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Left Bundle-Branch Block—Pathophysiology, Prognosis, and
Clinical Management
PIETRO FRANCIA, M.D., CRISTINA BALLA, M.D., FRANCESCO PANENI, M.D., MASSIMO VOLPE, M.D.
Chair and Division of Cardiology, II Faculty of Medicine, Sant’Andrea Hospital, University “La Sapienza,” Rome, Italy
Summary: Given its broad use as a screening tool, the electro-
cardiogram (ECG) has largely become one of the most com-
mon diagnostic tests performed in routine clinical practice. As
a result, the finding of left bundle-branch block (LBBB) in the
absence of a well-defined clinical setting has become relative-
ly frequent and raises questions and often concerns. While in
the absence of clinically detectable heart disease LBBB does
not necessarily imply poor outcomes, physicians should be
aware of the role of LBBB in stratifying risk of cardiovascular
events and death in subjects with both ischemic and nonis-
chemic heart disease. This paper reviews historical landmarks,
pathophysiologic features, prognostic implications, and clini-
cal management of LBBB in apparently healthy subjects and
those with heart disease.
Key words: left bundle-branch block, electrocardiogram, his-
tory of medicine
Clin. Cardiol. 2007; 30: 110–115.
© 2007 Wiley Periodicals, Inc.
Evolving Concepts, Misunderstandings, and Current
Appraisal of Left Bundle-Branch Block
As early as the beginning of the past century, Eppinger and
Tothberger, by means of a rudimental but efficient experi-
mental model, performed experiments destroying pieces of
dog myocardium by injecting silver nitrate and then observ-
ing the induced electrocardiographic (ECG) changes.1By
means of a single esophageal-anal lead, these and other inves-
tigators found that injuring the left and right bundle branches
resulted, respectively, in an upward and a downward QRS de-
flection on ECG.2Ironically, the mere extrapolation of data
obtained from this experimental canine model resulted in a
25-year misunderstanding of the real electrical abnormalities.
Left bundle-branch block (LBBB) pattern was incorrectly
identified as right bundle-branch block (RBBB), and vice ver-
sa. In fact, since the esophageal-anal lead was erroneously
judged to be “vertical” in the dog, the presence in humans of a
wide downward deflection in leads II and III was considered
to disclose RBBB.3
Almost 70 years after elucidation of this long-lasting mis-
interpretation, the electrogenesis and ECG pattern of LBBB
appear to be fully clarified. Under normal conditions, the elec-
trical impulse from the His bundle passes through a narrow
anterior fascicle, a broader early branching posterior fascicle,
and a third septal segment composed of many branches origi-
nating from each of the fascicles. The electrical impulse then
spreads through a rich peripheral Purkinje network that cou-
ples with individual myocardial cells.4, 5 The simultaneous
electrical activation of the right ventricle from its own branch
results in the QRS complex, which then represents the “sum”
of two parallel and independent electrical phenomena. Left
bundle-branch block completely modifies the electrical acti-
vation of the left ventricle and QRS complex on ECG. The ac-
tivation of the interventricular septum, which is left-sided in
physiologic conditions, originates on its right side. The elec-
trical impulse propagates then inferiorly, to the left, and slight-
ly anteriorly. This results in a nonhomogeneous and delayed
depolarization of the left ventricle, which can be only partial-
ly preserved in the presence of an efficient distal left bundle
branch and Purkinje network.6
Findings from three-dimensional (3-D) nonfluoroscopic
contact and noncontact mapping have recently provided new
insights into left ventricle activation sequence in patients with
LBBB and heart failure.7From its site of earliest left ventricu-
lar (LV) breakthrough, activation wave front spreads both su-
periorly and inferiorly, but it is unable to cross from the anteri-
or to the lateral wall because of the presence of a line of block
Clin. Cardiol. 30, 110–115 (2007)
Address for reprints:
Massimo Volpe, M.D.
Chair and Division of Cardiology
Ospedale Sant’Andrea
2nd Faculty of Medicine, University “La Sapienza”
Via di Grottarossa 1035
00189 Rome, Italy
e-mail: volpema@uniroma1.it
Received: January 10, 2006
Accepted with revision: April 4, 2006
Published online in Wiley InterScience
(www.interscience.wiley.com).
