Atrioventricular Nodal and Subnodal Conduction

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9
4
Atrioventricular Nodal
and Subnodal Conduction
Disturbances
Hein J.J. Wellens
Causes of Atrioventricular Conduction
Disturbances . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1991
Bundle Branch Block . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1992
Chronic Bundle Branch Block . . . . . . . . . . . . . . . . . . . . 1994
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1997
Key Points
icity, abnormalities in electrolyte levels, trauma (also during
open heart surgery), and fibrotic changes that occur with
aging.2 Abnormalities in conduction are common in acute
myocardial infarction (MI).3 They are usually transient (not
requiring long-term ventricular pacing), but have prognostic
implications both for hospital and long-term mortality. Their
site in the AV conduction system is related to the location of
the MI. As shown in Figure 94.1, a branch from the right
coronary artery perfuses the AV node. Therefore, AV nodal
block may occur in inferoposterior MI caused by an occlusion of the right coronary artery, especially when the occlusion is located proximal to the right ventricular branch. As
described elsewhere 3 and in Chapter 3, the location of the
obstruction in the coronary artery leading to inferoposterior
MI can easily be derived from the additional recording of
right precordial leads (Fig. 94.2).
In contrast, conduction abnormalities, distal to the AV
node may occur after a proximal occlusion of the left anterior
descending coronary artery. As shown in Table 94.1, both AV
nodal and subnodal conduction disturbances in acute MI
increase mortality. This also holds in the reperfusion era. 3–5
A common cause of abnormalities in the AV conduction
system is fibrosis of the intraventricular conduction system.
The incidence increases with age.2 This may lead to a primary
conduction system disorder and may involve the AV node,
the bundle of His, the right bundle branch, and the common
part and the fascicles of the left bundle branch.6–8
The ability to record the electrical activity of the bundle
of His makes it possible to identify the area of block or
impaired conduction.1 As indicated in Figure 94.3, block at
the different levels of the AV conduction system is traditionally divided into first-, second-, and third-degree types. Firstdegree block is a misnomer because each impulse is
conducted, but with a longer conduction time than normal.
Second-degree block is divided into two types: type 1
(Wenckebach), characterized by a series of impulses showing
progressive lengthening in conduction time, terminated by
• A common cause of chronic abnormalities in the atrioventricular (AV) conduction system is age-related fibrosis.
• AV nodal block in acute inferior infarction is usually
caused by an occlusion of the proximal part of the right
coronary artery.
• Block distal to the AV node (in His or the Bundle Branch
System) in acute anterior infarction indicates a very proximal occlusion in the left anterior descending coronary
artery.
• Both AV nodal and subnodal conduction abnormalities in
acute myocardial infarction increase mortality. This still
holds in the reperfusion era.
• In chronic AV block the site of block in the AV conduction system can usually be determined non-invasively.
• Left bundle branch block may hamper the diagnosis of
myocardial infarction. The decision to give reperfusion
therapy should be based upon the clinical impression.
• The cardiologist should be familiar with paroxysmal
complete AV block.
• Site and mechanism of AV block should determine decision making about pacemaker implantation.
Causes of Atrioventricular
Conduction Disturbances
After its origin in the sinus node region, the cardiac impulse
is conducted from atrium to ventricle over the atrioventricular (AV) node, the bundle of His, and the bundle branches.
Abnormalities in conduction may occur at any of these
levels, alone or in combination.1 These abnormalities can be
the result of developmental anomalies (congenital heart
disease), reversible or irreversible interruption of blood supply
to the conduction system (Fig. 94.1), inflammatory or infiltrative disease, calcified aortic valve disease, calcified mitral
annulus, cardiomyopathy, space-occupying lesions, drug tox-
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94
TABLE 94.1. Features of atrioventricular conduction disturbances
complicating acute myocardial infarction
Feature
Inferior MI
Anterior MI
Site of block
Artery involved
Escape rhythm
AV node
RCA
Narrow QRS
Rate 40–60/min
Dependable
Transient
2.5 times
Bundle branches
LAD
Wide QRS
Rate <40/min
Undependable
Transient
4 times
Duration of block
Increase in hospital
mortality (compared to
same infarct location
without block)
FIGURE 94.1. The components of the atrioventricular (AV) conduction system and the coronary arteries responsible for their blood
supply. The AV node is perfused by a branch from the right coronary
artery (RCA). The right bundle branch (RBB) and the anterior fascicle
(AF) of the left bundle branch are perfused by the left anterior
descending (LAD) coronary artery and are therefore vulnerable in
anteroseptal myocardial infarction. The posterior fascicle (PF) of the
left bundle branch is supplied by both the LAD and the RCA. CX,
circumflex coronary artery.
