1. No category

The His Bundle Electrogram
By JACOB I. HAFT, M.D.
SUMMARY
The His bundle electrogram is discussed with respect to its rationale, methods for its recording
and evaluation, findings with its use in the various forms of heart block and arrhythmias, its
clinical value, and its limitations.
Additional Indexing Words:
Intraventricular conduction
Heart block
similar manner, whether extra beats are of supraventricular or ventricular origin can be determined.
It is the purpose of this paper to review the
technics of His bundle electrography, the information that has already been learned with use of the
technic, and the clinical value of the His bundle
electrogram.
HE STANDARD electrocardiogram records
only electrical events of atrial and ventricular
depolarization and repolarization. The origin of the
impulse and information concerning conduction
from the atria to the ventricles are inferred from the
configuration and the relationship of the atrial to
the ventricular deflections. The conduction tissue
per se, however, whether within the atrium, the
node, the bundle of His, or the bundle branches,
does not have a representation on the electrocardiogram. Conclusions with regard to the integrity of
the conduction tissue are achieved only indirectly
from analysis of the depolarization of the various
areas of myocardial musculature. During the P-R
interval much of the depolarization of conduction
tissue occurs and cannot be seen on the ECG. The
A-V node is depolarized, the bundle of His is
depolarized, and then, in the normal, the two
bundle branches are depolarized relatively simultaneously. 2
With the use of the His bundle electrogram (fig.
1), a marker can be placed within the P-R interval
that will allow the separation of A-V conduction
into two periods: the time for conduction from (1)
the onset of atrial depolarization, through the
atrium, through the A-V node to the bundle of His,
and (2) from the depolarization of the bundle of
His through the bundle branches to the onset of
depolarization of the ventricular musculature. Using the bundle of His depolarization as a marker,
defects in A-V conduction can be localized either to
the areas above the His (atrial-nodal junction,
nodal, or nodal-His junction) or the areas below the
His (distal His bundle, bilaterally in both bundle
branches, or in the distal Purkinje system). In a
T
Technic
Alanis et al. were the first to record the
depolarization of the His bundle using fine-needle
electrodes directly on the bundle in the isolated dog
heart. Other investigators, similarly, were able to record
His bundle activity in the dog. In the human, bundle of
His depolarization was first recorded by Giraud et al.4
in a patient with atrial septal defect (ASD) in 1960.
Watson et al. reported similar records obtained from a
patient with Ebstein's anomaly in 1967.5 It was
Scherlag et al.,6 however, who were first to record
depolarization of the bundle of His in the normal intact
human using only the technics needed for right heart
catheterization, and it is their technic and its
modifications that are currently used by most investiga-
1
tors.
The heart is approached via the inferior vena cava. A
bipolar or multipolar electrode catheter is introduced
percutaneously into the right femoral vein either using
the Seldinger technic with a Desilets set (after the wire
has been introduced a dilator and then a thin sheath are
passed over the wire and then the electrode catheter is
passed into the sheath) or a no. 14 plastic-sheathed
needle (Jelco) with the electrode catheter then
replacing the needle. Under fluoroscopic control, the
catheter is passed up the inferior vena cava through the
right atrium into the right ventricle. The catheter is
then withdrawn slowly until a typical spike between
the P and QRS is seen on the monitored bipolar
electrogram. The HBE is recorded most often when the
position of the electrode on fluoroscopy in the PA
projection appears to be just at the left border of the
spinal column. At that point, the catheter electrodes are
just across the tricuspid valve and near the septum.
Often a few passes are required before an adequate
HBE is recorded. Applying a gentle clockwise torque to
the catheter as it is withdrawn will bring the catheter
From the Cardiac Section of the Bronx Veterans
Administration Hospital and Mount Sinai School of
Medicine, New York, New York.
Circulation, Volume XLVII, April 1973
897
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8HAFT
898
A H QfRS
X
¶
I
¾{
LAHJ
PH-J HV
Figure 1
A representative His bundle electrogram. A= atrial deflection: H - His deflection; QRS - ventricular depolarization. The intervals as measured are demonstrated. P-H is
the interval f rom the onset of the P wave either in a
standard lead ECG or a high atrial lead to the onset of the
rapid deflectioni of the His butndle spike. The A-H interval
begins from the onset of the atrial deflection on the His
bundle electrogram (low RA) to the His bundle deflection.
H-V is meastured from the first rapid deflection of the His
buindle to the onset of ventricular depolarization as seen
either on the HBE or on any of the standard leads.
electrode tips in contact with the septum and may aid
in achieving an adequate HBE recording.
There are many catheters available. The Damato
catheter has six poles 1 cm apart and requires the use of
a switch box that allows the recording of any bipolar
combination of the six poles.6 Various other catheters
with different distances between the poles have been
used for recording the HBE.7'- We have found that the
standard 4F bipolar or tripolar pacing catheter is
adequate, in most instances, and have discontiniued
using a switch box. We use a shielded two-wire cable
with two alligator clamps on one end that are attached
to the two poles or sequentially to two of the three
electrodes of a tripolar catheter, and a telephone jack
on the other end which is connected to the AC input
terminal of an ECG channel of an oscilloscopic
photographic recorder. Any monitoring and recording
system that has paper speeds of 100 mm/min or
greater, that has an ECG channel that will take a
bipolar signal, and that has frequen-cy limits that can be
set at 40-500 Hz is adequate (i.e., EEP eight channel
of an Electroniics for Medicine recorder). One or more
leads of the standard ECG are recorded simultaneously
on another channel to facilitate interpretation and interval measurement on the HBE.
In addition to the Scherlag-Damato technic that is
most commonly used, there are two other approaches to
recording of the His bundle depolarization that have
been successful. Lau, Bobb, and Damatol' obtained
records of the His bundle depolarization in intact dogs
using an arterial approach with an electrode catheter
introduced retrograde into the outflow tract of the left
ventricle and positioned above the aortic valve in the
posterior cusp or along the septal wall just below the
aortic valve. Recording of left bundle-branch activity
was also possible with the same catheter with minor
manipulation. In a similar manner, records of the bundle
of His from the left side of the heart were obtained in
man by Narula et al.' and by Rosen et al.2
Recently another approach to the His bundle hias
been developed by Gallagher et al., in Damato's
laboratory." Using a catheter with a J-curved tip anid a
device at the proximal end of the catheter that enables
the angle of the J curve to be changed, thelse
investigators have been able to approach the His
bundle from the arm via a cutdown in an anitecubital
vein rather than the femoral vein. Ease of achieving an
adequate HBE recording compares favorably with the
usual technic.
Clinical Findings with His Bundle Electrograms
The ability to determine the point in time of the
cardiac cycle at which the bundle of His is
depolarized has enabled investigators to study the
various forms of heart block and to verify
physiologically the concepts that were based
previously only on data from the routine ECG, the
autopsy table, or animal experiments. Stressing the
heart by atrial pacing and premature atrial
stimulation has aided in the study of normal and
abnormal conduction and of A-V node function.