DOI:10.1002/clc.20034
© 2007 Wiley Periodicals, Inc.
clc2006-010R.qxd 1/15/70 11:24 AM Page 110
P. Francia et al.: Clinical management of left bundle-branch block 111
Clinical Cardiology DOI:10.1002/clc
oriented from the base toward the apex of the left ventricle.
The wave front reaches the lateral and posterolateral regions
by propagating inferiorly around the apex and across the infe-
rior wall, thus defining a U-shaped activation pattern.7The
ECG shows wide QRS complexes (>120 ms), increased
intrinsecoid deflection time (80–120 ms), rS complexes in
V1–V2, and loss or large reduction of Q waves in leads I and
aVL. Likewise, repolarization forces mirror the electrical ab-
normality induced by the sequential activation of the two ven-
tricles. Since they early originate from the right ventricle, left
leads (I, aVL) usually show a negative ST-T pattern.
Asymptomatic Left Bundle-Branch Block:
Prevalence, Prognosis, and Concerns
Since its wide diffusion, undemanding feasibility, and low
cost, the ECG has become one of the most commonly per-
formed investigations in routine clinical practice in the last 30
years. Given its broad use as a screening tool in the general
healthy population, the finding of abnormal ECG patterns in
the absence of a well-defined clinical setting has become fre-
quent. Are we dealing with the preclinical stage of a structural
heart disease or rather with a borderline physiologic phenom-
enon not necessarily implying future clinical consequences?
This is exactly the case of LBBB in apparently healthy sub-
jects, a paradigmatic example of “medical rebus.” In the set-
ting of LBBB and apparent structural heart diseases, the avail-
able observational studies suggest caution and often concern
in the prognostic evaluation.8–10 On the other hand, new onset
LBBB in asymptomatic subjects raises several questions con-
cerning the diagnostic algorithm and the clinical behaviour,
with particular regard to the need for further investigation,
intensity and nature of follow-up, and indications for special-
ist referral.
In epidemiologic studies conducted during the last 30 years,
the prevalence of LBBB in the general population has been re-
ported to vary considerably according to population size and
sampling criteria, ranging from 0.1–0.8%11–15 (Table 1). Of
note, there is no consensus on LBBB-related prognosis, as the
latter is clearly influenced by study design, population size,
and heterogeneity. In a large population sample (3.983 sub-
jects) with a 29-year follow-up, Rabkin et al.16 found that the
incidence of LBBB was 0.7%. Of interest, in this study > 50%
of subjects with LBBB had a normal ECG before the conduc-
tion disturbance was detected. During follow-up, subjects with
LBBB displayed increased cardiovascular morbidity and mor-
tality compared with control subjects, with sudden death fre-
quently being the first clinical disease expression.
In 1979, the Framingham Study17 (5,209 subjects, 55 with
LBBB) showed a clear association between LBBB and main
cardiovascular diseases, such as hypertension, cardiac enlarge-
ment, and coronary heart disease. Coincident with or subse-
quent to the detection of LBBB, 48% of these individuals de-
veloped coronary artery disease (CAD) or congestive heart
failure (CHF). Within 10 years from LBBB detection, cardio-
vascular mortality was 50%, and at 18 years follow-up only
11% of subjects with LBBB remained free of detectable car-
diovascular abnormalities (Table 2).
In a large population of 110,000 subjects with a mean fol-
low-up of 9.5 years, Fahy et al.18 reported no difference in to-
tal actual survival between subjects with LBBB and their con-
trols. However, the LBBB group showed an increased
prevalence of cardiovascular disease at follow-up (21 vs. 11%
in controls) (Table 2).
In a formerly published review article, Rowlands19 summa-
rized the follow-up data from many studies concerning intra-
ventricular conduction defects. He concluded that mortality
risk in pre-existent LBBB without overt cardiac disease is
only 1.3. On the other hand, a newly acquired LBBB confers a
mortality risk of 10.0, mainly in subjects aged > 44 years at
LBBB onset.