one blocked impulse; and type 2 (Mobitz-2), in which
impulses are conducted with a normal or slightly prolonged
conduction time until one of the impulses is suddenly
blocked. Then there is 2 : 1 or 3 : 1 block, in which only every
second or third impulse is conducted over the conduction
system. In third-degree or complete block, each impulse fails
to be conducted through the conduction system. Seconddegree type 2, and third-degree or complete heart block are
treated with a pacemaker.
Table 94.2 illustrates how common or uncommon these
different forms of conduction disturbances are in relation to
the different components of the AV conduction system.
The Electrocardiogram in Atrioventricular
Conduction of the Heart
Figure 94.4 shows an example of type 1 second-degree AV
block (Wenckebach type). The narrow QRS places the con81660
I
V1
V2
II
V2
V1
V3
V3r
aVR
V4
V4r
aVL
V5
III
aVF
V6
duction abnormality in the AV node. Figure 94.5 gives an
example of type 2 second-degree AV block. The QRS complex
shows left bundle branch block (LBBB), indicating that the
most likely site of AV block is in the right bundle branch.
Figure 94.6 shows a 2 : 1 AV block with a sudden change to
complete AV block. The QRS complex on the left reveals a
complete block in the right bundle branch and the posterior
fascicle of the left bundle branch. Two-to-one conduction in
the anterior fascicle of the left bundle branch changes into
complete AV block.
Noninvasive Methods to Determine the Site
of an Atrioventricular Block
An AV block may be located in the AV node, bundle of His,
bundle branches, or any combination of these locations (Fig.
94.3). Because an AV nodal block has a better prognosis and
treatment differs from that of a subnodal block, the determination of the location and type of block is important. Much
can be learned on the surface electrocardiogram (ECG) from
the PR interval, the QRS duration, and the response of the
block to noninvasive interventions, such as atropine, exercise, and vagal maneuvers (Table 94.3).
Interventions that slow AV conduction, such as vagal
maneuvers, worsen the AV block, but because the number of
impulses passing through the AV node declines, such maneuvers improve the subnodal block (Fig. 94.7). On the other
hand, interventions such as atropine and exercise improve
AV nodal conduction, but because of the increase in number
of impulses conducted through the AV node, they worsen
subnodal conduction. Thus, carotid sinus massage worsens
AV nodal block and improves subnodal block; atropine and
exercise improve AV nodal block and worsen subnodal
block.
V5r
Bundle Branch Block
V6r
400 ms
FIGURE 94.2. Complete AV nodal block in a patient with an acute
inferoposterior myocardial infarction with right ventricular involvement. Right ventricular involvement is indicated by the ST segment
elevation in the right precordial leads.3
CAR094.indd 1992
AV, atrioventricular; LAD, left anterior descending coronary artery; MI, myocardial infarction; RCA, right coronary artery.
When discussing prognosis and treatment of bundle branch
block, it is important to make the distinction between (1)
bundle branch block in association with acute MI, and (2)
chronic bundle branch block in patients with or without
symptoms of transient neurologic impairment.
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at r iov en t r icu l a r noda l a n d su bnoda l con duct ion dist u r ba nces
Sinus node
I
P-A
1° AV block
A-H
AVN
II
1° AV block
2° AV block
type I
2:1; 3:1
3° AV block
III
1° AV block
2° AV block
type I
2:1; 3:1
type II
3° AV block
IV
1° AV block
2° AV block
type I
2:1; 3:1
type II
3° AV block
HIS
HIS
H-V
LB
RB
FIGURE 94.3. Location and types of block from the
sinus node area to the ventricles and measurements of
the AV intervals in the His bundle electrogram (HBE).