First-degree heart block (fig. 2), in the usual
situation with a normal QRS, has been found to be
due to block above the bundle of HiS.7 12' 13 The
His-QRS interval is normal in most instances, and
the delay in conduction occurs prior to the
recording of the bundle of His, presumably in the
A-V node, the atrial-nodal junction, or the node-His
junction. First-degree heart block can be produced
artifically by atrial pacing. As the rate of atrial
pacing increases, the P-R interval gradually increases due to block above the His bundle7' 12, 13
and is the normal response to an inappropriately
high atrial rate. (During sinus tachycardia the same
conditions that provoke the tachycardia, whether
fever, anxiety, hyperthyroidism, etc., also accelerate
conduction across the node. Hence, during sinus
tachycardia the P-R interval is normal or may even
be shortened in patients with normal A-V conduction.) Occasionally, especially in patients with left
bundle-branch block or in patients with other
intraventricular conduction defects, first-degree
heart block is found to be caused by block below
the bundle of His7 1416 in the trifascicular intraventricular conduction system. [The intraventricular
conduction system has three major pathways from
Circulaton, Volume XLVII, April 1973
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HIS BUNDLE ELECTROGRAM
P
H ORS
P
899
H ORS
P H ORS
P
P H ORS
H QRS
P
1,
_
1
------ M
PR- 32 SEC.
A H- 260 MSEC.
H-yV 45 MIEC.
.WNo,. .
PR - 24 SEC,
A-H 130 MSEC
H-V 68 MSEC.
1.
'-.
M.."
H ORS
O
~
0'mw--
PR g.45 SEC,
A- H- 345 MSEC.
H V- 78 MSECC
Figure 2
First-degree heart block. (Left) The usual findings in first-degree heart block with prolongation in the A-H
interval and a normal H-V interval. (Middle) First-degree heart block due to delay in the H-V interval with
a normal A-H interval (seen rarely except in the presence of LBBB). (Right) First-degree heart block with
block both in the A-H interval and the H-V interval.
the common bundle of His to the ventricular
musculature:'7 the right bundle branch, the anterior
superior radiations of the left bundle branch, and
the posterior inferior radiations of the left bundle
branch. Thus, RBBB on ECG is caused by block of
the right bundle; left-axis deviation can be caused
by block in the anterior radiations of the left
brundle; right-axis deviation, in the absence of
evidence for right ventricular hypertrophy, can be
caused by block in the posterior radiations of the
left bundle branch; and complete LBBB can be
caused by block either in the short main left bundle
branch before the formation of its two radiations or
by block in both the anterior and the inferior
radiations of the left bundle branch simultaneously.
Other combinations of lesions (e.g. of the right
bundle and the anterior radiations of the left) will
cause other combination lesions on ECG (i.e.
RBBB and left-axis deviation). In first-degree heart
block due to block beyond the His, when the
intraventricular conduction defects on ECG suggest
complete block in two of the three pathways of the
intraventricular conduction system (e.g. RBBB with
LAD), the assumption is made that there
is also incomplete block of the remaining
pathway.2 14, 18'21] A large number of patients with
LBBB and first-degree heart block are found to
have block below the His.'14 10 Because studies have
suggested that the left septum is depolarized earlier
than the right side22 and the anatomy of the LBB
shows earlier branching than the RBB, the time
from the onset of depolarization of the LBB to the
depolarization of LV musculature normally might
be shorter than the time from RBB to RV
depolarization. Then the conduction time from the
His to ventricular depolarization would be longer in
the presence of LBBB, even without incomplete
block of the RBB.2' Studies utilizing simultaneous
recording from the right and left bundle branches,
however, have suggested that the two bundle
branches are depolarized simultaneously.", 2 The
time from the RB depolarization to the onset of the
QRS is not prolonged in the presence of LBBB
iniduced by the artificial production of aberrant
conduction.2 Hence, 1° heart block in the presence
of LBBB found to be due to prolongationi of the HQRS time is probably due to disease of the RBB. It
is of interest that first-degree heart block accompanying uncomplicated RBBB, i.e. without concurrent marked axis deviation, is rarely due to block
heloxv the His, i.e. in the LBB system.2
Even in the absence of first-degree block the
finding of delay in conduction below the His has
been considered evidence of at least incomplete
trifascicular block.
Second-degree heart block can be divided into
two forms: Wenckebach (Mobitz type I) and
Mobitz type II (figs. 3, 4). In the great majority of
patients with Wenckebach block, study with His
bundle clectrograms has demonstrated the block to
be above the area of recording of the bundle of
His: at the node, the atrial-node junction or the
node-His juinction,7 9 as in most cases of firstdegree heart block. The gradual P-R interval
lengthening is due to block above the His. The
blocked P wave that terminates the Wenckebach
cycle is not followed by a His depolarization
indicating complete block in the node or perinodal
area (fig. 5). If the normal heart is accelerated by
atrial pacing, patients with normal conduction will
develop first-degree heart block and finally
Wenekebach block as the rate is further accelerated.23 It is this normal function of the nodal area
that guards against inappropriately high atrial rates
from being transmitted to the ventricles. Very
rarely Wenekebach-type block has been seen to
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900
-11
HAFT
M 01
m^.
P
lv
1
H QRS
~m im
-
.0^
P
m
ON
qww
E. E0..EE
HORs
.-
19 .
p
H
-1
ol^m
111111
P
p
RS
HORS
Figure 3
Weuickebach block (Mobitz I). Note the gradual increase in the P-H interval with the blocked P
followed by a His deflection. The H-V interval remains constacnt throughotut.
occur spontaneously below the His with the HisQRS interval progressively prolonged until block
occurs distal to the His spike.'5 24 Such Wenckebach block has been produced rarely by atrial
pacingl4 or atropine administration. 14
The presence of a "split His," i.e. two His bundle
spikes occurring on the record during the P-R
initerval with Wenckebach periods between the
spikes, has also been reported.25 26 In some of the
reporte.d cases of His to QRS Wenckebach, it is not
clear whether the "His spike" is not actually part of
the P wave.'5 24 This question can be settled only
by the various methods of verification of the bundle
of His (vide infra). Although Wenchebach block
below the His has been documented, block above
the His is the usual finding during Wenckebach
periods.
Second-degree heart block of the Mobitz II type
has been found on His bundle electrography to be
due in most instances to intermittent block of the
intraventricular conduction system below the
node.1t3 15. 16, 20, 25, 27 During the conducted beats,
the P-H interval is usually normal, and the H-QRS
25
H QR
P
HORS
P
HORS
not
interval can be normal or prolonged. Following each
blocked P wave, there is a His bundle depolarization but no QRS, demonstrating that the block is
below the bundle of His, usually in the intraventricular conduction system. Most patients with Mobitz
II who are found to have block below the His
during their nonconducted P waves have an
intraventricular conduction defect on their ECG in
the conducted beats. Mobitz type II, especially in
the presence of a prolonged QRS, is suggestive of
intermittent trifascicular block, and the patients
with this finding are at risk for the development of
complete heart block.28 9 Occasionally patients
with Mobitz II are found to have a "split" His
bundle spike with two deflections following each P
wave.2.1 Following the blocked P wave, only the
initial His spike is seen. This has been interpreted as
intra-His bundle block. It has been suggested that
patients with Mobitz II and a normal QRS
freqluently have block within the His bundle.25
A ntumber of cases recently have been reported of
Mobitz II where study with His bundle electrography revealed that block was proximal to the bundle
A
P
wave
P
A
Si~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~ ~- - -
H
P
HORS
_~
Figure 4
II.