Left Bundle-Branch Block and Risk Stratification
in Heart Disease
In several studies on chronic and acute CAD, LBBB was
found to be an excellent predictor of mortality and events20–24
(Table 2). In 681 patients with acute myocardial infarction
(AMI) enrolled in the Thrombolysis and Angioplasty in
Myocardial Infarction (TAMI) 9 and Global Utilization of
Streptokinase and t-PA for Occluded Arteries (GUSTO) 1
protocols,25 the incidence of LBBB was found to be 7%. The
occurrence of both RBBB and LBBB was closely related to
factors indicating more extensive myocardial damage (such
as number of diseased vessels, peak creatinine phosphoki-
nase, ejection fraction) and mortality. In patients showing per-
sistent rather than transient BBB, the 30 days-risk of death
was six times higher than in those without BBB, patients with
LBBB mostly contributing to this outcome.
TABLE 1 Studies of left bundle-branch block (LBBB) in apparently healthy populations
First author (Ref. No.) Year n Mean age (years) Male/female ratio Prevalence (%) of LBBB
Rodstein (12) 1951 30,000 51 131 (0.43)
Hiss (13) 1962 122,043 30 All male 231 (0.19)
Ostrander (56) 1965 5,129 40 0.9 18 (0.35)
Rotman (15) 1975 237,000 394 (0.16)
Siegman-Igra (57) 1978 5,204 50 All male 43 (0.82)
Modified from Ref. No. (18).
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Clin. Cardiol. Vol. 30, March 2007112
Clinical Cardiology DOI:10.1002/clc
Even when a community-based population of patients with
AMI and longer (3 years) follow-up was considered, unadjust-
ed postdischarge mortality was higher in subjects with
LBBB26 (Table 2).
To assess the independent contribution of LBBB to cause-
specific mortality in ischemic heart disease, Stenestrand et al.
recently analyzed data from a large cohort of patients with
AMI27 (Table 2). In striking contrast with the previous studies,
these authors reported that the extent of comorbidities such as
previous myocardial infarction, CHF, hypertension, diabetes,
renal failure, chronic pulmonary disease, and history of stroke
substantially reduces the independent prognostic impact of
LBBB in AMI, thus minimizing the differences in 1-year
mortality between subjects with and without LBBB. This
finding supports the concept that unadjusted differences in
mortality are mainly due to poorer LV function and concomi-
tant diseases.
In a random-sampled population of 855 men aged 50 years
in 1963, Eriksson et al.28 (Table 2) did not describe a signifi-
cant relationship between bundle-branch block and ischemic
heart disease in a 30-year follow-up. On the other hand, men
who had developed BBB also had a greater heart volume at
age 50 years and were more often diagnosed with CHF com-
pared with control subjects during follow-up. These findings
suggest that BBB results from a progressive disease affecting
not only the conduction system but the myocardium itself.
Furthermore, no increased mortality was noted in men with
BBB at follow-up, and there was no difference in the incidence
of ischemic heart disease or death due to cardiovascular dis-
eases compared with control subjects. Although these results
cannot be readily extrapolated to subjects with LBBB, the im-
pressive length of follow-up gives reason for a detailed analy-
sis and perhaps clarifies discrepancies with other studies. Left
bundle-branch block early affects prognosis of ischemic heart
disease; several different mechanisms account for such an ef-
fect. When LBBB expresses an unrecognized underlying non-
ischemic structural heart disease, LV performance may be de-
pressed and inadequate to face up to an acute ischemic event.
Moreover, LBBB itself induces intra- and interventricular
asynchrony,29, 30 abnormal LV diastolic filling patterns,31, 32
and impairment of LV systolic performance.33 Finally, in
LBBB the prolongation of the depolarization phase and the
subsequent increase in vulnerable repolarization time height-
ens the risk of life-threatening ventricular arrhythmias in the
presence of frequent ventricular ectopic beats, a common find-
ing in the setting of ischemic heart disease.34, 35 In the study by
Eriksson et al., the 30-year follow-up allowed the detection of
a slowly progressing degenerative heart disease-related BBB,
thus unmasking the real incidence of initially silent CAD-
unrelated dilated cardiomyopathy. Moreover, the long obser-
vational period likely balanced CAD-related mortality in sub-
jects with BBB compared with those with normal intraventric-
ular conduction.
