My 6-page notes to go along with the "debate" of whether new or presumed new LBBB per se (without any other qualification) should be treated as STEMI equivalent

1. 1
Five
Compelling
Reasons
Why
New
or
Presumed
New
LBBB
(without
any
other
qualification
such
as
Sgarbossa’s
or
Smith’s
criteria)
Should
NOT
be
treated
as
STEMI
Dr.
Chew
Keng
Sheng,
MD,
MMed
Emergency
Med
Dept,
School
of
Medical
Sciences,
Universiti
Sains
Malaysia
1. Recent
evidences
suggest
that
new
or
presumed
LBBB
does
not
predict
STEMI
any
more
than
old
LBBB
or
no
LBBB
a. Chang
et
al
(2009):
observational,
7937
patients
with
CP
admitted
to
ED;
55
with
new
or
presumed
new
LBBB,
136
had
old
LBBB,
and
7746
had
no
LBBB.
The
rate
of
AMI
was
not
significantly
different
between
the
3
groups
(7.3%
vs
5.2%
vs
6.1%;
P
=
0.75).
Authors
conclude,
“ED
patients
with
a
new
or
presumed
new
LBBB
are
not
at
increased
risk
of
AMI.
The
presence
of
LBBB,
whether
new
or
old,
did
not
predict
AMI.”
b. Jain
et
al
(2011):
Retrospective,
n
=
892,
only
36
(4%)
of
whom
had
new
LBBB.
Out
of
these
36,
only
14
patients
(39%)
had
final
diagnoses
of
acute
coronary
syndromes
(12
–
AMI,
2
UA),
13
(36%)
had
cardiac
diagnoses
other
than
acute
coronary
syndrome
(e.g.
acute
heart
failure,
complete
heart
block,
AF,
aortic
stenosis,
hypertensive
emergency)
and
9
(25%)
had
noncardiac
diagnoses.
Which
means,
only
approx
1/3
of
new
or
presumed
new
LBBB
ultimately
has
AMI.
Out
of
these
36
patients,
almost
all
patients
-­‐
32
underwent
PCI
(3
in
the
non-­‐ACS
cardiac
diagnoses
and
1
non-­‐cardiac
group
did
not).
Which
means,
new
or
presumed
LBBB
results
in
up
to
2/3
of
unnecessary
PCIs.
c. Kontos
et
al
(2011):
observational,
n=
401
LBBB
undergoing
their
institutional
MI
rule-­‐out
protocol,
including
serial
cardiac
biomarkers
and
PCI.
LBBB
were
classified
as
chronic,
new,
or
if
no
ECG
was
available,
as
presumably
new.
37%
new
LBBB,
27%
presumed
new
LBBB.
A
total
of
116
patients
(29%)
had
MI,
with
no
significant
difference
in
terms
of
frequency
as
well
as
the
infarct
size
of
MI
was
similar
among
patients
with
chronic
LBBB,
new
LBBB,
or
LBBB
of
unknown
duration.
Concordant
ST
changes
were
the
most
important
predictor
of
MI
(odds
ratio
17,
95%
CI
3.4-­‐81,
P
<
.001)
and
an
independent
predictor
of
mortality
(odds
ratio
4.3,
95%
CI
1.3-­‐15,
P
<
.001);
“new”
or
“presumably
new”
(a.k.a.
chronicity)
was
neither
predictive.

2. 2
d. Wong
et
al
(2005)
in
the
HERO-­‐2
(Hirulog
and
Early
Reperfusion
or
Occlusion)
trial;
n=
300
with
LBBB
(92
with
and
208
without
ST-­‐
segment
changes)
and
15,340
no
LBBB.
AMI
occurred
in
80.7%
of
LBBB
patients
and
88.7%
of
controls
(p
=
0.006).
What’s
more
interesting
is
when
they
analyzed
LBBB
with
or
without
concordant
ST
changes:
LBBB
with
ST-­‐segment
changes
similar
risk
of
30-­‐day
mortality
(even
slightly
higher)
compared
to
STEMI
patients
without
LBBB
(odds
ratio
[OR]
1.37,
95%
confidence
interval
[CI]
0.78
to
2.47).
