Modified shock index: A bedside clinical index for risk assessment of ST-segment elevation myocardial infarction at presentation

Abstract

Introduction
Prompt identification of higher-risk patients presenting with ST-segment elevation myocardial infarction (STEMI) is crucial to pursue a more aggressive approach.

Objective
We aimed to assess whether the modified shock index (MSI), the ratio of heart rate to mean arterial pressure, could predict six-month mortality among patients admitted with STEMI.

Methods
A retrospective observational cohort study was performed in a single center including 1158 patients diagnosed with STEMI, without cardiogenic shock on admission, between July 2009 and December 2014. They were divided into two groups: group 1 – patients with MSI <0.93 (72%); group 2 – patients with MSI≥0.93 (28%). The primary endpoint was six-month all-cause mortality.

Results
MSI≥0.93 identified patients who were more likely to have signs of heart failure (p=0.002), anemia (p<0.001), renal insufficiency (p=0.014) and left ventricular systolic dysfunction (p=0.045). They more often required inotropic support (p<0.001), intra-aortic balloon pump (p<0.001) and mechanical ventilation (p<0.001). Regarding in-hospital adverse events, they had a higher prevalence of malignant arrhythmias (p=0.01) and mechanical complications (p=0.027). MSI≥0.93 was an independent predictor of overall six-month mortality (adjusted HR 2.00, 95% CI 1.20-3.34, p=0.008).

Conclusion
MSI was shown to be a valuable bedside tool which can rapidly identify high-risk STEMI patients at presentation.

Full text

Rev
Port
Cardiol.
2018;37(6):481---488
www.revportcardiol.org
Revista
Portuguesa
de
Cardiologia
Portuguese
Journal
of
Cardiology
ORIGINAL
ARTICLE
Modified
shock
index:
A
bedside
clinical
index
for
risk
assessment
of
ST-segment
elevation
myocardial
infarction
at
presentation
Glória
Abreu∗,
Pedro
Azevedo,
Carlos
Galvão
Braga,
Catarina
Vieira,
Miguel
Álvares
Pereira,
Juliana
Martins,
Carina
Arantes,
Catarina
Rodrigues,
Alberto
Salgado,
Jorge
Marques
Cardiology
Department,
Braga
Hospital,
Braga,
Portugal
Received
5
March
2017;
accepted
13
July
2017
Available
online
26
May
2018
KEYWORDS
ST-elevation
myocardial
infarction;
Stratification;
Mortality;
Outcome;
Modified
shock
index
Abstract
Introduction:
Prompt
identification
of
higher-risk
patients
presenting
with
ST-segment
eleva-
tion
myocardial
infarction
(STEMI)
is
crucial
to
pursue
a
more
aggressive
approach.
Objective:
We
aimed
to
assess
whether
the
modified
shock
index
(MSI),
the
ratio
of
heart
rate
to
mean
arterial
pressure,
could
predict
six-month
mortality
among
patients
admitted
with
STEMI.
Methods:
A
retrospective
observational
cohort
study
was
performed
in
a
single
center
including
1158
patients
diagnosed
with
STEMI,
without
cardiogenic
shock
on
admission,
between
July
2009
and
December
2014.
They
were
divided
into
two
groups:
group
1
---
patients
with
MSI
<0.93
(72%);
group
2
---
patients
with
MSI≥0.93
(28%).
The
primary
endpoint
was
six-month
all-cause
mortality.
Results:
MSI≥0.93
identified
patients
who
were
more
likely
to
have
signs
of
heart
failure
(p=0.002),
anemia
(p<0.001),
renal
insufficiency
(p=0.014)
and
left
ventricular
systolic
dys-
function
(p=0.045).
They
more
often
required
inotropic
support
(p<0.001),
intra-aortic
balloon
pump
(p<0.001)
and
mechanical
ventilation
(p<0.001).
Regarding
in-hospital
adverse
events,
they
had
a
higher
prevalence
of
malignant
arrhythmias
(p=0.01)
and
mechanical
complications
(p=0.027).
MSI≥0.93
was
an
independent
predictor
of
overall
six-month
mortality
(adjusted
HR
2.00,
95%
CI
1.20-3.34,
p=0.008).
Conclusion:
MSI
was
shown
to
be
a
valuable
bedside
tool
which
can
rapidly
identify
high-risk
STEMI
patients
at
presentation.
©
2018
Sociedade
Portuguesa
de
Cardiologia.
Published
by
Elsevier
Espa˜
na,
S.L.U.
All
rights
reserved.
∗Corresponding
author.
E-mail
address:
gloriappabreu@gmail.com
(G.
Abreu).
https://doi.org/10.1016/j.repc.2017.07.018
0870-2551/©
2018
Sociedade
Portuguesa
de
Cardiologia.