Mobtiz
Note constant P to His and H-Q intervals with block of the nonconducted P
distal to the His bundle depolarization.
wave, occurring
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HIS BUNDLE ELECTROGRAM
901
::,j
--
P H
Qu
P H
P H
QeS
P H
P H
QRS
P H
t=}i
t
',I
w
vp
p
Figure 5
Complete heart block (third-degree heart block). (Top) Type of CHB usually seen in elderly patients with
each P wave being followed by depolarization of the buJndle of His and the ventricular depolarizations not
preceded by a His bundle spike. (Bottom) Type of CHB seen rarely in elderly patients (approximately
15%) but the usual type after diaphragmatic MI or with congenital heart block. Each QRS is preceded by
a His bundle depolarization suggesting that the beat originates either in the His bundle or possibly in the
lower node. The P waves are not followed by depolarization of the His bundle. Block is in the A-V node.
of His."" In three of the five cases reported,
however, there was concomitant evidence to
suggest that vagotonia was present, i.e., overdigitalization (case 1), carotid sinus massage (case 4), or
previous recent episodes of typical Wenckebach
block (case 5). In case 2, Mobitz II block
occurred only on pacing, and the remaining patient
(case 3) had corrected transposition, a lesion which
itself may have distorted the anatomy of the
conduction system, and what was called the His
spike may have originated in a bundle branch. All
of these cases had a normal QRS duration.30 What
appears to be Mobitz II but with block above the
His does not carry the same implications with
respect to the occurrence of complete heart block.
In most patients, without other evidence of
vagotonia, and with a prolonged QRS, however,
Mobitz II block is due usually to block below the
His and is indicative of trifascicular conduction
abnormality.
Second-degree A-V block with fixed ratio between a rapid atrial rate and the ventricular rate
(e.g. paroxysmal atrial tachycardia with 2:1 block or
flutter with 3:1 block) has been found to be due to
block above the area of recording of the bundle of
His, and is due to conduction delay at the A-V node
or perinodal area. In those instances of fixed-ratio
block with a normal atrial rate (either sinus or
otherwise, e.g. atrial rate of 90 beats/min and
ventricular rate of 45), however, the block can be
either proximal7' 25, 31, 32 or distal'3' 1G, 19, 24, 25 to the
His bundle depolarization. A 2:1 block with a
prolonged QRS (probably the most frequently seen
type) is usually due to block distal to the His. A 2:1
block associated with a normal QRS and with
preceding episodes of Wenckebach block and
evidence for vagotonia (e.g. dig toxicity)32 is
usually due to block proximal to the His. In the
individual case, definite determination can only be
made through use of a IBE. Block below the His
(or intra-His block) carries the same implication as
Mobitz II and is an indication for pacemaker
implantation.
During atrial fibrillation, as in flutter, the block
between the atria and the ventricles is in the node
area.32 34 Thus, preceding each QRS there is a His
bundle spike, and in the absence of a QRS there are
no His spikes recorded (fig. 6). Because of the
rapidly firing atria, it is occasionally difficult to
differentiate a His depolarization from the underlying "grass" on the record that is due to electrical
activity of the atrium.
From the anatomy of the conduction system it is
apparent that complete (third-degree) heart block
can occur due to discontinuity of conduction at
either the level of the A-V node, the bundle of His,
or simultaneously in both radiations of the left
bundle and the main right bundle. Pathologic
Circulation, Volume XLVII, April 1973
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HAFT
902
v
iv
H
1I'11
l
tIQ
HI VR
eHQF
F QW
H
il
Figure 6
Atrial flutter and fibrillation. (Top) Atrial flutter with a varying 3:1, 2:1 conduction. F flutter waves. Each
(RS is preceded by a His bundle depolarization suggesting that the nonconducted P waves are blocked in
the area of the A-V node. (Bottom) Atrial fibrillation. Note chaotic depolarization of the atrium and that
each QRS is preceded by a His bundle spike.
studies sinice the work of Mahaim,35 Yater et al..3"
and Lev and Unger37 have demonstrated that in the
majority of patienits with complete heart block
disease i.s usually present in the intraventricular
conduction system with the A-V node intact. More
recent studies by Lenegre 'I and by Davies and
Harris37 have confirmed their findings. There have
now beeni a number of reports of His bundle
electrography in patients with heart block. As was
predicted from the pathologic investigations, the
majority of patients with heart block, especially
among those in the latter decades of life, were
founid to have block beyond the His bundle:
with each P wave followed by His bundle spike and
each QRS not preceded by a recordable depolarization of the bundle of His. This suggests, physiologically, that there is block in the intraventricular
conduction system beyond the bundle of His. A
small number of patients with symptomatic heart
block have been found to have block at the level of
the A-V node, however, with His bundle spikes
preceding each QRS, but not following the blocked
P waves.9' 13. 19, 20, 24, 40-43 Complete block within
the bundle of His has also been reported.6 44 Those
with block distal to the His tend to have a wide
idioventricular QRS, a slow heart rate (35-± 5
beats/min), and usually do not respond to atropine
or exercise with increase in rate (fig. 7). In contrast,
those with block at the node (or the rare patient
with intra-His bundle block, with a His spike
following each P wave and another His spike precedinig each QRS) tend to have higher rates, over 40
beats/min, tend to be less symptomatic, have a
narrow, supraventricular-appearing QRS, and tend
to increase their rate with the administration of
atropine or on exercise. Most patients with congenital heart block have findings similar to the latter
group,45' 4(; with block at the level of the node.
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HIS BUNDLE ELECTROGRAM
P
-.
9
S
lmluw
HH
P HQR$
PH
P H QRS
M.mfn-t , I
:*
'
9()nu3
1
'1
i
Figure 7
A 2:1 A-V block with a low atrial rate. As in most instances of this phenomenon, the block is distal to the
His bundle spike.
Patients who develop heart block with digitalis
intoxication also tend to have block at the node34
(and usually are relatively asymptomatic because of
the relatively high rate of the idionodal or His
bundle focus that is controlling the heart).
Patients who develop heart block during acute
myocardial infarction have been studied with His
bundle electrography. Those with diaphragmatic
MI have been found usually to have their block
proximal to the His bundle spike at the level of the
node."2' 47 This is due probably to either ischemia of
the node seen with compromise of the circulation to
the diaphragmatic surface of the heart or to the
vagotonia that commonly accompanies diaphragmatic MI. These patients frequently have tolerable
rates, will respond to atropine, have a narrow QRS,
and in most instances will recover as collateral
circulation develops. They may require standby
pacing during the acute episode but rarely will
require implantation of a permanent pacemaker.