On the basis of the evidence presented so far, it is imperative
in clinical practice to consider the possibility that LBBB repre-
sents the clinical onset of an idiopathic dilated cardiomyopa-
thy36 or an infective, hypertensive, or valvular “dilated heart
disease.” This is particularly true in “tricky” forms of clinical-
ly silent structural heart disease, often characterized by border-
line values of LV volume and ejection fraction.
The Issue of Advanced Atrioventricular Block
Several studies published during the last three decades
have shown that patients with chronic BBB and nonfunction-
al atrioventricular (AV) block induced by incremental atrial
pacing and/or infranodal conduction time (His to ventricle
interval, HV) ≥70 ms had a significantly higher incidence of
progression to spontaneous second- or third-degree AV
block, with subjects with HV interval ≥100 ms presenting the
highest risk.37–39
TABLE 2 Outcomes in subjects and patients with left bundle-branch block (LBBB)
First author Mean age
(Ref No.) Year n (years) Sample Outcome
Eriksson (28) 1998 855 70 Men born 1913 Increased mortality for LBBB only in conjunction with CAD
Fahy (18) 1995 100,000 44 Screening Increased prevalence of cardiovascular disease at follow-up
Increased cardiac mortality for LBBB+CAD
No differences in all-cause mortality for LBBB
Schneider (17) 1981 5,209 50 Framingham Increased mortality for LBBB
Rotman (15) 1975 237,000 35 U.S. Air Force No increased mortality for LBBB
Hesse (58) 2001 7,073 60 Stress testing Increased all-cause mortality for LBBB
Freedman (20) 1987 15,609 55 Chronic CAD Increased mortality for LBBB
Wong (24) 2006 17,073 68 Acute MI Increased 30-day mortality for LBBB
Guerrero (23) 2005 3,053 69 Acute MI Increased in-hospital death for LBBB
Stenestrand (27) 2004 88.026 77 Acute MI Increased unadjusted 1-year mortality
Brilakis (26) 2001 894 76 Acute MI Lower pre-discharge ejection fraction
Higher in-hospital and long-term unadjusted mortality
Baldasseroni (10) 2002 5.517 63 CHF Increased 1-year mortality and sudden death
Abbreviations: CAD = coronary artery disease, MI = myocardial infarction, CHF = congestive heart failure.
clc2006-010R.qxd 1/15/70 11:24 AM Page 112
P. Francia et al.: Clinical management of left bundle-branch block 113
Clinical Cardiology DOI:10.1002/clc
Taken together, these studies claim that surface ECG analy-
sis is of limited value in identifying patients with LBBB at
higher risk for AV block, and that electrophysiologic evalua-
tion is of great help in defining prognosis of patients with BBB.
On the other hand, it has been reported that in symptomatic pa-
tients with BBB the practical usefulness of electrophysiologic
study is questionable, since risk stratification can be easily ob-
tained by ECG.40 Moreover, Rosen et al. failed to demonstrate
any relationship between prolonged HV interval and occur-
rence of spontaneous AV block.41
Recent data from the International Study on Syncope of
Uncertain Etiology (ISSUE)42 show that in patients with BBB
(patients with LBBB representing 38% of the study popula-
tion), syncope, and negative electrophysiologic study, most
syncopal recurrences are due to prolonged asystolic pauses
mainly attributable to paroxysmal AV block, as assessed by
implantable loop recorder traces. This finding claims a very
low negative predictive value of an invasive electrophysiolog-
ic study in ruling out a paroxysmal AV block as the cause of
syncope, since 33% of the patients with a negative study had a
documented episode of AV block. Notably, the study failed to
identify any risk predictor of future AV block. The authors
conclude that in patients with symptomatic BBB and negative
electrophysiologic study, an implantable loop recorder-guided
strategy is reasonable, with pacemaker implantation safely de-
layed until symptomatic bradycardia is documented.
The Long and Winding Road of Clinical Management
As stated in a consensus document of the Study Group of
Sport Cardiology of the European Society of Cardiology,43
subjects who have positive findings at basic clinical evalua-
tion, as in the case of LBBB, should be referred for additional
testing, initially noninvasive such as echocardiography, 24-h
ambulatory Holter monitoring, and exercise testing. In select-
ed cases, invasive tests such as coronary angiography and elec-
trophysiologic study may be necessary to confirm or rule out
the suspicion of heart disease.