Published
by
Elsevier
Espa˜
na,
S.L.U.
All
rights
reserved.
2174-2049

482
G.
Abreu
et
al.
PALAVRAS-CHAVE
Enfarte
com
supradesnivelamento
do
segment
ST
(EAMCSST);
Estratificac¸ão;
Mortalidade;
Prognóstico;
Índice
de
choque
modificado
(ICM)
Índice
de
choque
modificado:
um
índice
clínico
simples
para
estratificac¸ão
de
risco
nos
doentes
admitidos
com
enfarte
com
supradesnivelamento
do
segmento
ST
Resumo
Introduc¸ão:
A
identificac¸ão
precoce
dos
doentes
(dts)
de
maior
gravidade
que
se
apresentam
com
enfarte
com
supradesnivelamento
do
segment
ST
(EAMCSST)
é
fundamental
para
uma
abordagem
mais
eficaz
e/ou
segura.
Objetivo:
Avaliar
se
o
índice
de
choque
modificado
(ICM)
---
razão
entre
a
frequência
cardíaca
e
a
pressão
arterial
média
---
poderá
ser
um
preditor
de
mortalidade
aos
seis
meses,
nos
doentes
admitidos
com
enfarte
com
EAMCSST.
Métodos:
Estudo
observacional,
unicêntrico,
retrospetivo
que
incluiu
1158
doentes
admitidos
com
o
diagnóstico
de
EAMCSST,
sem
choque
cardiogénico
à
admissão,
desde
julho
de
2009
a
dezembro
de
2014.
Os
doentes
foram
divididos
em
dois
grupos:
grupo
1
---
dts
com
ICM<0,93
(72%);
grupo
2
---
dts
com
ICM≥0,93
(28%).
O
endpoint
primário
foi
a
ocorrência
de
morte
por
todas
as
causas
aos
seis
meses.
Resultados:
Os
doentes
com
ICM≥0,93
apresentavam
mais
frequentemente
sinais
de
insuficiên-
cia
cardíaca
(p=0,002),
anemia
(p<0,001),
insuficiência
renal
(p=0,014)
e
disfunc¸ão
ventricular
esquerda
(p=0,045)
à
admissão.
Estes
doentes
necessitaram
mais
frequentemente
de
suporte
aminérgico
(p<0,001),
suporte
com
balão
intra-aórtico
(p<0,001)
e
ventilac¸ão
mecânica
invasiva
(p<0,001).
Relativamente
aos
eventos
hospitalares
adversos,
os
doentes
com
ICM≥0,93
apresen-
taram
mais
frequentemente
arritmias
malignas
(p=0,01)
e
complicac¸ões
mecânicas
(p=0,027).
O
valor
de
ICM≥0,93
mostrou-se
um
preditor
independente
de
mortalidade
por
todas
as
causas
aos
seis
meses
---
HR
ajustada
2,00,
95%
CI
(1,20-3,34),
p=0,008.
Conclusão:
O
índice
de
choque
modificado
mostrou
ser
uma
ferramenta
útil,
capaz
de
estrati-
ficar
rapidamente
os
doentes
com
EAMCSST
de
maior
risco.
©
2018
Sociedade
Portuguesa
de
Cardiologia.
Publicado
por
Elsevier
Espa˜
na,
S.L.U.
Todos
os
direitos
reservados.
Introduction
In
daily
practice,
when
dealing
with
ST-segment
elevation
myocardial
infarction
(STEMI),
it
is
important
to
identify
patients
who
may
potentially
suffer
complications.
Risk
assessment
provides
an
opportunity
to
estimate
the
patient’s
prognosis,
alerting
the
physician
to
possible
hazards,
in
order
to
pursue
a
more
aggressive
approach.1
Several
risk
stratification
systems
have
been
developed,
such
as
Thrombolysis
In
Myocardial
Infarction
(TIMI)
and
the
Global
Registry
of
Acute
Coronary
Events
(GRACE),
but
they
are
time-consuming
and
difficult
to
perform
routinely
at
the
bedside.2 --- 5 It
is
crucial
to
find
an
easier
method
to
stratify
STEMI
patients,
in
order
to
recognize
subclini-
cal
indicators
of
worse
prognosis,
such
as
cardiogenic
shock,
early.
In
the
GUSTO
trial,
cardiogenic
shock
was
reported
to
occur
on
average
12
hours
after
STEMI
presentation
in
patients
who
were
not
considered
to
have
cardiogenic
shock
at
the
time
of
initial
assessment.
Some
of
these
patients
may
have
had
subclinical
shock
with
no
sign
of
organ
hypoperfusion.1
The
shock
index
---
the
ratio
of
heart
rate
to
systolic
blood
pressure
(SBP)
---
is
recognized
as
a
predictor
of
hemody-
namic
instability.
