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
di Giampaolo Merlini, Centro per lo Studio e la Cura delle Amiloidosi Sistemiche, Fondazione IRCCS Policlinico San Matteo, Dipartimento di Medicina Molecolare Università di Pavia.
Slide per l'intervento tenuto in Fondazione Giannino Bassetti in occasione del primo incontro del ciclo "La medicina di precisione", primo progetto dalla convenzione tra Università di Pavia e Fondazione Bassetti.
12 marzo 2018
di Giampaolo Merlini, Centro per lo Studio e la Cura delle Amiloidosi Sistemiche, Fondazione IRCCS Policlinico San Matteo, Dipartimento di Medicina Molecolare Università di Pavia.
Slide per l'intervento tenuto in Fondazione Giannino Bassetti in occasione del primo incontro del ciclo "La medicina di precisione", primo progetto dalla convenzione tra Università di Pavia e Fondazione Bassetti.
12 marzo 2018
1. Discuss normal vs. abnormal semen analysis
2. Evaluate different treatments of varicocele
3. Assess azoospermia and discuss micro dissection testicular sperm extraction
4. Diagnose Klinefelter syndrome and genetic abnormalities in men with infertility
Role of Plasma Exchange in ABO-incompatible Kidney TransplantationApollo Hospitals
In the past, ABO incompatibility was an absolute contraindication for solid organ transplantation. However,
multiple recent trials have suggested strategies for overcoming the reactions between graft antigens and recipient antibodies that cause graft rejection.
Logistics excellence: creating a harmonious performanceMarco Tieman
Creating a harmonious performance of a supply chain is an art. How fit is your supply chain? A balanced symphony can be achieved by a systematic approach towards supply chain design and control. A supply chain model is introduced to assess and design supply chains. A 4-step approach is proposed to effectively implement logistics excellence in the supply chain for an organisation.
My talk in April 2015 in Malaysia on Best Practices and Resuscitation Workflow. The new 2015 resuscitation guidelines is expected to be released in Oct 2015.
An introduction to the rationale and the two types (Write-in and Select-Menu) of Key Feature Questions. This presentation is based on an original article by Page and Bordage (1995).
My talk in April 2015 Malaysia on Best Practices and Resuscitation Workflow. The new 2015 resuscitation guidelines is expected to be released in Oct 2015.
1. Discuss normal vs. abnormal semen analysis
2. Evaluate different treatments of varicocele
3. Assess azoospermia and discuss micro dissection testicular sperm extraction
4. Diagnose Klinefelter syndrome and genetic abnormalities in men with infertility
Role of Plasma Exchange in ABO-incompatible Kidney TransplantationApollo Hospitals
In the past, ABO incompatibility was an absolute contraindication for solid organ transplantation. However,
multiple recent trials have suggested strategies for overcoming the reactions between graft antigens and recipient antibodies that cause graft rejection.
Logistics excellence: creating a harmonious performanceMarco Tieman
Creating a harmonious performance of a supply chain is an art. How fit is your supply chain? A balanced symphony can be achieved by a systematic approach towards supply chain design and control. A supply chain model is introduced to assess and design supply chains. A 4-step approach is proposed to effectively implement logistics excellence in the supply chain for an organisation.
My talk in April 2015 in Malaysia on Best Practices and Resuscitation Workflow. The new 2015 resuscitation guidelines is expected to be released in Oct 2015.
An introduction to the rationale and the two types (Write-in and Select-Menu) of Key Feature Questions. This presentation is based on an original article by Page and Bordage (1995).
My talk in April 2015 Malaysia on Best Practices and Resuscitation Workflow. The new 2015 resuscitation guidelines is expected to be released in Oct 2015.
ACLS 2015 Updates - The Malaysian PerspectiveChew Keng Sheng
This set of slide was presented during the Kelantan Resuscitation Update 22 Nov 2015 in accordance to the latest ACLS/ILCOR 2015 Guidelines. However, I have emphasized on certain important aspects relevant within the Malaysian context. Nonetheless, in general, there are no major changes for this year 2015
Sensitivity, specificity and likelihood ratiosChew Keng Sheng
A short tutorial on sensitivity, specificity and likelihood ratios. In this presentation, I demonstrate why likelihood ratios are better parameters compared to sensitivity and specificity in real world setting.
This slide was first presented during the Malaysian 1st Emergency Medicine Annual Scientific Meeting, in conjunction with the Academy of Medicine Malaysia, Academy of Medicine Singapore and the Academy of Medicine Hong Kong Tripartite Meeting in Aug 2016.
Acute myocardial infarction associated with right bundle branch block and cha...YasserMohammedHassan1
Acute myocardial infarction may be associated right bundle branch block.
Accompanied trifascicular heart block had pre-streptokinase left anterior fascicular block
with left axis deviation and post-streptokinase left posterior fascicular block with right axis
deviation.
Methods: The current clinical study was conducted at Gaza city. It involved 90 patients who were scheduled for coronary angioplasty procedure. The patients were divided into three groups: The first group (n = 30), underwent BMS implantation and received colchicine 0.5 mg twice daily for six months. The second group (n = 30), underwent BMS implantation alone. The third group (n = 30) underwent DES implantation. All the patients were followed up for six months. The primary endpoint was clinical ISR at 6months. Secondary endpoints included Target Vessel Revascularization (TVR) and Stent Thrombosis (ST).
Brugada syndrome (BrS) is an inherited cardiac disorder,
characterised by a typical ECG pattern and an increased
risk of arrhythmias and sudden cardiac death (SCD).