Complete LBBB is also listed among the medical disqual-
ifications for flying duties.44 Both the U.S. Federal Aviation
Administration (FAA) and the Joint Aviation Requirements
standards (the European approach to medical standards for
flying fitness)45 consider LBBB as a disqualifying condition
unless structural heart disease is excluded. According to the
UK Civil Aviation Authority policy, the exact requirements to
rule out heart disease in the presence of LBBB are set out in a
specific CAA Medical Division protocol. The finding of
LBBB on resting ECG requires a complete cardiology evalu-
ation including exercise ECG, 24-h ECG, echocardiogram,
evaluation of possible CAD at least with myocardial perfu-
sion scan in subjects aged > 40 years, and electrophysiologic
study in the presence of LBBB and I degree AV block. Class
1 certificate applicants need to show no abnormal instrumen-
tal findings and a 3-year period of stability before a certificate
can be issued.
Unless we are dealing with such particular kinds of patients,
it is reasonable that routine patients with new onset LBBB un-
dergo second-step investigations, that is, echocardiogram and
Holter ECG. This latter is particularly helpful in identifying
both advanced AV blocks and heart disease-related tach-
yarrhythmias. The clinical suspicion of ischemic heart disease,
based on the presence of risk factors and typical symptoms,
should lead the physician to assess myocardial perfusion by
means of imaging techniques, given the low specificity of
ECG ST-segment changes during stress test in the presence of
Exclude Myocardial perfusion
imaging
EP study
- IDCM
- CAD
- VHD
- Myocarditis
- Alcoholic CM
- Amyloidosis
- Other forms of
secondary DCM
Consider for
coronary
angiography
Follow up Loop recorderConsider for
permanent
pacing
Follow up
Left bundle-branch block
Symptomatic subjects
CHF symptoms CAD symptoms
CAD risk factors Syncope
Incidental finding
in apparently
healthy subjects
Holter ECG
echocardiogram
Holter ECG
echocardiogram
Holter ECG
echocardiogram
Holter ECG
echocardiogram
FIG. 1 Flow-chart of proposed clinical approach to an individual or patient presenting with left bundle-branch block. CHF = congestive heart
failure, CAD = coronary artery disease, EP = electrophysiologic, IDCM = idiopathic dilated cardiomyopathy, VHD = valvular heart disease,
CM = cardiomyopathy, DCM = dilated cardiomyopathy.
clc2006-010R.qxd 1/15/70 11:24 AM Page 113
Clin. Cardiol. Vol. 30, March 2007114
Clinical Cardiology DOI:10.1002/clc
LBBB. In the absence of significant instrumental and clinical
findings, a cautious “wait and see” attitude is probably the pre-
ferred choice, and annual clinical follow-up may be scheduled.
Only apparent anomalous clinical and/or instrumental find-
ings should lead to a third-step investigation (i.e., coronary an-
giography or electrophysiologic study) (Fig. 1).
Future Perspectives: Should We Treat Patients
or Electrocardiographic Traces?
Recent successes of cardiac resynchronization therapy
(CRT) in chronic heart failure46–49 highlight the hemodynam-
ic effects of LBBB, so far considered roughly an electrocar-
diographic entity. Prolongation of QRS complex > 120 ms
results in some degree of intra- and interventricular dyssyn-
chrony, usually characterized by noncoordinated contraction
of interventricular septum and LV posterior or posterolateral
wall. This results in waste of energy contraction, inability to
generate effective intraventricular pressure, and increased wall
tension at the level of latest activated regions of the LV.50
Conventional echocardiography- and TDI-based techniques
for intra- and interventricular dyssynchrony quantification
currently offer the potential for an accurate definition of the ef-
fects of LBBB on cardiac contraction51–53 and seem to identi-
fy with some degree of accuracy those patients who will most
benefit from CRT.54, 55
While referral for resynchronization therapy currently
applies to subjects with severe heart disease, indications for
physiologic pacing are expanding. The new millennium is
marking the transition of LBBB from risk stratification factor
to rational therapeutic target.
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