It
is
an
easy
tool
to
assess
prognosis
in
different
settings,
including
STEMI.6 --- 9 A
more
recent
index,
the
modified
shock
index
(MSI),
which
is
the
ratio
of
heart
rate
to
mean
arterial
pressure
(MAP),
has
been
shown
in
small
studies
to
predict
mortality
in
medical
and
trauma
emergency
patients.10---12 The
purpose
of
the
present
study
was
to
assess
the
MSI
as
a
predictor
of
six-month
all-cause
mortality
among
patients
admitted
with
STEMI.
Methods
Study
population
The
study
population
included
1234
patients
admitted
with
a
diagnosis
of
STEMI
between
July
2009
and
December
2014,
either
directly
from
the
community
to
our
cen-
ter
or
transferred
from
one
of
its
satellite
hospitals,
to
perform
emergent
percutaneous
coronary
interven-
tion.
Of
these,
26
patients
were
excluded
as
lost
to
follow-up
(2%),
and
50
patients
(5%)
presented
with
cardiogenic
shock,
defined
as
Killip
class
IV,
on
admis-
sion.
Therefore,
the
study
population
consisted
of
1158
patients
without
cardiogenic
shock,
presenting
within
12hours
of
symptom
onset
and
with
persistent
ST-segment
elevation
or
new
left
bundle
branch
block,
or>12hours
after
symptom
onset
and
with
ongoing
ischemia,
life-
threatening
arrhythmias
or
stuttering
electrocardiogram
(ECG)
changes.
The
diagnosis
of
STEMI
was
based
on
the
presence
of
chest
pain
suggestive
of
myocardial
ischemia,
a
12-lead
ECG
showing
persistent
ST-segment
elevation
of≥2.5mm
in
men

Modified
shock
index:
A
clinical
index
for
risk
assessment
of
STEMI
patients
483
aged<40
years,
>2mm
in
men
aged≥40
years,
and>1.5mm
in
women,
in
leads
V2-V3
and/or>1mm
in
other
leads
(in
the
absence
of
left
ventricular
hypertrophy
or
left
bun-
dle
branch
block),
or
new
left
bundle
branch
block,
and
increased
serum
biomarkers
of
cardiac
injury.
The
biomark-
ers
used
were
cardiac
troponin
I
and
CK-MB,
with
a
positive
threshold
of
0.06
and
3.5
ng/ml,
respectively.
Heart
failure
was
defined
as
Killip
class≥2
during
hospi-
talization.
Malignant
arrhythmias
were
defined
as
ventricular
fibril-
lation
or
sustained
ventricular
tachycardia.
Clinical
data
and
the
Modified
Shock
Index
Demographic,
clinical,
laboratory,
echocardiographic
and
coronary
angiographic
data
were
collected
prospectively
and
recorded
in
an
electronic
database
(SIMACARDIO),
in
accordance
with
our
department’s
protocol
for
patients
admitted
to
the
coronary
care
unit.
Regarding
laboratory
data,
N-terminal
pro-brain
natri-
uretic
peptide
(NT-proBNP)
levels
were
measured
within
24hours
of
admission.
Estimated
glomerular
filtration
rate
(eGFR)
was
obtained
at
presentation
using
the
abbre-
viated
Modification
of
Diet
in
Renal
Disease
(MDRD)
formula.
Anemia
was
defined
according
to
the
World
Health
Organization
criteria
(hemoglobin<12g/dl
in
women
and
<13g/dl
in
men).
Echocardiographic
data
were
obtained
from
the
first
echocardiogram
performed
within
24hours
of
admission
or
as
soon
as
a
mechanical
complication
was
suspected.
Left
ventricular
systolic
dysfunction
was
defined
as
left
ven-
tricular
ejection
fraction≤40%.
Right
ventricular
systolic
dysfunction
was
defined
as
tricuspid
annular
plane
systolic
excursion<16mm.
Significant
coronary
artery
disease
on
coronary
angiog-
raphy
was
defined
as≥50%
stenosis
of
the
left
main
artery
or≥70%
in
other
coronary
arteries.
Severe
coronary
disease
was
defined
as
left
main
disease
and/or
three-vessel
dis-
ease.
Coronary
revascularization
was
defined
as
successful
percutaneous
or
surgical
coronary
intervention
in
order
to
restore
blood
flow.
Preprocedural
systolic
blood
pressure
(SBP)
and
diastolic
blood
pressure
(DBP)
were
measured
in
the
catheterization
laboratory
with
the
guide
catheter
placed
in
the
ascending
aorta.
Heart
rate
was
obtained
at
the
same
time
from
the
corresponding
ECG.
MAP
was
calculated
using
the
formula
((2×DBP)+SBP)/3.
Preprocedural
MSI
was
calculated
using
the
formula
heart
rate/MAP.