It
is
those
STEMI
patients
with
LBBB
that
has
NO
concordant
ST-­‐
segment
changes
that
has
demonstrated
lower
mortality
than
STEMI
patients
without
any
LBBB
(OR
0.52,
95%
CI
0.33
to
0.80).
LBBB
with
concordant
ST-­‐segment
elevation
or
lead
V1
to
V3
ST-­‐segment
depression
independently
predicted
higher
30-­‐day
mortality
but
the
absence
of
concordant
ST-­‐segment
elevation
or
lead
V1
to
V3
ST-­‐
segment
depression
during
LBBB
independently
predicted
a
lower
30-­‐
day
mortality
rate
than
that
of
patients
with
no
LBBB.
2. Questionable
historical
origin
-­‐
Recognition
of
LBBB
in
AMI
dates
back
to
1917
in
an
account
by
Oppenheimer
and
Rothschild.
As
noted
by
Bauer
(1965)
many
of
the
patients
with
BBB
had
many
other
confounding
risks:
they
were
significantly
older,
higher
frequency
of
HPT,
CHF,
previous
MI,
and
cardiogenic
shock.
Therefore,
it
is
difficult
to
discern
whether
increased
mortality
risk
(approximately
2-­‐fold)
in
BBB
were
actually
due
to
the
BBB
it
self
or
it
was
confounded
by
age
and
comorbid
conditions.
Furthermore,
in
her
article
published
in
the
Journal
of
Electrocardiology
Vol.
33
(2000),
Sgarbossa
questioned
whether
many
of
the
ECGs
recorded
in
the
pre-­‐
thrombolytic
era
were
actually
recorded
in
real
time
when
the
patients
were
having
acute
myocardial
infarction
or
not.
In
that
article
the
authors
say:
“In
the
prethrombolytic
era,
however,
the
management
of
patients
with
myocardial
infarction
(MI)
consisted
only
of
pain
relief,
observation,
and
treatment
of
complications.
In
patients
with
ECG
confounders,
such
as
LBBB,
the
diagnosis
of
MI
was
confirmed
through
biochemical
determinations
over
several
hours
or
days
after
admission.
Because
there
was
no
incentive
to
collect
information
on
early
ECG
signs
of
MI,
most
studies
on
the
diagnosis
of
MI
in
the
presence
of
LBBB
included
ECGs
with
old
infarctions
as
well
as
recordings
obtained
at
widely
scattered
time-­‐points
after
acute
infarction”
Furthermore,
the
recommendation
by
ACC/AHA
to
use
the
criteria
of
new
or
presumed
new
LBBB
is
based
on
the
findings
more
than
20
years
ago.
It
was
based
on
the
pooled
data
of
9
trials
in
the
FTT
group
(FTT
=
Fibrinolytic
Therapy
Trialists)
back
in
1991
(more
than
20
years
ago)
showing
that
STEMI
patients
with
BBB
treated
with
fibrinolysis
had
lower
mortality
rate
than

3. 3
placebo
(18.7%
vs
23.6%)
but
this
is
at
the
expense
of
increased
major
bleeding
risk
(1.3%
vs
0.3%)
and
increase
in
stroke
(2.1%
vs
1.1%).
Furthermore,
there
are
three
important
caveats
in
interpreting
the
FTT
group
results:
o these
trials
did
not
specify
whether
the
ECG
showed
RBBB
or
LBBB
o whether
the
conduction
abnormalities
were
new,
or
whether
there
were
associated
ST-­‐segment
changes
(a.k.a.
the
chronicity
of
the
BBB
unknown)
o the
cohort
of
STEMI
patients
with
BBB
in
FTT
group
was
very
small,
3.6%
of
the
total
cohort
3. Confounding
pathogenetic
mechanisms:
There
are
just
too
many
confounders
to
the
pathogenetic
mechanism
of
LBBB
in
AMI.
In
a
commentary
article
for
example,
Neeland
et
al
(2012)
say
that
for
an
AMI
to
result
in
LBBB,
it
would
have
required
a
rather
large
infarct.