Heart block during acute anterior myocardial
infarction, however, is usually founid on His bundle
electrography to be associated with block distal to
the site of recording of the bundle of His.32 It is felt
that block during anterior MI is due to simultaneous damage to the right bundle branch and the
anterior radiations of the left bundle which lie
directly opposite each other on the anterior septum
and have a commoni blood supply, and to the
inability of the posterior radiations of the left
bundle to conduct adequately, due either to prior
damage or to ischemia also of these conduction
fibers. Most patients with such heart block have
fairly extensive damage to the septum and frequently succumb whether temporary pacing is instituted
promptly or not.48 They have slow rates with wide
idioventricular QRS and do not respond to atropine.
Those that survive the acute episode not infrequent-
ly have residual complete block or recurrent
episodes of complete block requiring permanent
pacing.
Measurement
of Intervals on the
Electrograms
His
Bundle
Measurements of conduction time can be made
from the His bundle electrogram. The P-His
interval is measured from the onset of the P wave to
the first rapid deflection of the His bundle spike.
Some investigators use the intraatrial high-frequency deflections as the onset of the interval (A-H),7
whereas others use the first deflection of atrial
depolarization whether it is seen on intraatrial
electrogram or the peripheral standard ECG
(P-H ).13 30" 49 Varius investigators have put in other
electrode catheters to simultaneously measure the
high atrial electrogram and use the interval from
the first deflection of the high atrial electrogram to
the onset of the atrial deflection as seen on the HBE
(low atrial electrogram) as a measure of intraatrial
conduction.7 4 Using the onset of the P wave as
seeni on the His electrogram (A-H), the normal
value varies from 50 to 120 msec.25 Others have
noted the normal P-H to be 80-140 msec.14 Depending on how it is measured, this interval may comprise coonduction from the sinus node through the
atrium, through the atrial-nodal junction, the A-V
nlode, the node-His junction, and the proximal
bundle of His; yet abnormal prolongation of this
interval is considered due to delay at the perinodal
area.
The interval from the His bundle depolarization
to the onset of ventricular depolarization has been
considered the more important interval. Prolongation of this initerval among patients with intraventricular conduction abnormalities on standard ECG
may be predictive of complete heart block. The lack
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HAFT
904
of a specific definition for this interval complicates
its evaluation. Some workers measure the interval
from the first rapid deflection of the His spike to the
onset of the earliest QRS seen on the peripheral
ECG leads.'14 50-52 Others use only the onset of
ventricular depolarization seen on the His bundle
electrogram lead as the limit of the H-Q interval,53
while other workers have used the earliest depolarization on either the intracardiac His bundle
electrogram or the peripheral EGG.20
Thus
normal limits are quoted as 35-45 msec,7 25-55
msec,34 or 35-55 msec.2, 26
Evaluation of His bundle electrogram intervals is
complicated also by the mistaken identification of
depolarization of the atrial deflections as His
spikes. This error can be obviated by verification of
the His spike, by atrial pacing,6 or by direct pacing
of the His bundle.55 The atrial pacing procedures
utilize the physiologic response to inappropriate
atrial acceleration, i.e. increase in the P-His interval,
to demonstrate that the spike to be evaluated is not
part of the P wave. Coupled pacing of the atrium,
i.e. delivering a spike at an interval of 300-400 msec
after the sinus P wave, will cause a paced APC.
Ordinarily after an early APC there-will be a delay
in conduction from the P wave to the His deflection
with an increase in the P-R interval.57 If there is no
such delay, the spike considered the His deflection
may be part of the P wave. Verification of the His
can be done also by direct pacing of the His bundle
through the catheter used for recording of the
His.9 55 If the catheter had been recording the His
spike, the QRS resulting from such pacing will have
the same configuration as the normal QRS and will
follow the pacing spike after the same interval as
the H-Q interval. Occasionally, the H-Q interval
appears very short, and differentiation between a
His deflection and a right bundle-branch deflection
must be made. This can be done by either pacing
the His or by delivering sequentially more premature stimuli to the atrium.57 In most patients, as the
prematurity of the atrial impulse is progressively
shortened, the QRS will develop a right bundlebranch block type of aberration.58 If the spike
remains in the presence of RBBB, this is evidence
that the spike was not due to the right bundle but
to the His depolarization (fig. 8). If the spike is due
to the right bundle branch, it will disappear with
development of RBBB conduction.
One of the chief promises that the His bundle
electrogram offers is the possibility of predicting
which of the many patients with intraventricular
conduction defects (right bundle-branch block with
left-axis deviation, right bundle-branch block with
right-axis deviation, or left bundle-branch block,
block in two of the three pathways of intraventricular conduction) will develop complete heart block
(CHB). Lasser et al.59 found that 59% of patients
with CHB were found to have had RBBB and LAD
on ECGs with orthograde conduction, but that only
9% of the patients with this pattern went on to
develop CHB. The figures are somewhat higher for
RBBB and RAD,60 but are entirely unknown for
LBBB. In the normal heart, conduction through the
right and left bundles occurs almost simultaneously.l,2 One would expect that those patients with
ECG patterns suggestive of block in two of the
three conduction pathways with a prolonged H-Q
interval might have disease also in the remaining
intact conduction pathway, and thus be more prone
to develop heart block. If a prolonged H-Q were
found on His bundle electrography, prophylactic
implantation of a permanent pacemaker might be
indicated. Over the past few years a number of
centers have been collecting His bundle electrograms in patients with these ECG patterns to
evaluate prospectively the predictive value of the
HBE. A number of reports with a small number of
cases have appeared in which HBE were recorded
during normal conduction and subsequently CHB
with block distal to the His developed.'6' 19 Of the
11 patients reported by Narula and Samet,'9 10 had
prolonged H-Q intervals during orthograde conduction. Berkowitz et al.'6 reported three such cases,
one with definite H-V prolongation during NSR,
and two others who were not specifically identified
except as having LBBB. All of his patients with
LBBB had an H-Q interval of 54 msec or more
(upper limit of normal or above). In the author's
laboratory, however, four of five patients who
developed intermittent CHB had H-Q intervals
within normal limits during HBE recording during
their normal conduction periods. Although this
finding does not suggest that a patient with a
prolonged H-Q interval might not be more prone to
develop heart block, the presence of a normal H-Q
interval does not preclude CHB in patients with
ECG patterns that have been epidemiologically
found to precede CHB.18
His Bundle Electrography in the Evaluation
of Arrhythmias
In addition to localization of conduction abnormalities, the ability to record depolarization of the
bundle of His aids in the determination of the
Circulation, Volume XLVII, April 1973
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905
HIS BUNDLE ELECTROGRAM
P H QRS
H9RS
ORS
P H
S
t_
A
HO
S
._~~~~~~~~~~~~~~~~~~~~~~il
P H
HORS P
tiX,
P
1I
;-wk~~~~~~~~~~~~
P H
_
\
_.s
P
P H
P HQs
P HS
P
H
1w ; , ti-
RS
Figure 8
hIis bundle electrogram during extrasystoles. (Top) A VPC originating in the ventricle. Note that no His
burndle depolarization precedes the extra beat. Following this interpolated VPC the following P-His
interval is prolonged suggesting that retrograde conduction from the ventricle into the A-V node has
occurred following the VPC. (Middle) A His bundle (or possibly low nodal) escape beat following an APC.