Follow-up
and
adverse
events
The
study’s
primary
endpoint
was
six-month
all-cause
mor-
tality
and
the
secondary
endpoint
was
the
occurrence
of
cardiogenic
shock
during
hospital
stay.
Patients
in
this
study
were
included
in
the
National
Reg-
istry
of
Acute
Coronary
Syndromes
and
were
monitored
for
six
months
or
until
occurrence
of
the
primary
outcome.
Follow-up
was
by
phone
calls
and
consultation
of
hospital
records.
Statistical
analysis
Receiver
operating
characteristic
(ROC)
curve
analysis
was
used
to
determine
the
optimal
threshold
of
MSI.
Categori-
cal
variables
were
expressed
as
percentages
and
compared
by
the
chi-square
test
or
Fisher’s
exact
test.
Continu-
ous
variables
were
tested
for
normal
distribution
by
the
Kolmogorov-Smirnov
test;
all
continuous
variables
had
a
normal
distribution,
and
so
between-group
differences
were
compared
using
the
t
test
and
were
expressed
as
means±standard
deviation.
Binary
logistic
regression
analy-
sis
was
performed
to
determine
the
independent
predictors
of
occurrence
of
cardiogenic
shock
during
hospital
stay.
Only
four
variables
with
statistical
significance
on
univariate
analysis
were
included,
given
the
small
numbers
of
events
in
the
study.
Cox
proportional
hazards
regression
analysis
was
used
to
determine
independent
predictors
of
six-month
all-cause
mortality,
including
only
variables
with
statisti-
cal
significance
on
univariate
analysis.
Kaplan-Meier
survival
curves
were
constructed
to
compare
event-free
survival
at
six
months
according
to
the
threshold
value
obtained
for
MSI.
The
log
rank
test
was
used
to
test
the
equality
of
the
survival
function
across
groups.
A
two-sided
p<0.05
was
con-
sidered
statistically
significant.
All
statistical
analyses
were
performed
with
SPSS
software,
version
21
(IBM
SPSS
Inc.,
Chicago,
IL).
Results
The
optimal
threshold
for
MSI
was
determined
based
on
ROC
curve
analysis.
The
area
under
the
curve
(C-statistic)
was
0.636
(95%
confidence
interval
[CI]:
0.573-0.700;
p<0.001).
The
shortest
distance
to
the
upper
left
corner
and
Youden’s
index
were
used
to
identify
the
optimal
threshold,
which
was
0.93
(sensitivity
of
65%
and
specificity
of
73%).
Patients
were
divided
into
two
groups:
group
1
---
those
with
MSI<0.93
(n=843,
72%);
and
group
2
---
those
with
MSI≥0.93
(n=324,
28%)
(Figure
1).
The
groups
were
compared
in
terms
of
base-
line
characteristics,
laboratory
findings
and
adverse
events.
Figure
1
Flowchart
of
patient
selection.

484
G.
Abreu
et
al.
Table
1
Baseline
patient
characteristics,
clinical
presentation,
echocardiographic
findings
and
coronary
angiography,
according
to
the
Modified
Shock
Index.
MSI<0.93
(72%;
n=834)
MSI≥0.93
(28%;
n=324)
p
Demographic
Age
(years),
mean
(SD)
61±13
62±14
0.235
Female
(%)
16.5
(138)
21.9
(71)
0.033
Cardiovascular
risk
factors
(%)
Diabetes
21.6
(180)
28.4
(92)
0.014
Hypertension
56.6
(472)
57.4
(186)
0.802
Dyslipidemia
50.8
(423)
47.8
(155)
0.369
Active
smoker 38.5
(321) 38.9
(126)
0.900
Ex-smoker
18.1
(150) 15.3
(49) 0.259
BMI
(kg/m2),
mean±SD 27±427±4 0.169
Previous
cardiovascular
history
(%)
Myocardial
infarction
9.6
(80)
8.6
(28)
0.618
Angina
8.8
(73)
7.1
(23)
0.359
CABG
1.1
(9)
1.2
(4)
0.822
PCI
7.0
(58)
5.6
(18)
0.388
Stroke
5.4
(45)
8.0
(26)
0.09
Previous
medication
(%)
Aspirin
14.6
(122)
14.8
(48)
0.936
Beta-blockers
16.2
(135)
10.5
(34)
0.359
Statins
26.6
(222)
26.9
(87)
0.822
ACE
inhibitors
or
ARBs
31.9
(266)
38.3
(124)
0.045
Diuretics
15.8
(105)
19
(47)
0.205
Anticoagulants
2.1
(14)
1.6
(4)
0.660
Clinical
presentation
SBP
(mmHg),
mean±SDa135±26
112±20
<0.001
DBP
(mmHg),
mean±SDa83±15
69±13
<0.001
HR
(bpm),
mean±SDa72±14
92±16
<0.001
MAP
(mmHg),
mean±SDa100±18
83±14
<0.001
Acute
heart
failure
(%)a14
(117)
21.6
(70)
0.002
eGFR<60
ml/min/1.73
m2(%)a14.3
(119)
20.2
(65)
0.014
Anemia
(%)a17.8
(148)
29.2
(94)
<0.001
Troponin
peak
level
(ng/ml),
mean±SD 83±101 100±139
0.02
NT-proBNP
(pg/ml),
mean±SD 2228±4515 2816±4401 0.066
CRP
(mg/l),
mean±SDa12.3±20.43 20.4±38.88
<0.001
Anterior
infarction
(%)
65.9
(549)
63
(204)
0.346
Echocardiographic
findings
(%)
LVEF≤40%
39.1
(293)
45.9
(135)
0.045
RV
dysfunction
5.1
(41)
7.1
(22)
0.18
Coronary
angiography
(%)
Left
main
or
three-vessel
disease
15.5
(129)
18.8
(61)
0.168
aon
admission.
