Download His Bundle Electrograms in Healthy Adolescents with Persistent

His Bundle Electrograms in Healthy
Adolescents with Persistent Second Degree
A-V Block*
Paul R. Lightfoot, M.D.; Lewis Sasse, M.D.;
Wil2iam 1. Mandel, M.D.;** and Hirokazu Hayakawa, M.D.
H
i
s bundle recordings were obtained in two healthy young adult men without
organic heart disease whose resting electrocardiograms demonstrated second
degree A-V block with Wenckebach periods. The area of block was found to
be proximal to the His bundle. Exercise and atropine produced both prompt sinus
node acceleration and elimination of the A-V block. This evidence, coupled
with additional pharmacologic studies, strongly indicated excessive vagal tone
as a major causal factor in production of the electrocardiographic abnormalities in these patients.
numerous authors1-l1have commented
Recently,
on the diverse nature of A-V block both in
terms of pathologic and electrophysiologic correlates. Of late particular attention has been placed
on defining the site of conduction disturbance by
utilizing His bundle recording techniques, especially in the setting of second degree A-V b l ~ c k . ' ~ - ' ~
In this regard, the occurrence of second degree A-V
block with Wenckebach periods ( Mobitz Type I ) is
rare in patients without overt cardiac disease. Two
asymptomatic healthy young adult men who were
noted to have second degree A-V block with
Wenckebach periods prompted this report.
This 16-year-old Negro boy was first seen because of
an irregular heart beat discovered during a routine physical examination. There was no history of any significant
previous disease or symptoms related to the cardiovascular
system. Resting ECG's over a six month period demonstrated
persistent second degree A-V block with Wenckebach periods and rare junctional escape beats occurring after the
nonconducted P wave. The QRS complexes were normal with
physiologic ST-T elevation ( early repolarization changes )
"From the D e artments of Cardiology, Kaiser-Permanente
Hospitals, cdiars-sinai Medical Center, and the Department of Medicine, University of California, Los Angeles.
Su ported in part b USPHS Grant No. 5S01 RR 05468.
" " ~ i i yFactor clinicar investigator, Western Cardiac Foundation.
Reprint requests: Dr. Lightfoot, Kaiser Foundation Hospital,
Fontam, Californiu 91711
( Fig 1A). During exercise, physiologic acceleration of the
sinus node ensued. Wenckebach periods were abolished and
replaced with 1:1 A-V conduction and a normal PR interval
(0.20 sec) (Fig l B ) .
This 19-year-old Negro youth was first seen for a preemployment physical examination. At that time, an irregular, slow cardiac rate was detected. An electrocardiogram
(Fig 2A) demonstrated second degree A-V block with
Wenckebach periods. The patient denied any history of
previous disease or symptoms referable to the cardiovascular
system. Physical examination demonstrated blood pressure
of 120/80 rnm Hg and an irregular pulse of approximately 40
per minute, without other significant abnormalities.
His bundle electrograms were recorded by standard techniques with a bipolar or tripolar catheter positioned at the
tricuspid valve.17 Recordings were made on Electronics for
Medicine DR-8 a t filter frequencies of 40 to 500 Hz with a
variable paper speed ( 75-200 mm/sec ) . Atrial electrogram
recordings were obtained by utilizing a specially constructed quadripolar catheter. This catheter was positioned
at the right atrium-superior vena caval junction for the
purpose of both atrial pacing and recording the atrial electrogram. Ventricular pacing was also performed in one patient
while atrial electrograms were recorded to assess the state of
VA conduction. In addition, pharmacologic studies were
carried out using ( 1 ) atropine, 1.0 mg IV; ( 2 ) edrophonium
10 mg IV; ( 3 ) propranolol, 8 mg IV, while simultaneous His
bundle recordings were obtained. Furthermore, exercise electrocardiographic studies were performed with the use of a
variable speed, variable incline treadmill.
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HIS BUNDLE ELECTROGRAMS IN HEALTHY ADOLESCENTS
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RESULTS
Case 1
Two types of A-V block were observed: ( A )
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FIGURE1. Case 1: Electrocardiograms and His bundle recordings: ( A ) Standard 12 lead
electrocardiogram with lead I1
rhythm strip. Note Wenckebach
periodicity in rhythm strip. ( B)
Lead I1 rhythm strip during
treadmill exercise. Note normal
A-V conduction time with 1 : l
A-V conduction. ( C ) His bundle
electrogram recordings. The record shows evidence of atypical
Wenckebach periodicity with
progressive AH prolongation for
four beats with subsenuent AH
shortening. Blocked P' wave is
not associated with H deflection.