This
is
because,
unlike
the
RBB,
which
is
a
discrete
bundle
that
can
be
injured
by
a
small
focal
insult,
the
LBB
is
a
large
bundle
that
is
further
branched
into
the
anterior
superior
and
posterior
inferior
fascicles,
and
therefore,
the
infarct
would
have
either
affected
the
LBB
just
distal
to
the
bundle
of
His
or
an
infarct
that
affect
both
anterior
and
posterior
fascicles.
As
such,
although
LBBB
can
occur
de
novo
in
AMI,
LBBB
is
more
likely
a
pre-­‐existing
marker
of
underlying
structural
heart
disease
such
as
a
fibrotic
conduction
system
–
thus,
a
reflection
of
the
patient’s
baseline
CVS
risks
such
as
long
standing
HPT
causing
LVH
or
left
ventricular
remodeling
resulting
from
CHF.
This
is
consistent
with
the
observations
by
Bauer
(1964)
that
show
that
LBBB
in
AMI,
although
can
be
transient
or
permanent
but
most
permanent
LBBB
in
AMI
are
not
due
to
true
AMI-­‐related
LBBB
because
these
true-­‐AMI
related
LBBB
has
very
high
mortality.
4. Ethical
issue
of
giving
fibrinolytics
when
it
is
not
needed
The
bleeding
risk:
E.g.,
FTT
group
data:
bleeding
risk
of
fibrinolysis
1.1
–
1.3%.
NNT
for
streptokinase
is
25;
based
on
the
studies
like
Chang
et
al
(2009)
where
the
incident
of
STEMI
is
the
same
in
the
new
LBBB
vs
old
LBBB
vs
no
LBBB,
and
the
incident
of
STEMI
is
only
1/3rd
of
the
total
cases
of
new
or
presumed
LBBB,
is
it
ethical
to
subject
the
patient
to
fibrinolytic
merely
because
of
new
or
presumed
new
LBBB
per
se?
To
quote
Neeland
et
al
(2012):
“In
centers
where
primary
PCI
is
not
readily
available,
these
issues
obviously
are
more
concerning
given
the
risks
of
bleeding,
particularly
intracranial
bleeding,
with
fibrinolytic
therapy;
the
risks
of
fibrinolytic
therapy
may
be
magnified
in
patients
with
LBBB
who
generally
are
older
and
have
higher
rates
of
hypertension.”
5. Unnecessary
PCIs.
As
commented
in
Neeland
et
al
(2012),
presumed
LBBB
has
emerged
as
a
frequent
reason
for
false
activation
cath
lab.
In
a
single
study
of
1335
patients,
Larson
et
al
(2007)
–
overall
false
+ve
cath
lab

4. 4
activation
was
14%,
but
in
the
LBBB
cohort,
the
rate
was
44%!
Lopes
et
al
(2011)
–
39%
out
of
98
patients
with
new
LBBB,
even
including
those
with
concordant
ST-­‐changes
on
ECG
did
not
have
positive
angio
finding.
Even
worse
is
in
centers
that
do
not
have
24/7
PCI
service.

5. 5
ADDITIONAL
NOTES:
What’s
the
alternative?
If
new
or
presumed
new
LBBB
per
se
should
not
be
treated
as
STEMI
equivalents,
what
are
the
alternatives?
1.
Add
on
the
Sgarbossa’s
3
criteria
Concordant
ST
elevation
>/=
1
mm,
weighted
score
5;
Concordant
ST
depression
>/=
1
mm
in
V1-­‐V3,
weighted
score
3;
Discordant
ST
elevation
>/=
5
mm,
weighted
score
2
Tabas
et
al
(2008)
in
a
meta-­‐analysis
on
the
Sgarbossa’s
criteria,
N
=
2100
11
trials
For
a
total
score
of
>/=
3
points,
sensitivity
is
20%
(95%
CI
18
–
23%);
specificity
of
98%
(95%
CI
97
–
99%)
For
a
total
score
of
>/=
2
points,
sensitivities
ranged
from
20%
to
79%;
specificities
ranged
from
61%
to
100%
Sokolove
et
al
(2000)
Sgarbossa’s
criteria
has
an
excellent
inter-­‐observer
agreement
(kappa=0.81,
95%
CI
0.80
to
0.83)
between
cardiologists
and
emergency
physicians
for
diagnosing
AMI.