ACE:
angiotensin-converting
enzyme;
ARB:
angiotensin
receptor
blocker;
BMI:
body
mass
index;
CABG:
coronary
artery
bypass
grafting;
CRP:
C-reactive
protein;
DBP:
diastolic
blood
pressure;
eGFR:
estimated
glomerular
filtration
rate;
HR:
heart
rate;
LVEF:
left
ventricular
ejection
fraction;
MAP:
mean
arterial
pressure;
MI:
myocardial
infarction;
NT-proBNP:
N-terminal
pro-brain
natriuretic
peptide;
PCI:
percutaneous
coronary
intervention;
RV:
right
ventricular;
SBP:
systolic
blood
pressure.
Baseline
patient
characteristics
The
mean
age
of
the
study
population
was
61.70±13.5
years;
there
was
no
significant
age
difference
between
the
groups
(Table
1).
The
group
with
MSI≥0.93
had
a
higher
proportion
of
women
(21.9%
vs.
16.5%;
p=0.033)
and
patients
with
diabetes
(28.4%
vs.
21.6%;
p=0.014).
There
were
no
sta-
tistically
significant
differences
between
groups
regarding
other
conventional
cardiovascular
risk
factors
such
as
hyper-
tension,
dyslipidemia
or
smoking,
or
regarding
previous
cardiovascular
history.
On
admission,
patients
with
MSI≥0.93
more
frequently
presented
signs
of
acute
heart
failure
(21.6%
vs.
14%;

Modified
shock
index:
A
clinical
index
for
risk
assessment
of
STEMI
patients
485
Table
2
In-hospital
treatment
and
procedures
and
in-hospital
adverse
events,
according
to
the
Modified
Shock
Index.
MSI<0.93
(72%;
n=834)
MSI≥0.93
(28%;
n=324)
p
In-hospital
medication
(%)
Aspirin
100
(834)
100
(324)
1.00
Clopidogrel
100
(834)
100
(324)
1.00
Beta-blockers
90.1
(750)
84.0
(272)
0.004
ACE
inhibitors
90
(749)
83
(269)
0.001
Statins
99
(824)
98.1
(318)
0.214
UHF
72.8
(606)
78.4
(254)
0.061
LMWH
31.9
(265)
30.2
(98)
0.581
Nitrates
19.5
(162) 14.2
(46) 0.037
GP
IIb/IIIa
inhibitors 18.3
(152) 24.7
(80) 0.015
Inotropics
4.1
(34) 12.4
(40) <0.001
Diuretics
29.2
(199)
40.1
(101)
0.002
Procedures
(%)
Symptom-to-balloon
time
(min)
336±578
373±636
0.375
FMC-to-balloon
time
(min)
151±120
166±132
0.08
Revascularization 96.9
(808)
97.7
(316)
0.548
CABG
7.1
(46) 6.7
(16)
0.847
Intra-aortic
balloon
pump 1.3
(9) 7.9
(20) <0.001
Non-invasive
ventilation 1.1
(7) 6.9
(16)
<0.001
Mechanical
ventilation 1.8
(11) 5.2
(12) <0.001
In-hospital
events
(%)
New-onset
heart
failure
24.6
(205)
36.1
(117)
<0.001
Cardiogenic
shock
4.4
(20)
6.5
(21)
0.001
Angina
after
MI
3.5
(29)
2.5
(8)
0.381
Reinfarction
1.9
(16)
1.2
(4)
0.423
Acute
stent
thrombosis
1.2
(10)
0.6
(2)
0.526
Mechanical
complications
0.9
(16)
2.8
(7)
0.027
Malignant
arrhythmias
6.1
(51)
10.2
(33)
0.017
New-onset
atrial
fibrillation
8.4
(70)
14.2
(46)
0.003
High
grade
heart
block
7.0
(58)
4.9
(16)
0.206
Respiratory
tract
infection
3.2
(27)
8.6
(28)
<0.001
Stroke
0.8
(7)
1.5
(5)
0.289
Mortality
2.4
(20)
5.2
(17)
0.013
ACE:
angiotensin-converting
enzyme;
CABG:
coronary
artery
bypass
grafting;
FMC:
first
medical
contact;
GP
IIb/IIIa:
glycoprotein
IIb/IIIa;
LMWH:
low-molecular-weight
heparin;
MI:
myocardial
infarction;
UHF:
unfractionated
heparin.
p=0.002),
anemia
(29.2%
vs.