Top tracing is a lead I1 electrocardiogram and bottom tracing
is a His bundle electronram recording. Low right at ha^, His
bundle and ventricular depolarizations are marked A, H and V
respectively.
classic Wenckebach periodicity ( Fig 1A ) characterized by progressive lengthening of the PR
interval until a beat was dropped; ( B ) less frequently, the A-H intervals, after gradually length-
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b
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FI(;UHE2. Pharmacologic interventions in case 1. Panel A is recorded following atropine
administration. Leads and abbreviations a< in Figure 1C. Note the increase in heart rate
associated with a pronor~nced shortening of AH time and 1:l A-V conduction. Panel B is
recorded following edrophonir~madministration. Note the development of Wenckebach periods
with 1 : 3 and 3:2 A-\' concluction ratios. The nonconducted P wave is blocked above the His
bundle. Panel C is the record obtained following propranolol administration. Note, as compared to the record ohtained after atropine (panel A ) , the AH time is prolonged but 1 : l AV
conduction is seen.
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.
ening, either stabilized at a constant interval, or
were shortened by small decrements before a beat
was dropped ( Fig 1C ) . During these periods, block
occurred proximal to the His bundle and the
subsequent A-H interval was short.
The patient was then given 1 mg of atropine
intravenously and maximum acceleration of the
sinus node rate occurred at four minutes with
a cycle length of 410 msec. At this peak vagolytic
effect, there was constant 1 : l A-V conduction with
a stable low normal A-H interval of 60 msec (Fig
2A). Ten milligrams of edrophonium (Tensilon)
was then given in a bolus intravenously. Maximum
effect was manifest by slowing of the sinus cycle to
496 msec and the reappearance of Wenckebach
periods with a 3:2 A-V ratio (Fig 2B). After
dissipation of the transient cholinergic effect of
edrophonium, 1:1 A-V conduction with a normal AH interval resumed, secondary to the prolonged
effect of atropine.
Eight milligrams of propranolol (Inderal) was
then given slowly by vein ( 1 mglmin), in an effort
to block sympathetic tone and indirectly enhance
vagal activity. During peak effect (30 minutes after
atropine), the sinus node cycle length was 550
msec, the A-H interval was high normal at 120 msec
and Wenckebach periods did not occur (Fig 2C).
The secondary or indirect vagotonic effect of propranolol was apparently negated by the vagolytic
effect of atropine. It is to be noted that HV times
were within the normal range throughout the study.
Case 2
His bundle recordings initially demonstrated
Wenckebach cycles with the blocked P wave not
conducting to the proximal His bundle. Atrial
pacing at rates up to 150 per minute demonstrated
further increases in A-V block (Fig 3B, C ) and the
site of block remained proximal to the His bundle.
Ventricular pacing produced a 1:1 ventricular response but V-A conduction was absent (Fig 4 ) . As
with patient 1 ( 1) intravenous atropine resulted in
prompt sinus acceleration and eliminated A-V
block; ( 2 ) HV times were within the normal range
throughout the study. One week later the patient
underwent exercise studies which demonstrated
prompt sinus acceleration with elimination of A-V
block.
Reports of Wenckebach type A-V block in cases
without organic heart disease or drug intoxication
are very sparse. Cullen and Collin,ls in a review of
the literature in 1964, could find only 11 welldocumented cases of persistent Wenckebach phenomenon. In addition, they reported their observations in two men, ages 36 and 41, whose resting
ECG demonstrated Wenckebach periods which
.
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FIGURE3. Electrocardiogram and His bundle
recordings for case 2. ( A ) Standard 12
lead electrocardiogram with lead I1 rhythm
strip. Note Wenckebach periods in rhythm
strip with 2 : l and 3:2 A-V conduction. ( B
and C ) His bundle recordings dunng atr~al
pacing. The tracings are, from top to bottom,
atrial electrogram ( AEG ), His bundle electrogram ( HBE ) and standard electrocardiographic leads I, I1 and 111. The low right
atrium, His bundle and ventricular depolarizations are labled A, H and V respectively.
In Panel B, the right atrium was paced at a
cycle length of 667 msec (90/niin ) with the
development of 3:2 A-V conduction. AH
times prolong from 210 to 340 msec and the
third P wave is blocked proximal to the HIS
bundle. In Panel C the atrium was paced at
a cycle length of 400 msec (150/min) with
the development of advanced A-V block.
Note the differences in PR interval9 in the
conducted beats, possibly reflecting concealed conduction.
111
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(~01.
