H1085.[Abstract/Free Full Text]
18.
Mancia G, Bonazzi O, Pozzoni L, Ferrari A, Gardumi M,
Gregorini L, Perondi R. Baroreceptor control of
atrioventricular conduction in man. Circ
Res. 1979;44:752–758.[Abstract/Free Full Text]
19.
Martin P. Secondary AV conduction responses during
tonic vagal stimulation. Am J Physiol.
1983:245;H584–H591.
20.
Irisawa H, Caldwell WM, Wilson MF. Neural regulation of
atrioventricular conduction. Jpn J
Physiol. 1971;21:15–25.[Medline]
[Order article via Infotrieve]
21.
Salata JJ, Gill RM, Gilmour RF, Zipes DP. Effects of
sympathetic tone in vagally induced phasic changes in heart rate and AV
nodal conduction in the anesthetized dog. Circ Res. 1986;58:584–594.[Abstract/Free Full Text]
22.
Boineau JP, Canavan TE, Schuessler RB, Cain ME, Corr
PB, Cox JL. Demonstration of a widely distributed atrial pacemaker
complex in the human heart. Circulation. 1988;77:1221–1237.[Abstract/Free Full Text]
23.
Geesbreght JM, Randall WC. Area localization of
shifting cardiac pacemakers during sympathetic stimulation.
Am J Physiol. 1971;220:1522–1527.
24.
Goldberg JM. Intra-SA nodal pacemaker shifts induced by
autonomic nerve stimulation in the dog. Am J Physiol. 1975;229:1116–1123.
25.
Mazgalev T, Dreifus LS, Michelson EL, Pellag A. Effect
of postganglionic vagal stimulation on the organization of
atrioventricular nodal conduction in isolated rabbit
heart tissue. Circulation. 1986;74:869–880.[Abstract/Free Full Text]
26.
Janse MJ. Influence of the direction of the atrial
wavefront on AV nodal transmission in isolated hearts of rabbits.
Circulation.. 1969;25:439–449.
27.
Zipes DP, Mendez C, Moe GK. Evidence for summation and
voltage dependency in rabbit atrioventricular nodal
fibers. Circ Res. 1973;32:170–177.[Abstract/Free Full Text]
28.
Mazgalev TL, Dreifus S, Iinuma H, Michelson EL. Effects
of the site and timing of atrioventricular nodal input
on atrioventricular conduction in the isolated perfused
rabbit heart. Circulation. 1984;70:748–759.[Abstract/Free Full Text]
29.
van den Berg MP, Haaksma J, Brouwer J, Tieleman RG,
Mulder G, Crijns HJEM. Heart rate variability in patients with
fibrillation is related to vagal tone. Circulation. 1997;96:1209–1216.[Abstract/Free Full Text]
30.
Nagayoshi H, Janota T, Hnatkova K, Camm AJ, Malik M.
Autonomic modulation of ventricular rate in atrial
fibrillation. Am J Physiol. 1997;272:H1643–H1649.[Abstract/Free Full Text]
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Abstract
Introduction