The His spike precedes the QRS with the same H-V interval as noted during orthograde conduction. (Bottom) A VPC originating in the bundle-branch system. Note that the H-V interval of the extra beat is
shorter than duiring the normally conducted beats, suggesting that the His is being depolarized retrograde
simultaneously with antegrade conduction into the ventricles.
origin of ectopic beats and tachycardias (fig. 9).
This is especially valuable in the differentiation
between supraventricular beats with aberration and
beats that originate in the ventricle.33 34 61 63 If a
beat or a succession of beats (tachycardia) is
preceded by a His spike and the H-Q interval is
similar to that of the normal beats, the focus is
either in the atrium, the perinodal area, or the
proximal bundle of His. If, on the other hand, an
adequate bundle of His electrogram is recorded
during the normal beats, but no His spike is seen
preceding the ectopic beats, the origin of the
ectopia is well below the His in the ventricles.
Occasionally, ectopic beats are found to be
preceded by a bundle of His depolarization but the
H-Q interval is shorter than the H-Q recorded
during a normally conducted beat.51' 64, 65 The QRS
frequently is of the right bundle-branch block
configuration suggesting that such a beat originates
from a focus high in the left bundle system, either
in the anterior or posterior radiations of the left
Circulation, Volume XLVII,
April
bundle branch, and that the His depolarization has
been conducted retrograde from the focus. That is,
the impulse is propagated orthograde to the
ventricles and simultaneously retrograde to the site
of recording of the His depolarization. Since the
ectopic focus is closer to the His bundle than to the
ventricular musculature, depolarization of the His
will precede the onset of the QRS but by less than
the H-Q interval recorded during normally conducted beats.
Spontaneous retrograde conduction from the
ventricle to the bundle of His (e.g. after a
spontaneous VPC), except in the situation noted
above, usually is not recorded during His bundle
electrography. This pattern is not discernible
because depolarization of the His occurs simultaneously with the QRS and is buried within the
QRS.8 Patton et al.t.1 have reported one case in
which retrograde His depolarization was recorded
during CHB in a patient with a His bundle rhythm.
Retrograde His potentials can be seen, however,
1973
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HAFT
906
P ORS
H
QRS
P
ORS
H
QRS P
OR~ H
QRS P
?~~
<,9''H'
8,tv,'
:4
'
~ ~~~~~
01:~ ~ 'I
blocked His prermatures were responsible for what
appeared on ECG to be both Mobitz I and II in a
patient who otherwise had normal A-V conduction.
Massumi et al. documented that interpolated His
extrasystoles could produce a supraventricular
tachycardia."'t.
Various other arrhythmic phenomena such as
supernormal conduction, 711-72 concealed conduction)7t entrance block into the sinus73 and A-V
node,74 and the initiation of supraventricular
tachycardia-'7"8, have been elucidated using His
bundle electrographic technics.
Effects of Drugs on Conduction and Refractory
Period Measurement
P HOfS
PH
QRS
Using the bundle of 1-is electrogram the effects
P HQR
conduction of various drugs used in the
disorders have been
investigated (table 1). Vagolytic drugs, such as
atropine, have been shown to shorten the P-H
on
treatment of cardiovascular
I^s
:
#
E
interval but to have
Figure 9
(Top) His bundle electrogram during arrhythmia. This
patient had a ventricuilar rate of 180 beats/mmn with A-V
di.ssociation (note that the P-P intervals are regular and
have no relation to the R-R interval): The diagnosis of ventricular tachycardia was made. On study with a His bundle
electrogram, each QRS was demonstrated to be preceded
by a His bundle depolarization suggesting that the arrhythmia was suipraventricular in origin. (Bottom) After terminating the arrhythmia by pacing, HBE during normal sinus
rhylthm suiggested that the previously diagnosed His spike
teas indeed the His bundle depolarizationi.
during ventricular pacing especially if coupled
pacing of the ventricle is performed.8' 66 During
spontaneous ventricular activity, the occurrence of
retrograde conduction can be inferred from the
effects on the HBE of subsequent orthograde beats.
Hence, following most VPCs, retrograde conduction
through the His to the node can be documented in
the presence or absence of retrograde atrial
depolarization by the finding of a prolonged P-H
interval after an interpolated VPC or of a P wave
blocked proximal to the His following a usual
VPC.67 Using this type of analysis, complete heart
l)lock with retrograde conduction to the node was
found in a patient with block distal to the bundle
of His both in the absence and presence of retrograde atrial depolarization.68
In the diagnosis of bizarre arrhythmias His
bundle electrography has occasionally been of
utmost value. Rosen et al.52 documented that
no
effect
on
the H-Q interval.'2
Sympathomimetic drugs, such as isoproterenol
(Isuprel), have effects similar to vagolytic drugs
with shortening of the P-H and little effect on the
H-Q. 12 Vagotonic drugs and ouabain have been
shown to increase the length of the P-H but to have
no effect on the H-Q.'2 Lidocaine, an antiarrhythmic drug, has been found to have a varying effect
on the P-H interval: slight shortening or no effect in
most patients, and slight prolongation in two of 10
patients studied.76 The H-Q was unaffected, but
lidocaine lead to slight prolongation of the H-S
(intraventricular conduction) in four of 10 patients.
Diphenylhydantoin shortened (five of 12 patients)
had no effect on the P-H interval, and had no
effect on the H-Q interval in any patient.32
Propraniolol increased the P-H time but did niot
or
Efects of Drugs
on
Druig
Table 1
A-V Conduction
A-11 interval
l-l-V interval
Vagotollic:
D)igitalis
Vagolytic:
Ati0pime
I
Syrnpat homimet 1(:
Jsolpiotereitol
1
Synmpatholytic
I
Propranolol
Anttiai.lhvthmic:
Procaine arnide
I)ipheiiylhydaiitoiii
I T
1
Lidocaime
i
(I)
Circulaton, Volume XLVII, April 1973
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HIS BUNDLE ELECTROGRAM
9()7
diagnosis.80 Patients with recurrent arrhythmias, in
whom the differential diagnosis between ventricular
tachycardia and nodal tachycardia with aberration
cannot be made definitely, can have their diagnosis
clarified by demonstrating the presence or absence
of a His spike before each beat. Similarly, the origin
of an ectopic beat, i.e. whether it is ventricular or
supraventricular, can be ascertained by His bundle
electrography. As noted above, elucidation of
bizarre arrhythmias can be achieved sometimes if a
His bundle electrogram is recorded.
Insufficient data exist at this time as to the use of
His bundle electrography in predicting which
patients among those with the ECG patterns during
orthograde conduction that predispose to CHB
(RBBB and LAD, RBBB and RAD, and LBBB)
are at greatest risk for the development of CHB.
The majority of patients reported in the literature
who have had HBE and subsequently developed
heart block have been found to have a prolonged
H-Q interval during the initial HBE study. Therefore, it seems reasonable to assume that the presence
of a prolonged H-Q interval in patients with intraventricular conduction defects would make them
more prone to the development of CHB. However,
the author recently collected five patients with HBE
before the onset of CHB, only one of whom had a
prolonged H-Q interval. Although those with a
prolonged H-Q may be more prone to develop
CHB, the finding that the H-Q is normal should not
falsely reassure the physician that CHB may not
develop.