17.8%;
p<0.001)
and
renal
insufficiency
(eGFR<60ml/min/1.73
m2)
(20.2%
vs.
14.3%;
p<0.001).
On
echocardiographic
assessment,
almost
half
of
patients
with
MSI≥0.93
had
left
ventricular
dysfunction
(45.9%
vs.
39.1%;
p=0.045).
Treatment
and
in-hospital
procedures
There
were
no
statistical
differences
in
terms
of
antithrom-
botic
therapy,
but
patients
with
MSI≥0.93
were
less
often
treated
with
beta-blockers
(84%
vs.
90%;
p=0.004),
angiotensin-converting
enzyme
(ACE)
inhibitors
(83%
vs.
90%;
p=0.001)
and
nitrates
(14.2%
vs.
19.5%,
p=0.037)
(Table
2).
On
the
other
hand,
they
more
often
required
inotropic
support
(12.4%
vs.
4.1%;
p<0.001),
levosimendan
(2.8%
vs.
0.4%;
p=0.002)
and
diuretics
(40.1%
vs.
29.2%;
p=0.002)
(Table
2).
Total
ischemic
time
and
first
medical
contact-to-balloon
time
were
not
statistically
different
between
groups.
Regarding
revascularization,
there
were
no
significant
dif-
ferences
between
groups,
but
patients
with
MSI≥0.93
more
frequently
required
glycoprotein
IIb/IIIa
inhibitors
(24%
vs.
18.3%;
p=0.015)
due
to
evidence
of
massive
thrombus
dur-
ing
the
angiographic
procedure
and
no-reflow
or
slow
flow
situations.
Intra-aortic
balloon
pump
support
(7.9%
vs.
1.3%;
p<0.001)
and
non-invasive
(6.9%
vs.1.1%;
p<0.001)
and
mechanical
ventilation
(5.2%
vs.
1.8%;
p<0.001)
were
used
more
frequently
in
patients
with
MSI≥0.93.
In-hospital
adverse
events
In
the
study
population,
27.8%
(n=322)
of
patients
developed
acute
heart
failure
and
3.5%
(n=41)
developed
cardio-
genic
shock.
The
proportion
of
patients
with
acute
heart
failure
(36.1%
vs.
24.6%;
p<0.001)
and
cardiogenic
shock
(6.5%
vs.
2.4%;
p=0.001)
was
higher
in
patients
with
MSI
≥0.93.

486
G.
Abreu
et
al.
Table
3
Cox
proportional
hazards
regression
analysis
for
six-month
all-cause
mortality.
Variable
HR
(95%
CI)
p
Age
1.06
(1.04-1.09)
<0.001
eGFR<60
ml/min/1.73
m23.71
(2.11-6.55)
<0.001
Acute
heart
failure
1.29
(0.74-2.26)
0.376
MSI≥0.93
2.00
(1.20-3.34)
0.008
RV
systolic
dysfunction
1.13
(0.54-2.35)
0.746
LV
systolic
dysfunction
(LVEF<40%)
2.55
(1.45-4.45)
0.001
Anemia
1.52
(0.87-2.61)
0.145
Gender
1.18
(0.66-2.10)
0.890
CI:
confidence
interval;
eGFR:
estimated
glomerular
filtration
rate
by
the
MDRD
formula;
HR:
hazard
ratio;
LV:
left
ventricular;
LVEF:
left
ventricular
ejection
fraction;
MSI:
Modified
Shock
Index;
RV:
right
ventricular.
Binary
logistic
regression
analysis
was
performed
for
development
of
cardiogenic
shock
during
hospital
stay
using
the
previously
identified
predictors.
Right
ventricular
dys-
function
(adjusted
odds
ratio
[OR]
5.0,
95%
CI
2.05-12.21;
p<0.001)
and
left
ventricular
dysfunction
(adjusted
OR
4.87,
95%
CI
1.12-4.78;
p=0.001)
were
the
strongest
independent
predictors,
although
the
presence
of
acute
heart
failure
on
admission
(adjusted
OR
3.41,
95%
CI
1.63-7.16;
p<0.001)
and
MSI≥0.93
(adjusted
OR
2.731,
95%
CI
1.12-4.78;
p=0.023)
provided
additional
information.