In the left lower portion of the figure, an HBE and lead
II electrocardiogram (ECG) tracing are schematically
shown. The intervals noted are P-A, A-H, and H-V;
normal values are shown in milliseconds. The figure
also indicates possible sites and types of block that may
occur in the atrioventricular conduction system.
V
mixed lesions
at multiple sites
I, II, III, IV
HBE
P-A
30 – 50
A-H
60 – 125
H-V
35 – 55
II
Bundle Branch Block in Acute
Myocardial Infarction
As pointed out by Lie and associates8 in case of MI, the prognosis depends on whether the bundle branch block is the
consequence of the MI or was present before the MI. Acquired
right bundle branch block is more common in anterior wall
MI and LBBB in inferior wall MI. The risk of progression to
high-degree AV block is lower in old (preexistent) versus new
(acquired) bundle branch block. It would be helpful, therefore, to be able to distinguish old from new bundle branch
block if the bundle branch block is already present on admission. Lie and associates pointed out that age >70 years and
an rSR rather than a QR pattern in lead V1 favor preexistent
rather than new right bundle branch block (RBBB) (Fig. 94.8).
In anterior wall MI, acquired RBBB carries a higher in-hospital mortality than does preexistent RBBB in the reperfusion era.3,5,9,10
In patients with RBBB, the complication of complete
sub–AV nodal block is greater when anterior or posterior left
fascicular block is present as well.
The significance of preexistent versus acquired LBBB in
association with an acute MI is less clear. An LBBB is often
a sign of more generalized left ventricular disease, and as
such has a more ominous significance than RBBB. In contrast to RBBB, it is often not possible to make the distinction
between preexistent versus acquired LBBB, unless an older
ECG with LBBB, before chest pain, is present.
Sgarbossa et al.11 called attention to ECG fi ndings of help
in recognizing acute MI in patients with LBBB. Their findings are listed in Table 94.4. They were criticized by Shlipak
et al.,12 who could not confirm the value of the algorithm
proposed by Sgarbossa et al.
Recently, Wong et al.13 indicated that the ST segment
changes in LBBB patients described in criteria 1 and 2 in
Table 94.4 were highly specific but not sensitive for an enzymatic diagnosis of MI. Importantly, patients having those ST
segment changes, had a higher 30-day mortality than LBBB
patients with an enzyme rise in the absence of ST segment
changes. We conclude that the ECG can be helpful in decision making about a myocardial reperfusion attempt in the
patient with LBBB, but that in the majority of LBBB patients
with acute chest pain the decision should be based on the
clinical impression rather than the ECG.
83465
I
II
III
TABLE 94.2. Prevalence of the different forms of conduction
disturbances at different sites of the atrioventricular conduction
system
V5
Second degree
AVN
His bundle
Branches
First degree
Type 1
Type 2
2:1
Third degree
C
C
C
C
U
U
N
C
C
C
C
C
C
C
C
AVN, atrioventricular
uncommon.
CAR094.indd 1993
node;
C,
common;
N,
V1
virtually
never;
V6
U,
400 ms
FIGURE 94.4. Type 1 (Wenckebach) second-degree AV block. There
is progressive PR prolongation of the fi rst, second, or third P wave
with AV block after the third or fourth P wave.
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TABLE 94.3. Noninvasive interventions to determine site of
atrioventricular block: effects on atrioventricular conduction
I
II
III
V1
V5
Intervention
AV nodal
conduction
Subnodal
conduction
Atropine
Exercise
CSM
Improves
Improves
Worsens
Worsens
Worsens
Improves
AV, atrioventricular; CSM, carotid sinus massage.
V6
400 ms
FIGURE 94.5. Type 2 (Mobitz-2) second-degree AV block. The PR
intervals stay the same before and after the blocked P wave. The
QRS has a typical left bundle branch block configuration indicating
that the most likely site of Mobitz-2 block is in the right bundle
branch.