Among the patients with the clinical diagnosis of
Mobitz IL or 2:1 block with a slow atrial rate,
affect the H-Q.77 Procaine amide has been found to
work differently: to increase the P-H in eight of 15
patients and to prolong the H-Q in all patients.78
Damato's group has used the His bundle
electrogram to measure the refractory period of the
conduction system proximal and distal to the site of
His bundle recording.79 By delivering premature
atrial stimuli in a programmed manner, they have
been able to determine the refractory period of the
A-V node and of the intraventricular conduction
system. Studies in patients with LBBB have defined
the refractory periods of the right bundle and the
anterior radiations of the left bundle.54 Further
information from studies of this type may further
refine the ability to predict the probability of heart
block in individual patients. Effects of drugs on the
refractory periods measured in this way may be a
means of defining in man the more subtle effects of
drugs on the intraventricular conduction system.
Clinical Value and Indications for His Bundle
Electrocardiography
At present His bundle electrography is primarily
an investigational technic that is useful in studying
A-V conduction and aiding in understanding the
physiology of the various conduction abnormalities
(table 2). However, there
are a
number of clinical
situations where critical information can be gotten
only through His bundle electrography. In those
instances where the differential diagnosis between
W-P-W and myocardial infarction, or left bundlebranch block, cannot be made with certainty from
the ECG or VCG alone the presence or absence of
the typical finding of W-P-W (short H-Q with
change with pacing) on the HBE can clarify the
Table 2
Site of Block in Atrioventricular Conduction Disturbances
Proximal to His
Heart block
First-degree
Second-degree:
Wenckebach
Mobitz II
Complete:
Congenital
Elderly
Anterior MI
Diaphragmatic MI
Traumatic (surg)
Flutter
Fibrillation
2:1 with slow atrial rate:
Normal QRS
Prolonged QRS
Distal to His
Intra-His
Usual
Rare
Usual
Very rare
Rare
Usual
Very rare
Very rare
Usual
Usual
Very rare
Usual
Rare (approx
15%/)
Occasional
Usual
Usual
Usual
Usual
Usual
Frequent
Rare
Usual
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Occasional
Occasiona
908
HAFT
especially those with a normal QRS duration, the
finding of block before the His (at the node) does
not carry the same significance with regard to the
development of CHB as does block distal to the
His. Prophylactic pacemakers are indicated in
patients with P waves blocked distal to the His
bundle depolarization.
The determination of the site of block in all
patients with CHB is currently being done in a
number of centers. It may develop that those
patients with block above the His who are not
symptomatic may not require chronic pacemakers.
Evidence of this type may help to end the
controversy as to which patients with chronic heart
block (and no symptoms) require a permanent
pacemaker.
In patients with acute myocardial infarction and
heart block distal to the His as proven by HBE, it
commonly is the practice in the author's institution
to implant permanent pacemakers. However, this is
not instituted necessarilv in those with block
proximal to the His bundle deflection.
Currently, patients with symptomatic sinus bradycardia are frequently treated with implantation of
permanent transvenous ventricular pacemakers.
With futher technologic advances and development
of a reliable permanent transvenous atrialpacing
system, atrial pacing with its preservation of the
atrial pump-priming function will be treatment of
choice for many of these patients. His bundle
electrographic studies in a number of these patients,
however, have demonstrated that A-V conduction
is also compromised in many patients with sinus
bradycardia,81' 82 and in these patients ventricular
pacing will remain the optimum treatment. In the
future, when atrial pacers are available, prior to
their implantation, investigation of the A-V conduction system using HBE will be indicated to determine which patients will require ventricular rather
than atrial pacing.
Critique of His Bundle Electrography
Although recording the depolarization of the His
bundle has been of great value in the understanding
of conduction and rhythm disturbances, for intelligent interpretations of the literature on the HBE
certain problems with the procedure must he
considered. The chief difficulty relates to the fact
that in reality we are recording a rapid deflection
that occurs between the atrial and ventricular
depolarizations and are interpreting this as the
bundle of His depolarization. Although in most
cases this deflection is the depolarization of the His
bundle, occasionally what has been called the His
in published articles may be either the proximal
right bundle branch or a part of the atrial
deflection. Verification of the His as described
above is usually sufficient to allay doubts as to the
origin of the deflection, but it is conceivable that
conduction delay in the atrium may give the
appearance of an increase in A-H interval on atrial
pacing or coupled atrial beats and suggest that
what is really part of the atrial deflection is the His
spike. Differentiation from the right bundle branch
may also be difficult to accomplish if premature
atrial beats lead to block in the right bundle branch
below the level of the area of recording. Unfortunately, pacing of the His bundle, which would
appear to be the optimum method of verification, is
frequently difficult to achieve and is not used
routinely in many centers. In addition to the
problems with verification, reading of the literature
is complicated by the fact that frequently, especially in records of the arrhythmias, no form of
verification of the His deflection has been attempted.
Another problem at this time is the absence in the
literature of a large series of normal patients, i.e.
patients who have completely rnormal hearts, not
just those with normal electrocardiograms. Interpretations of whether intervals measured on the HBE
are normal or abnormal must be tempered by the
fact that the actual normal limits have not been
accurately defined. The absence of a uniform
method for measuring the various intervals and the
lack of an accepted nomenclature with regard to
the intervals has!also complicated the field.
In the future many of these problems may be
resolved. Currently it is important to realize that
His bundle electrography is a new technic and, as
with all new methods, constant evaluation and
reevaluation will be necessary before the full
beneficial results of the technic can be assessed.
References
1. NARULA
OS, JAvIElR RJ, SAMET P, MARAMBA LC:
Significance of His and left bundle recordings from
the left heart in man. Circulation 42: 385, 1970
2. ROSEN KM, RAHIMTOOLA SH, SINNO MZ, GUNNAR
RM: Bundle branch and ventricular activation in
man: A study using catheter recordings of left and
right bundle branch potentials. Circulation 43: 193,
1971
3. ALANIS J, CONZALEZ H, LOPEZ E: Electrical activity of
the bundle of His. J Physiol 142: 127, 1958
Cifculation, Volume XLVII, April 1973
Downloaded from http://circ.ahajournals.org/ by guest on February 6, 2015
HIS BUNDLE ELECTROGRAM
4. GIRAUD G, PEUCH P, LATOUR H: L'activite electrique
physiologique du noeud de Tawara et du Faisceueau
de His chez l'homme. Acad Nat Med, May 1960, p
363
5. WATSON H, EMSLIE-SMITH D, LOWE KG: Intracardiac
electrocardiogram of human atrioventricular conducting tissue. Amer Heart J 74: 66, 1967
6. SHERLAG BJ, LAU SH, HELFANT RH, BERKOWITZ WD,
STEIN E, DAMATO AN: Catheter technique for
recording His bundle activity in man. Circulation
39: 13, 1969
7. NARULA OS, COHEN LS, SAMET P, LISTER JW,
SCHERLAG B, HILDNER FJ: Localization of A-V
conduction defects in man bv recording of the His
bundle electrogram. Amer J Cardiol 25: 228, 1970
8. CASTILLO CA, CASTELLANOS A JR: Retrograde activation of the His bundle during intermittent paired
ventricular stimulation in man. Circulation 42: 1079,
1970
9. PUECH P, LATOUR H. GROLLEAU R, DUFOIX R,
CABASSON J, ROBIN j: L'activite electrique du tissu
de conduction auriculo-ventriculaire: I. Identification.