Concordant
STE
is
the
single
most
specific
criteria
(Lopes
et
al,
2011;
Jain
et
al,
2011)
Although
Sgarbossa’s
criteria
is
specific,
it
is
not
sensitive.
But
we
should
remember
Sgarbossa’s
for
LBBB
is
an
add-­‐on
criteria
for
STEMI.
Without
Sgarbossa’s,
the
usual
definition
of
STEMI
should
be
applied.
2.
Smith’s
et
al
(2011)
Address
the
weak
criteria
of
discordant
ST
elevation
Absolute
5
mm
was
used
by
Sgarbossa
et
al
Changed
it
to
ST/S
</=
-­‐0.25
(meaning
magnitude
of
at
least
25%
of
the
R
or
S
whichever
greater)
increases
sensitivity
from
52%
to
91%
at
the
expense
of
reducing
specificity
from
98%
to
90%.
3.
Neeland
et
al’s
algorithm
(2013)
If
hemodynamically
unstable,
e.g.
cardiogenic
shock,
refer
for
PCI/thrombolytics
If
stable,
use
a
more
specific
criteria
(Sgarbossa’s)
If
Sgarbossa’s
criteria
suggestive
STEMI
–
PCI/thrombolytics
If
Sgarbossa’s
criteria
not
suggestive
–
depends
on
other
clinical
parameters
including
echo/serial
biomarker
Suggested
free
web
resources:
1. A
MUST
READ
-­‐
Neeland
IJ,
Kontos
MC,
de
Lemos
JA.
Evolving
considerations
in
the
management
of
patients
with
left
bundle
branch
block
and
suspected
myocardial
infarction.
J
Am
Coll
Cardiol
2012;60(2):96-­‐105.
Available
at:

6. 6
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402162/pdf/nihms-­‐
388154.pdf
2. Amal
Mattu's
ECG
Case
of
the
Week:
Nov
4,
2013.
Available
at
URL:
https://www.youtube.com/watch?v=tf4rjJMSrgQ
3. Modified
Sgarbossa
Criteria:
Ready
for
Primetime?
In:
Academic
Life
in
Emergency
Medicine
(ALiEM)
website
Available
at
URL:
http://www.aliem.com/modified-­‐sgarbossa-­‐criteria-­‐ready-­‐primetime/
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o Chang
AM,
Shofer
FS,
Tabas
JA,
et
al.
Lack
of
association
between
left
bundle-­‐branch
block
and
acute
myocardial
infarction
in
symptomatic
ED
patients.
Am
J
Emerg
Med
2009;27(8):916-­‐21.
o Jain
S,
Ting
HT,
Bell
M,
et
al.
Utility
of
left
bundle
branch
block
as
a
diagnostic
criterion
for
acute
myocardial
infarction.
Am
J
Cardiol
2011;107(8):1111-­‐6.
o Kontos
MC,
Aziz
HA,
Chau
VQ,
et
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Outcomes
in
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with
chronicity
of
left
bundle-­‐
branch
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with
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Am
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CK,
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and
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left
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J
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o Neeland
IJ,
Kontos
MC,
de
Lemos
JA.
Evolving
considerations
in
the
management
of
patients
with
left
bundle
branch
block
and
suspected
myocardial
infarction.
J
Am
Coll
Cardiol
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results
from
all
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o Lopes
RD,
Siha
H,
Fu
Y,
et
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Diagnosing
acute
myocardial
infarction
in
patients
with
left
bundle
branch
block.
Am
J
Cardiol
2011;108(6):782-­‐8.
o Tabas
JA,
Rodriguez
RM,
Seligman
HK,
et
al.
Electrocardiographic
criteria
for
detecting
acute
myocardial
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in
patients
with
left
bundle
branch
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a
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o Smith
SW,
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KW,
Henry
TD,
et
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ST-­‐elevation
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in
the
presence
of
left
bundle
branch
block
with
the
ST-­‐elevation
to
S-­‐wave
ratio
in
a
modified
Sgarbossa
rule.
Ann
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o Sokolove
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