85063
I
II
III
V1
p
p
p
p
p
V5
Treatment of Bundle Branch Block Associated with
Acute Myocardial Infarction
The development of RBBB in acute MI signifies a proximal
occlusion of the left anterior descending coronary artery and
the presence of an extensive area at risk. Immediate reperfusion of that region, therefore, should be attempted, preferably
by a percutaneous coronary intervention. If that possibility
is not available, thrombolytic therapy should be given.3 If
RBBB with anterior or posterior left fascicular block persists
after reperfusion, temporary prophylactic pacing is recommended.14 Prophylactic pacing avoids the need for a cardiopulmonary resuscitation associated with the low ventricular
rate usually seen in complete block with anterior infarction.
As pointed out elsewhere, if complete AV block develops, it
is usually transient.3 Permanent pacing should be reserved
for patients who have persistent or recurrent high-degree AV
block.14,15 A special problem is the patient presenting with
acute chest pain and LBBB because the ECG is less accurate
in diagnosing acute MI.3,11–13 In that situation, the clinical
impression should decide on the administration of reperfusion therapy.3
Pacing in MI with LBBB is required only if the MI occurs
in the setting of high-degree AV block. Prophylactic pacing
is not required if LBBB occurs with 1 : 1 AV conduction.
V6
400 ms
FIGURE 94.6. On the left, a 2 : 1 AV block with a QRS configuration
indicating a block in the right bundle branch and the posterior fascicle of the left bundle branch. This suddenly changes into a complete AV block, with an escape rhythm arising in the left posterior
fascicle.
Chronic Bundle Branch Block
Bundle branch block is a common fi nding, and the incidence
increases with age.16 With the exception of LBBB, males are
more frequently affected than females.17–19 The prognostic
significance varies in relation to the type of patient studied
84073
I
II
720
440
1280
III
1300
1280
1500
V1
V5
V6
CSM
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Atropine
FIGURE 94.7. Example of the value of carotid
sinus massage (CSM) and atropine administration in locating the site of block in a patient
with complete AV block with a narrow QRS.
As shown, slowing of the sinus node by CSM,
improves AV conduction, whereas atropine
worsens conduction. This indicates a sub–AV
nodal location of the block in the bundle of
His.
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at r iov en t r icu l a r noda l a n d su bnoda l con duct ion dist u r ba nces
FIGURE 94.8. Preexisting versus acquired right bundle branch block (RBBB)
after myocardial infarction (MI). (A) Preexisting RBBB in a patient with an acute
inferior MI. The QRS during RBBB
shows an RSR’ configuration in lead V1.
(B) An ECG of a patient with an acute
anterior wall MI with acquired RBBB
and left posterior hemiblock. The QRS
during RBBB shows a qR pattern in lead
V1.
A
B
I
V1
I
V1
II
V2
II
V2
III
V3
III
V3
aVR
V4
aVR
V4
aVL
V5
aVL
V5
aVF
V6
aVF
V6
05002
400 ms
and is less when the chance finding of bundle branch block
in the community-dwelling patient is compared with that in
the asymptomatic and symptomatic hospital patient.17–23 In
general, prognosis is determined by the overall cardiac status
of the patient, rather than by bundle branch block (BBB)
alone. Table 94.5 summarizes the issues to be addressed
when treating a patient with chronic bundle branch block.
Frequently, BBB is accompanied by significant pathologic
changes in the intraventricular conduction system.2 Widespread fibrosis is often present, especially if there is associated hemiblock. Many diseases can cause chronic impairment
of intraventricular conduction, including coronary artery
disease, hypertension, aortic valve disease, idiopathic degenerative diseases of the conduction system, and cardiomyopathy. In the young population, bundle branch block is rare,
especially LBBB. The presence of LBBB should raise the suspicion of underlying heart disease. An LBBB, because it
results in desynchronized cardiac contraction, may lead to
impaired cardiac function and the development of heart
failure. Recent studies have indicated that in an appreciable
number of those patients, resynchronization of cardiac contraction by biventricular pacing can lead to marked improvement of cardiac function.