Arch Mal Coeur 63: 500, 1970
10. LAU SH. BOBB GA, DAMATO AN: Catheter recording
and validation of left bundle branch potentials in
intact dogs. Circulation 42: 375. 1970
11. GALLAGHER JJ, DAMATO AN, LAU SH, TOWER A,
CARACTA AR, VARCHESE PJ, JOSEPHSON ME:
Antecubital vein approach to recording His bundle
activity. Clin Res 20: 373, 1972
12. DAMATO AN, LAU SH, HELFANT RH, STEIN E,
BERKOWMIZ WD, COHEN SI: Study of atrioventricular
conduction in man using electrical catheter recordings
of His bundle activity. Circulation 39: 287, 1969
13. DAMATO AN, LAU SH. HELFANT RH, STEIN E, PATTON
RD. SCHERLAG BT. BERKOWITZ WD: A study of heart
block in man using His bundle recordings. Circulation 39: 297, 1969
14. ROSEN KM, RAHTMTOOLA SH. CHUQUIMIA R, LOEB
HS, GUNNAR RM: Electrophysiological significance
of first degree atrioventricular block with intraventricular conduction disturbance. Circulation 43: 491,
1971
15. RANGANATHAN N. DHURANDHAR R, PHILLIPS JH,
WIGLE ED: His bundle electrogram in bundlebranch block. Circulation 45: 282. 1972
16. BERKOWITZ WD, LAU SH. PATTON RD, ROSEN KM,
DAMATO AN: The use of His bundle recordings in
the analysis of unilateral and bilateral bundle branch
block. Amer Heart J 81: 340. 1972
17. ROSENBAUM MB, ELIZARI MV, LAZZARI JO: Los
Hemibloqueos. Buenos Aires, Paidos, 1968
18. HAFr JI, LASSER R: ECG patterns helpful in the
diagnosis of complete heart block. JAMA. In press
19. NARULA OS, SAMET P: Right bundle branch block with
normal, left or right axis deviation. Amer J Med 51:
432, 1971
20. SCHUILENBUYRG RM, DURRER D: Observations on
atrioventricular conduction in patients with bilateral
bundle-branch block. Circulation 41: 967, 1970
21. HAFT JI, WEINSTOCK M, DEQUIA PK, GUPTA P, FANO
A: Assessment of atrioventricular conduction in left
909
and right bundle branch block using His bundle
electrograms and atrial pacing. Amer J Cardiol 27:
474, 1971
22. SODI-PALLARES D, CALDEC RN: The New Bases of
Electrocardiography. St. Louis, C. V. Mosby Co.,
1956
23. LISTER JW, STEIN E, KosoWsKY BD, LAU SH,
DAMATO AN: Atrioventricular conduction in man:
Effect of rate, exercise, isoproterenol and atropine on
the P-R interval. Amer J Cardiol 16: 516, 1965
24. PUECH P, GROLLEAU R, LATOUR H, DuFoIx R,
CABASSON J, ROBIN J: L'enregistrement del l'activite
electrique du faisceau de His dans les blocs A-V
spontanees. Arch Mal Coeur 63: 784, 1970
25. NARULA OS, SAMET P: Wenckebach and Mobitz type II
A-V block due to block within the His bundle and
bundle branches. Circulation 41: 947, 1970
26. SCHUILENBURG RM, DURRER D: Conduction disturbances located within the His bundle. Circulation
45: 612, 1972
27. HAS-r JI, WEINSTOCK M, DEQuLi R: Electrophysiologic studies in Mobitz type II second degree heart
block. Amer J Cardiol 27: 682, 1971
28. DONoso E, ADLER LN, FRIEDBERG CK: Unusual forms
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
of second degree atrioventricular block, inicluding
Mobitz type II block associated with MorgagniAdams-Stokes syndrome. Amer Heart J 67: 150,
1964
LANGENDORF R, PICK A: Atrioventricular block type II
(Mobitz): Its nature and clinical significance.
Circulation 38: 819, 1968
ROSEN KM, LOEB HS, GUNNAR RM, RAHIMTOOLA SH:
Mobitz type II block without bundle branch block.
Circulation 44: 1111, 1971
ROSEN K, LOEB HS, CHUQUIMA R, SINNO MZ,
RAHIMTOOLA SH, GUNNAR RM: Site of heart block
in acute myocardial infarction. Circulation 42: 925,
1970
DAMATO AN, BERKOWITZ WD, PATTON RD, LAU SH:
The effect of dinhenvlhydantoin on atrioventricular
and intraventricular conduction in man. Amer Heart J
79: 51, 1970
LAU SH, DAMATO AN, BERKOWITZ WD, PATTON RD: A
study of atrioventricular conduction in atrial fibrillation and flutter in man using His bundle recordings.
Circulation 40: 71, 1969
CASTELLANOS A, CASTILLO CA, AGHA AS: Contribution
of His bundle recording to the understanding of
clinical arrhythmias. Amer J Cardiol 28: 499, 1971
MAHAIM I: Les Maladies Organiques du Faisceau de
His Tawara. Paris, Messon et cie, 1931
YATER YM, CORNEL VH, CLAYTOR T: Auriculoventricular heart block due to bilateral bundle branch
lesions: Review of the literature and report of three
cases with detailed histopathologic studies. Arch
Intern Med (Chicago) 57: 132, 1936
LEV M, UNGER PM: Pathology of the conduction
system in acquired heart disease: I. Severe atrioventricular block. Arch Path (Chicago) 60: 502, 1955
LENEGRE J: Etiology and pathology of bilateral bundle
branch block in relation to complete heart block.
Progr Cardiovasc Dis 6: 409, 1964
Circulation, Volume XLVII, April 1973
Downloaded from http://circ.ahajournals.org/ by guest on February 6, 2015
910
HAFT
39. DAV'IES M, HARRIS A.: Pathologic basis of primary
heart block. Brit Heart J 31: 219-226, 1969
40. NARULA OS, SCHERLAG BJ, JAVIER RP, HILDNER FJ,
SAMET P: Analysis of the A-V conduction defect in
complete heart block utilizing His bundle electrograms. Circulatinn 41: 437. 1970
41. STEINER C, LAU SH, STEIN E, WIT AL, WEiss MB,
DAMATO AN, HAFT JI, WEINSTOCK M, GUPTA P:
Electrophysiologic documentation of trifascicular
block as the common cause of complete heart block.
Amer J Cardiol 28: 436, 1971
42. HAFT JI, WEINSTOCK M, DEQUIA R, GUPTA P, FANO
A: Localization of conduction defects in patients with
complete heart block using His bundle recordings.