Patients
with
MSI≥0.93
had
more
episodes
of
malig-
nant
arrhythmias
(10.2%
vs.
6.1%;
p=0.017),
new-onset
atrial
fibrillation
(14.2%
vs.
8.4%;
p=0.003),
mechanical
complications
(2.8%
vs.
0.9%;
p=0.027)
and
respiratory
tract
infections
(8.6%
vs.
3.2%;
p<0.001).
Adverse
outcomes
Of
the
total
population,
3.2%
(n=37)
died
during
hospitaliza-
tion,
and
six-month
all-cause
mortality
was
recorded
in
7.2%
(n=88)
of
patients.
Patients
with
MSI≥0.93
had
a
higher
proportion
of
in-
hospital
mortality
(5.2%
vs.
2.4%;
p=0.013;
OR
2.25;
95%
CI
1.17-4.36;
p=0.016).
Due
to
the
low
rate
of
in-hospital
mor-
tality
it
was
not
possible
to
calculate
independent
predictors
of
in-hospital
mortality
in
this
sample.
Predictors
of
longer-term
mortality
Patients
with
MSI≥0.93
had
also
higher
six-month
all-cause
mortality
(13.3%
vs.
5.4%;
p<0.001);
OR
2.68;
95%
CI
(1.73
---
4.16);
p<0.001).
Table
3
shows
the
results
of
Cox
proportional
hazards
regression
analysis
for
six-month
all-cause
mortality.
After
adjusting
for
different
baseline
characteristics
and
possible
confounding
factors,
MSI≥0.93
remained
as
an
independent
predictor
(adjusted
hazard
ratio
[HR]
2.00;
95%
CI
1.20-3.34;
p=0.008).
Kaplan-Meier
curves
(Figure
2)
show
that
patients
with
MSI≥0.93
had
higher
mortality
early
after
hospital
admis-
sion,
but
their
worse
prognosis
remained
throughout
the
follow-up
period
(log
rank
p<0.001).
Figure
2
Kaplan-Meier
curves
for
six-month
mortality
accord-
ing
to
the
Modified
Shock
Index.
Discussion
Our
study
presents
data
on
all-comers
who
met
the
crite-
ria
for
STEMI,
irrespective
of
age
and
comorbidities.
The
study
reflects
modern
primary
percutaneous
coronary
inter-
vention
(PCI)
practice
and
modern
care
procedures,
which
enabled
short
door-to-balloon
and
total
ischemic
times,
as
well
as
the
use
of
GP
IIb/IIIa
inhibitors
and
drug-eluting
stents.
MSI
is
an
easily
accessible
index
that
does
not
depend
on
subjective
information,
previous
patient
history
or
blood
tests;
it
only
depends
on
invasive
measures
of
blood
pres-
sure
and
heart
rate
at
the
beginning
of
the
primary
PCI
procedure,
which
are
less
susceptible
to
fill-in
errors.
MSI
has
been
demonstrated
to
be
a
valid
prognostic
tool
in
medical
or
trauma
patients
admitted
to
the
emer-
gency
department.
Liu
et
al.
showed
that
an
MSI
of≥1.3
was
associated
with
increased
probability
of
intensive
care
unit
admission
or
death.10 Other
studies
have
compared
the
standard
shock
index
with
MSI
for
predicting
prognosis
in
emergency
patients
and
showed
that
MSI
is
a
better
predic-
tor
of
mortality
in
this
setting.11,12
The
MSI
has
been
tested
in
STEMI
patients
as
well
as
in
emergency
patients.
Our
results
are
in
line
with
Shangguan

Modified
shock
index:
A
clinical
index
for
risk
assessment
of
STEMI
patients
487
et
al.,13 who
found
higher
rates
of
all-cause
mortality
and
major
adverse
cardiac
events
at
seven
days
in
STEMI
patients
who
presented
MSI≥1.4.
They
compared
the
shock
index
with
MSI
and
concluded
that
the
latter
better
predicted
prognosis:
MSI≥1.4
predicted
higher
rates
for
all-cause
mor-
tality
(20.4%
vs.
13.9%)
and
major
adverse
cardiac
events
(44.9%
vs.
36.1%)
than
SI≥0.7.
As
the
calculation
of
MSI
uses
MAP,
its
greater
predictive
power
in
STEMI
patients
is
logical,
since
it
more
accurately
reflects
myocardial
perfu-
sion
and
systemic
vascular
resistance.13 The
cut-off
used
by
Shangguan
et
al.
was
determined
on
the
basis
of
ROC
curve
analysis,
as
in
our
study.
A
possible
explanation
for
their
higher
cut-off
is
that
they
did
not
exclude
patients
admit-
ted
in
cardiogenic
shock.