PI-PI ;.to0 msec
CHEST, VOL. 63, NO. 3, MARCH, 1973
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HIS BUNDLE ELECTROGRAMS IN HEALTHY ADOLESCENTS
FIGURE
4. Ventriclilar pacing. The traces are, from top to bottom, the atrial electrograrn ( A E G )
and standard leads I, I1 and 111. Right ventricular pacing was performed at a cycle length of
667 msec (90/min) with absence of VA conduction.
were abolished by exercise. One case, however,
was transient; the other case could well have been
due to carditis. Grimby and Saltinlg demonstrated
Wenckebach phenomenon in two athletes, ages 53
and 51. Both men, however, were hypertensive and
also had Wenckebach periods during exercise. Lamb
and others,'O in their report of 67,375 asymptomatic
healthy fliers, could find only one case of second
degree A-V block. Their case, retrospectively, had
suspected carditis and a resting normal ECG without block on reexamination eight months later. In a
recent report, Sarghin and co-workers2' describe an
asymptomatic 27-year-old marathon runner with
persistent Wenckebach A-V block at rest and normal A-V conduction after atropine or exercise. Their
case was not investigated by utilizing His bundle
recordings so that a more precise localization of the
site of A-V block was unavailable.
\Venckebach periods are the most common form
of second degree A-V block and can occur in
myocardial ischemia, during drug therapy, during
or after acute carditis, after surgical manipulation
or trauma to the A-V conduction system, during
severe vagotonia, or during atrial tachycardias and
rapid atrial pacing. Its occurrence during normal
sinus rhythm in the basal state is usually considered
pathologic.
Recent studies with His bundle recordings during
MTenckebach type A-V block have usually demonstrated an area of block proximal to the His
b ~ n d l e . ' ~ . ' ~Other
.~'
investigator^^^ have demonstrated Wenckebach periodicity in the His-Purkinje
system distal to the His bundle. The phenomenon,
however, is apparently rare, and is usually associated with a widened QRS.
During characteristic Wenckebach periods in our
patients, under basal conditions, His bundle recordings demonstrated block proximal to the His bundle. Two types of A-V block were demonstrated:
(1) the usual progressive prolongation of the A-H
interval before the dropped beat; ( 2 ) at other
times, the A-H interval stabilized or shortened
before the dropped beat and simulated Mobitz type
I1 A-V block (Fig. 1 C ) . Other recent reportsl1*l4
have shown that Mobitz type I1 A-V block can
occur proximal to the His bundle during slight
variations in the P-P interval, or during constant PP intervals. In these reports, however, the A-H
interval following the dropped beat was usually
slightly or moderately decreased, and the QRS
complexes were narrow. These investigations, as
well as the findings in our patients, demonstrate
that HBE recordings are essential in defining the
area of A-V blocks as Type I and Type I1 A-V block
can occur either above or within the His bundle.
Atropine decreased the A-H interval in both cases
and abolished the Wenckebach phenomenon. The
restoration of normal A-V conduction by both a
vagolytic agent and exercise points toward excessive vagal tone as a cause of the prolonged refractory period of the A-V node and the resulting
1Venckebach phenomenon. An interesting corollary
is the observation of incomplete A-V block with
Wenckebach periods in approximately 15 percent of
normal horses at rest.24 In addition, these animals
invariably demonstrate sinus arrhythmia unrelated
to the respiratory cycle, a phenomenon also observed in our patients.
Edrophonium abolished the vagolytic action of
atropine and reproduced Wenckebach periods in
CHEST, VOL. 63, NO. 3, MARCH, 1973
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Case
Its neutralization of the atropine effect
and its mimicking of the resting A-V block supports
the supposition that excessive parasympathetic tone
is a major factor in the etiology of our patients' A-V
block.
Propranolol, although significantly lengthening
the A-H interval, probably did not produce A-V
block related to the prolonged vagolytic action of
atropine. The combined opposing effects of atropine and propranolol resulted in a near normal A-H
time without A-V block. Ventricular pacing demonstrated absence of VA conduction in Case 2. This
finding by itself, however, is not indicative of
intrinsic heart disease as up to 11 percent of patients
with normal A-V conduction do not have 1 : l VA
~onduction.~~
Therapeutic implications based on findings in our
present cases and those previously reported are
unclear. We have elected to observe these patients
without resorting to pharmacologic or pacemaker
therapy. Longterm follow-up will presumably clarify the natural history of this arrhythmia.
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2 Lenegre J: Etiology and pathology of bilateral bundle
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4 Lev M, Unger PN: Pathology of the conduction system in
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5 Lev M : Anatomic basis for atrioventricular block. Am J
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6 Davies hl, Harris A: Pathologic basis of primary heart
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7 James TN: Morphology of the human atrioventricular
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14 Rosen KSI, Loeb HS, Gunnar Rhl, et al: hlobitz type I1
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15 Mandel WJ, Lozano J, Carrasco H, et al: Coexisting intra
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19 Grimby G, Saltin B: Letters to the Editor. Lancet 2:962,
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20 Lamb LE: The first international symposium on cardiology in aviation. 1959, p 313
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