In older patients with RBBB, clinical cardiovascular
disease is present in 50%, according to a general population
survey, rising to about 80% in a hospital population, especially when bifascicular block is present.19–21 An LBBB has an
even higher incidence of associated cardiac disease.17–19 The
prognosis for patients with chronic bundle branch block is
determined by the presence and the type of associated cardiovascular disease. McAnulty et al.21 reported a cumulative
mortality after 3 years of 56% in hospitalized patients with
coronary artery disease with a previous MI and 20% in those
without a previous MI. In community surveys, a lower mortality rate is found.
Of the patients with bundle branch block who die,
approximately 50% die suddenly. In those patients in whom
the terminal rhythm was documented, ventricular tachyarrhythmias were found more commonly than was a complete
block with asystole.21,23
There is a low incidence of progression to documented
complete AV block, and it is therefore difficult to determine
such risk in patients with bundle branch block, in relation
to the type and cause of their conduction disturbance. In a
general population study, Kulbertus and coworkers17 found a
2% increase of complete heart block in patients with RBBB
TABLE 94.5. Issues to be addressed in treating the patient with
chronic bundle branch block
TABLE 94.4. Electrocardiogram criteria to diagnose myocardial
infarction in the presence of left bundle branch block11
Criteria
1. ST elevation >1 mm in leads I, aVL, V5, V6
2. ST depression >1 mm in leads V1, V2, or V3
3. ST elevation >5 mm in leads V2 –V4
Odds ratio
Score
25.2
6.0
4.3
5
3
2
To obtain a sensitivity of 78% and a specificity of 90%, the minimal total
score should be 3.
CAR094.indd 1995
Underlying pathology
Prognosis of the patient
Risk of progression to complete heart block
Value of electrophysiologic studies
Management of patients with bundle branch block and syncope
but no documentation of bradycardia
Role of permanent pacing in the asymptomatic patient with
bundle branch block
Management of the patient with bundle branch block under
circumstances such as general anesthesia, open heart surgery,
and use of His–Purkinje system–depressant drugs
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80224
I
II
III
250
V1
250
280
280
V6
80041
FIGURE 94.9. Example of alternating bundle branch block. The left
part of the figure shows sinus rhythm with left bundle branch block
and a PR interval of 250 ms. This suddenly changes into a right
bundle branch block with a PR interval of 280 ms.
and left anterior hemiblock after a mean follow-up period of
3 years. In a hospital-based series, Dhingra et al.22 found a
7% cumulative incidence of documented complete heart
block after 5 years of follow-up in patients with bifascicular
block (RBBB with left anterior or left posterior hemiblock)
and LBBB. Rarely, there are ECG fi ndings in patients with
bundle branch block that indicate an ominous prognosis,
such as alternating bundle branch block (Fig. 94.9) and paroxysmal AV block24 (Figs. 94.10 and 94.11).
The hope that information on the AV conduction system
obtained by using His bundle recordings and atrial pacing
would help in predicting the risk for complete block in the
asymptomatic patient with bundle branch block, with or
without accompanying hemiblock, has not been fulfilled.
Most studies did not find a correlation between a prolonged
94
His-ventricle (HV) interval and the development of complete
block.25,26 Only patients with documented transient AV block
or syncope in whom ventricular tachyarrhythmias and noncardiac causes of syncope can be excluded have a high incidence of progression to complete block in cases of prolonged
HV interval.25,26 Scheinman and co-workers26 reported a high
incidence of complete block in patients with an HV interval
of 100 ms or greater. Dhingra et al.27 pointed to the prognostic
value of the development of block distal to the His bundle
during 1 : 1 AV nodal conduction with atrial pacing at rates
less than 140 beats/minute.
A special problem is the patient with bundle branch block
and syncope, but no documentation of bradycardia. In these
patients other causes for syncope must be excluded. After the
prolonged use of an event recorder has not revealed bradyarrhythmias, an electrophysiologic study should be performed.
If high-degree AV block can be induced, a permanent pacemaker is indicated. This should also be done in case of an
HV interval of 100 ms or longer. If no AV block is inducible
and the HV interval is not severely prolonged, programmed
stimulation should be performed in the ventricle to exclude
sustained ventricular tachycardia as the cause of syncope.