Such
patients
are
known
to
have
higher
heart
rate,
which
can
increase
the
cut-off
obtained.
Excluding
patients
in
cardiogenic
shock
on
admission
may
have
led
us
to
use
a
lower
cut-off
value,
but
it
also
helped
to
determine
whether
MSI
could
identify
patients
in
the
early
phase
of
decompensation,
at
a
stage
when
cardiogenic
shock
is
not
yet
established.
In
our
study,
the
MSI
was
shown
to
be
valuable
in
iden-
tifying
more
critical
and
morbid
patients
presenting
at
a
pre-shock
stage.
Those
with
higher
MSI
more
often
had
dia-
betes
and
on
admission
more
often
presented
anemia,
renal
insufficiency
and
acute
heart
failure.
By
identifying
patients
with
worse
prognosis,
this
index
can
enable
closer
monitoring
and
increase
alertness
for
possible
complications.
In
the
present
study,
patients
with
higher
MSI
had
a
higher
prevalence
of
malignant
arrhyth-
mias,
mechanical
complications,
and
respiratory
tract
infections.
It
was
also
a
strong
independent
predictor
of
cardiogenic
shock
during
hospital
stay
(OR
2.73,
95%
CI
1.12-
4.78;
p=0.001).
In
the
early
management
of
high-risk
patients
with
rela-
tive
hypotension
and
tachycardia,
this
tool
can
be
used
not
only
to
assess
risk
but
also
to
prevent
iatrogenic
cardiogenic
shock
by
avoiding
certain
therapies,
such
as
beta-blockers
or
ACE
inhibitors.14
Interestingly,
in
our
study
MSI
was
also
an
independent
predictor
of
six-month
mortality
in
STEMI
patients
on
multi-
variate
analysis.
One
possible
explanation
for
this
is
that
a
high
MSI
may
identify
more
frail
patients
with
comorbidities
that
in
themselves
impart
a
worse
prognosis,
such
as
female
gender,
renal
insufficiency,
anemia,
and
left
ventricular
sys-
tolic
dysfunction.
Another
is
its
association
with
in-hospital
adverse
events
such
as
mechanical
complications,
new-
onset
heart
failure,
cardiogenic
shock
and
respiratory
tract
infections,
which
also
increase
frailty.
A
third
possible
expla-
nation
is
the
inherent
hemodynamic
profile
of
this
patient
group,
which
may
hamper
the
introduction
or
titration
of
treatments
that
could
modify
prognosis.
Although
various
systems
have
been
applied
for
risk
strat-
ification
in
STEMI
patients,
including
the
TIMI
and
GRACE
scores,
the
complex
and
lengthy
calculations
involved
usu-
ally
make
them
impractical
in
daily
clinical
practice.
The
MSI
is
a
valuable
prognostic
tool,
based
only
on
patients’
hemodynamic
profile
assessed
on
admission,
that
has
the
advantage
of
being
calculated
rapidly.
MSI
may
be
used
in
addition
to
conventional
risk
scores
to
complement
risk
assessment,
helping
physicians
to
implement
differ-
ent
strategies
in
this
population
in
order
to
change
their
outcomes,
such
as
providing
hemodynamic
support
and
introducing
well-timed
treatments
that
could
modify
prog-
nosis.
Study
limitations
Firstly,
although
our
patients
were
included
in
a
prospective
registry,
this
was
a
retrospective,
non-randomized,
observa-
tional
study
conducted
in
a
single
center,
and
so
the
results
may
have
been
influenced
by
identified
or
unidentified
con-
founding
factors.
Secondly,
most
variables
were
determined
by
consulting
medical
records,
which
may
have
been
incom-
plete.
Finally,
as
the
study’s
primary
endpoint
was
all-cause
mortality,
this
may
have
included
not
only
cardiovascular
death,
but
also
death
from
other
causes,
which
could
bias
our
findings.
Conclusion
In
summary,
MSI≥0.93
was
an
independent
predictor
of
six-
month
mortality.
MSI
is
an
easily
accessible
tool
that
can
be
used
to
stratify
STEMI
patients
and
guide
clinical
manage-
ment.
Nevertheless,
it
needs
to
be
externally
validated
and
compared
to
existing
validated
indices.
Conflicts
of
interests
The
authors
have
no
conflicts
of
interest
to
declare.
References
1.
Hasdai
D,
Holmes
DRJ,
Califf
RM,
et
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Cardiogenic
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acute
myocardial
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GUSTO
investigators.
Global
Utilization
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and
Tissue-Plasminogen
Activator
for
Occluded
Coronary
Arteries
Am
Heart
J.
1999;138:21---31.
2.
O’Gara
PT,
Kushner
FG,
Ascheim
DD,
et
al.,
2013
ACCF/AHA
guideline
for
the
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