Clin Res 18: 310, 1970
43. PATTON RD, HEINLE RA: A study of chronic heart
block using His bundle electrograms. J Electrocardiol
4: 24, 1971
44. NARULA OS, SCHERLAG BJ, SAMET P, JAVIER RP:
Atrioventricular block: Localization and classification
by His bundle recordings. Amer J Med 50: 146,
1971
45. ROSEN KM, MEHTA A, RAHIMTOOLA SH, MILLER RA:
Sites of congenital and surgical heart block as defined
by His bundle electrocardiography. Circulation 44:
833, 1971
46. KELLY DT, BRODSKY SJ, MIROWSKI M, KROVETZ LJ,
RoWE RD: Bundle of His recordings in congenital
complete heart block. Circulation 45: 277, 1972
47. GERSHENGORN K, HAFT JI: Intermittent heart block
related to treatment of hypertension in a patient with
acute myocardial infarction. Chest 61: 402, 1972
48. GODMAN MJ, LASSERS BW, JULIAN DG: Complete
bundle branch block complicating acute myocardial
infarction. New Eng J Med 282: 237, 1970
49. CASTELLANOS A, CHAPUNOFF E. CASTILLO C, MAYTIN
0, LEMBERG L: His bundle electrograms in two cases
of Wolff-Parkinson-White (pre-excitation) syndrome.
Circulation 41: 399, 1970
50. DAMATO AN, LAU SH, BERKOWITZ WD, ROSEN KM,
Lisi KR: Recording of specialized conducting fiber
(A-V nodal, His bundle, and right bundle branch) in
man using an electrode catheter technique. Circulation 39: 435, 1969
51. MASSUMI RA, ERTEM GE, VERA Z: Aberrancy of
junctional escape beats. Amer J Cardiol 29: 351,
1972
52. ROSEN KM, RAHIMTOOLA SH, GUNNAR RM: Pseudo
A-V block secondary to premature nonpropagated His
bundle depolarizations. Circulation 42: 367, 1970
53. COLDREYER BN, WEISS MB, DAMATO AN: Supraventricular tachycardia initiated by sinus beats. Circulation 44: 820, 1971
54. CANNOM DS, GOLDREYER BN, DAMATO AN: Atrioventricular conduction in left bundle branch block with
normal QRS axis. Circulation 46: 129, 1972
55. NARuLA OS, SCHERLAG BJ, SAMETr P: Pervenous pacing
of the specialized conducting system in man.
Circulation 41: 77, 1970
56. CASTELLANOS A, CASTILLO CA, AGHA AS, TESSLER M:
His bundle electrograms in patients with short P-R
intervals, narrow QRS complexes and paroxysmal
tachyeardias. Circulation 43: 667, 1971
57. DAMATO AN, LAU SH, PATTON RD, STEINER C,
BERKOWITZ WD: A study of atrioventricular conduction in man using premature atrial stimulation and
His bundle recordings. Circulation 40: 61, 1969
58. COHEN SI, LAU SH, HAFT JI, DAMATO AN:
Experimental production of aberrant ventricular
conduction in man. Circulation 36: 673, 1967
59. LASsim RP, HAFT JI, FRIEDBERG CK: Relationship of
right bundle branch block and marked left axis
deviation (with left parietal or peri-infarction block)
to complete heart block and syncope. Circulation 37:
429, 1968
60. ROSENBAUM MB, ELIZARI MV, LAZZARI JO: The
61.
62.
63.
64.
65.
66.
67.
68.
69.
70.
71.
72.
73.
74.
Hemiblocks. Tampa, Florida, Tampa Tracings,
1970
DAMATO AN, LAU SH: His bundle rhythm. Circulation
40: 527, 1969
GALLAGHER JJ, DAMATO AN, LAU SH: Electrophysiologic studies during accelerated idioventricular
rhythms. Circulation 44: 671, 1971
PATTON RD. STEIN E. POSEN KM, LAU SH, DAMATO
AN: Bundle of His electrograms: A new method for
analyzing arrhythmias. Amer J Cardiol 26: 324,
1970
CASTILLO C, CASTELLANOS A, AGHA AS: Significance of
His bundle recordings with short H-V intervals. Chest
60: 143, 1971
COHEN HC, Cozo EG, PICK A: Ventricular tachycardia
with narrow QRS complexes (left posterior fascicular
tachycardia). Circulation 45: 1035, 1972
CASTILLO C. CASTELLANOS A: Retrograde activation of
the His bundle in the human heart. Amer J Cardiol
27: 264, 1971
HAFT JI, GUPTA P: The effect of ventricular premature
contractions on A-V conduction and rhythm as
studied by His bundle electrograms. Circulation 44
(suppl II): II-174, 1971
GUPTA P, HAFr JI: Retrograde ventriculo-atrial
conduction in complete heart block: Studies with His
bundle electrography. Amer J Cardiol. In press
MASSUMI RA: Interpolated His bundle extrasystoles, an
unuisual cause of tachycardia. Amer J Med 49: 265,
1970
DAMATO AN, LAU SH: Concealed and supernormal
atrioventricular conduction. Circulation 43: 967,
1971
DAMATO AN, WIT AL, LAU SH: Observations on the
mechanism of one type of so-called supernormal A-V
conduction. Amer Heart J 82: 725, 1971
MAsSuMI RA, AmSTERDAM E, MASON DT: Phenomenon of supernormality in the human heart. Circulation 46: 264, 1972
COLDREYER BN, DAMATO AN: Sinoatrial-node entrance
block. Circulation 44: 789, 1971
VARCHESE PJ, DAMATO AN, PAULAY KL, GALLAGHER
JJ, LAU SH: Demonstration of entrance block into
the atrioventricular node of man. Circulation 46:
123, 1972
Circulation, Volume XLVII, April 1973
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911
HIS BUNDLE ELECTROGRAM
75. COLDREYER BN, DATMATO AN: The essential role of
atrioventricular conduction delay in the initiation of
paroxysmal supraventricular tachycardia. Circulation
43: 679, 1971
76 ROSEN KM, LAU SH, WEISS MB, DAMATO AN: The
effect of lidocaine on atrioventricular and intraventricular conduction in man. Amer J Cardiol 25: 1,
1970
77. BERKOWITZ WD, WIT AL, LAU SH, STEINER C,
DAMATO AN: The effects of propanolol on cardiac
conduction. Circulation 40: 855, 1969
78. DAMATO AN, LAU SH: Clinical value of the
electrography of the conduction system. Progr
Cardiovasc Dis 13: 119, 1970
79. WIT AL, WEISS MB, BERKowIrz WD, ROSEN KM,
STEINER C, DAMATO AN: Patterns of atrioventricular
conduction in the human heart. Circ Res 27: 345,
1970
80. NARRULA OS: Wolff-Parkinson-White syndrome: A
review. Circulation 47:874, 1973
81. ROSEN KM, LOEB HS, SINNO MZ, RAHIMTOOLA SH,
GUNNAR RM: Cardiac conduction in patients with
symptomatic sinus node disease. Circulation 43: 836,
1971
82. NARULA OS: Atrioventricular conduction defects in
patients with sinus bradyeardia. Circulation 44:
1096, 1971
Circulation, Volume XLVII, April 1973
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The His Bundle Electrogram
JACOB I. HAFT
Circulation. 1973;47:897-911
doi: 10.1161/01.CIR.47.4.897
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