The patient with paroxysmal AV block presents a diagnostic challenge. Characteristically, these patients experience periods of asystole on reaching a critical duration of the
PP interval; this may occur after a premature (atrial, AV
junctional or retrogradely conducted ventricular) beat (Fig.
94.10) or carotid sinus massage (Fig. 94.11). The mechanism
is the development of local phase 4 depolarization in the
subnodal (intrahisian or bundle branch) tissue.24
Outside the episodes of asystole, the ECG may be perfectly normal (Fig. 94.10) or show only bundle branch block
(Fig. 94.11). Especially in these patients, Holter or event monitoring is particularly useful.
In the asymptomatic patient with chronic bundle branch
block, an electrophysiologic study is not indicated unless a
systemic disease is present with rapidly progressive conduction system disease, such as dystrophia myotonica.28
94001
I
I
II
II
III
III
aVR
aVR
aVL
760 560 840
aVF
aVL
aVF
V1
V1
V2
V2
V3
V3
V4
V4
V5
V5
V6
932179
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V6
400 ms
FIGURE 94.10. Paroxysmal complete AV block after a
conducted atrial premature beat (occurring after 560 ms
during sinus rhythm) is followed by an interval to the
next sinus P wave of 840 ms. This P-P interval is sufficiently long to induce local phase 4 depolarization in
the bundle of His, resulting in complete AV block for
subsequent atrial impulses. The escape rhythm shows
a narrow QRS complex indicating an origin high in the
specific AV conduction system.
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at r iov en t r icu l a r noda l a n d su bnoda l con duct ion dist u r ba nces
CSM
I
I
II
III
III
aVL
aVF
FIGURE 94.11. Paroxysmal complete AV block on
reaching a critical length of the P-P interval during
carotid sinus massage. Note that there is no change in
the PR interval up to the moment of complete AV block,
indicating that the block is not in the AV node. Local
phase 4 depolarization in the left bundle branch is
responsible for this type of AV block.
aVR
aVL
aVF
V1
V1
V2
V2
V3
V3
V4
V4
V5
V5
V6
V6
Occasionally, the question arises of prophylactic acute or
long-term pacing in asymptomatic patients with bundle
branch block, in situations such as general anesthesia, cardiac
catheterization, cardiac surgery, and use of His–Purkinje
system–depressant antiarrhythmic drugs. In general, prophylactic pacing during general anesthesia is not recommended,
because the risk for progression to high-degree AV block is
very low.29 Electrocardiogram monitoring should be performed during the procedure. Placement of temporary epicardial pacing electrodes is indicated in patients with bundle
branch block who are undergoing cardiac surgical procedures
in the vicinity of the conduction system. Antiarrhythmic
drugs that depress the His-Purkinje system, such as quinidine, procainamide, and amiodarone can be used safely in
patients without symptoms that are suggestive of paroxysmal distal heart block.30,31 When in doubt, especially when
high dosages of these drugs are required to control ventricular tachyarrhythmias, the effect of the drug should be tested
during an electrophysiologic study.
Summary
Atrioventricular conduction disturbances are common.
There are many different causes and its significance is determined by site (AV nodal vs. sub–AV nodal) and the presence
and severity of additional heart disease. When the practitioner is familiar with ECG characteristics, noninvasive
methods often facilitate the correct identification of the site
of block in the AV conduction system and the decision
making about treatment.
After an acute MI, when an AV block that occurs at the
AV nodal (inferior MI) or sub–AV nodal (anterior MI) level
worsens, prognosis stresses the necessity of a reperfusion
attempt preferably by a primary intracoronary intervention.
Electrophysiologic studies are of limited value in decision
making about treatment in chronic bundle branch block.
Holter or event monitoring is helpful to diagnose block
related bradycardia or asystole, especially in patients with
paroxysmal AV block.
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400 ms
References
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Arrhythmias: Electrophysiology, Diagnosis and Management.
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334:481–487.
12. Shlipak MS, Lyons WL, Go AS, et al. Should the electrocardiogram be used to guide therapy in patients with left bundle
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