BrS is a challenging entity, in regard to diagnosis as
well as arrhythmia risk prediction and management.
Nowadays, asymptomatic patients represent the majority
of newly diagnosed patients with BrS, and its incidence
is expected to rise due to (genetic) family screening.
Progress in our understanding of the genetic and
molecular pathophysiology is limited by the absence
of a true gold standard, with consensus on its clinical
definition changing over time. Nevertheless, novel
insights continue to arise from detailed and in-depth
studies, including the complex genetic and molecular
basis. This includes the increasingly recognised
relevance of an underlying structural substrate. Risk
stratification in patients with BrS remains challenging,
particularly in those who are asymptomatic, but recent
studies have demonstrated the potential usefulness
of risk scores to identify patients at high risk of
arrhythmia and SCD. Development and validation of
a model that incorporates clinical and genetic factors,
comorbidities, age and gender, and environmental
aspects may facilitate improved prediction of disease
expressivity and arrhythmia/SCD risk, and potentially
guide patient management and therapy. This review
provides an update of the diagnosis, pathophysiology
and management of BrS, and discusses its future
perspectives.
Beta blockers in SIHD: Yes, all patients should receive them !cardiositeindia
A presentation made by Dr. Akshay Mehta on the topic- Beta blockers in SIHD: yes, all patients should receive them !.
This was presented at the SIHD conference, Mumbai, 2015.
Presentatie Prof. dr. Deckers en Prof. dr. BotsCVON
Combining Atherosclerosis Imaging and New and Novel Markers in Asymptomatic Subjects at Intermediate CVD Risk: Implications for Pathophysiology, Prediction and Prevention.
Disaster and Mass Casualty Incidents (updated 7th July 2020)Chew Keng Sheng
A new updated slide on an overview of disaster management in Malaysia, including the formation of NADMA as the dedicated agency to coordinate disaster management in Malaysia.
Predatory publishing is a relatively recent phenomenon that seems to be exploiting some key features of the open access publishing model, sustained by collecting APCs that are far less than those found in legitimate open access journals. This CME aims to introduce to the participants on the phenomenon of predatory journals, why they continue to thrive, characteristics that are suggestive of a predatory journal, and how one can take step to minimize the risk of faling into predatory journal publication
A short sharing on doctor-patient communication to First year medical students in Universiti Malaysia Sarawak, to be supplemented with anecdotal accounts.
My presentation slides during the 1st National Symposium in Emergency and Acute Care (S.E.M.A.C). I presented some of the obstacles and challenges in scientific writing in emergency medicine within the Malaysia context as academic emergency medicine is still progressing in Malaysia,
Managing Cardiovascular Emergencies In A Malaysian Hospital - Challenges and ...Chew Keng Sheng
This is the talk I gave during ICEM 2010 under the International Experience of Cardiology Track. In this presentation, I highlighted some of the challenges I see within the Malaysian setting, I focus mainly on prehospital and A&E setting. Issues that are conventionally under the care of the cardiologists are not discussed.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
New or Presumed New LBBB To Be Treated As a STEMI Equivalent? A Contra Argument (Companion Notes)
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/
References:
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
al.
Outcomes
in
patients
with
chronicity
of
left
bundle-‐
branch
block
with
possible
acute
myocardial
infarction.
Am
Heart
J
2011;161(4):698-‐704.
o Wong
CK,
French
JK,
Aylward
PE,
et
al.
Patients
with
prolonged
ischemic
chest
pain
and
presumed-‐new
left
bundle
branch
block
have
heterogeneous
outcomes
depending
on
the
presence
of
ST-‐segment
changes.
J
Am
Coll
Cardiol
2005;46(1):29-‐38.
o Sgarbossa
EB.
Value
of
the
ECG
in
suspected
acute
myocardial
infarction
with
left
bundle
branch
block.
J
Electrocardiol
2000;33
Suppl:87-‐92.
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
2012;60(2):96-‐105.
o Fibrinolytic
Therapy
Trialists'
(FTT)
Collaborative
Group.
Indications
for
fibrinolytic
therapy
in
suspected
acute
myocardial
infarction:
collaborative
overview
of
early
mortality
and
major
morbidity
results
from
all
randomised
trials
of
more
than
1000
patients.
Lancet
1994;343(8893):311-‐22.
o Larson
DM,
Menssen
KM,
Sharkey
SW,
et
al.
"False-‐positive"
cardiac
catheterization
laboratory
activation
among
patients
with
suspected
ST-‐segment
elevation
myocardial
infarction.
JAMA
2007;298(23):2754-‐60.
o Lopes
RD,
Siha
H,
Fu
Y,
et
al.
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
infarction
in
patients
with
left
bundle
branch
block:
a
meta-‐analysis.
Ann
Emerg
Med
2008;52(4):329-‐36
o Smith
SW,
Dodd
KW,
Henry
TD,
et
al.
Diagnosis
of
ST-‐elevation
myocardial
infarction
in
the
presence
of
left
bundle
branch
block
with
the
ST-‐elevation
to
S-‐wave
ratio
in
a
modified
Sgarbossa
rule.
Ann
Emerg
Med
2012;60(6):766-‐76.
o Sokolove
PE,
Sgarbossa
EB,
Amsterdam
EA,
et
al.
Interobserver
agreement
in
the
electrocardiographic
diagnosis
of
acute
myocardial
infarction
in
patients
with
left
bundle
branch
block.
Ann
Emerg
Med
2000;36(6):566-‐71.