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Skripsi ACINTYA 15329 Final
Skripsi ACINTYA 15329 Final
COVER PAGE
A graduating paper
Submitted to the board of examiners as
partial fulfillment of the requirement of
Bachelor Degree in Faculty of Medicine
Universitas Gadjah Mada
By:
ACINTYA SEKAR MAHARDHIKA
12/338670/KU/15329
FACULTY OF MEDICINE
UNIVERSITAS GADJAH MADA
YOGYAKARTA
2015
APPROVAL PAGE
by
ACINTYA SEKAR MAHARDHIKA
12/338670/KU/15329
Material advisor
Methodology advisor
Examiner
ii
AUTHENTICITY STATEMENT
IMPACT OF ON ADMISSION OSMOLALITY ON MAJOR ADVERSE
CARDIOVASCULAR EVENTS IN ACUTE MYOCARDIAL INFARCTION
PATIENT
By
Acintya Sekar Mahardhika
12/338670/KU/15329
iii
PREFACE
spending
much
time
in
helping
me
writing
this
They
are
all
hard-working
doctors
and
deepest
gratitude
for
my
best
friends
who
iv
TABLE OF CONTENTS
COVER PAGE...................................................................................................................... i
APPROVAL PAGE ............................................................................................................. ii
AUTHENTICITY STATEMENT ....................................................................................... iii
INDEX OF ABBREVIATIONS ........................................................................................ x
ABSTRACT .........................................................................................................................xi
CHAPTER I ....................................................................................................................... 1
INTRODUCTION ................................................................................................................ 1
A.
Background..................................................................................................... 1
B.
C.
Objectives..................................................................................................... 3
D.
E.
CHAPTER II..................................................................................................................... 5
LITERATURE REVIEW .................................................................................................... 5
A.
1.
2.
3.
4.
B.
C.
Hypothesis................................................................................................... 18
D.
Theoretical Framework
E.
................................................................... 19
B.
C.
D.
E.
F.
G.
H.
I.
J.
CHAPTER IV................................................................................................................... 31
A.
CHAPTER V ..................................................................................................................... 43
CONCLUSION AND SUGGESTION ............................................................................... 43
A.
Conclusion................................................................................................... 43
B.
Suggestion................................................................................................... 43
REFERENCES................................................................................................................... 44
APPENDIX ....................................................................................................................... 53
vi
INDEX OF TABLE
Table 1
vii
Table 28 ....................................................... 59
viii
INDEX OF FIGURE
Figure 1. Incidence of MACE in the research.................................... 36
ix
INDEX OF ABBREVIATIONS
Abbreviation
ACS
AMI
ATPase
aVF
aVL
BUN
CAD
CK-MB
CKD
df
dl
ECG
ESRD
Exp(B)
ICCU
kg
LL
MACE
mEq/l
mg
mm
mmol
mOsmol
NSTEMI
NYHA
PCI
STEMI
VF
VT
WHO
Full Citation
Acute Coronary Syndrome
Acute Myocardial Infarction
Adenosine Triposphatase
Augmented Voltage Foot
Augmented Voltage Left
Blood Urea Nitrogen
Coronary Artery Disease
Creatinin Kinase MB
Chronic Kidney Diseasae
Degree of freedom
deciliter
Electrocardiogram
End Stage Renal Disease
Exponentiation of B coefficient
Intensive CardioCare Unit
kilogram
Log Likelihood
Major Adverse Cardiac Event
Milliequivalent per liter
milligram
millimeter
millimol
milliosmol
Non-ST Elevation Myocardial Infarction
New York Heart Association
Percutaneous Coronary Intervention
ST Elevation Myocardial Infarction
Ventricular Fibrilation
Ventricular Tachycardia
United Nation World Health Organization
ABSTRACT
Background: The main cause of death around the world is
cardiovascular disease. According to WHO, in 2008 there
are 17.3 million deaths caused by cardiovascular
disease, with 7.3 million is the result of myocardial
infarction. Some studies suggested that there is an
association between elevated blood glucose and BUN on
admission and mortality due to acute myocardial
infarction. As plasma glucose, BUN, and sodium are the
main component of osmolality, we should also analyze
the effect of on admission osmolality on clinical
endpoints in AMI patient. Previous studies show that
the value of osmolality significantly related with
clinical outcome in ACS patient.
Objective: The objective of this research is to
investigate the influence of increasing osmolality on
to the incidence of MACE in AMI patients hospitalized
in ICCU
Method:
The
objective
of
this
research
is
to
investigate the influence of increasing osmolality on
to the incidence of MACE in AMI patients hospitalized
in ICCU.
Results:This study is an observational study. The study
design is a prospective cohort. The study is a part of
the
previous
study
conducted
in
Department
of
Cardiology and Vascular Medicine. Plasma osmolality was
calculated using concentration of sodium, plasma
glucose, and blood urea nitrogen on admission.
Conclusion:There
is
strong
association
between
increasing value of on admission osmolality and the
increasing of MACE occurrence.
Key Words: osmolality, AMI, MACE
xi
CHAPTER I
INTRODUCTION
A.
The
main
cause
Background
of
death
around
the
world
is
there
are
17.3
million
deaths
caused
by
deaths)
is
infarction.
Cardiovascular
around
of
10%
the
the
result
disease
disability
of
give
adjusted
myocardial
contribution
life
years
clinical
setting,
serum
biomarkers
are
sensitive
and
specific
for
acute
myocardial
association
admission
and
between
mortality
elevated
due
to
plasma
acute
glucose
on
myocardial
we
should
also
analyze
the
effect
of
on
admission
related
Osmolality
There
relationship
is
between
with
is
clinical
closely
also
related
reported
worsening
outcome
with
that
kidney
in
ACS
kidney
there
is
function
a
in
significant
relationship
with
MACE
(Major
large
predictor
of
death,
recurrent
myocardial
osmolality
on
clinical
endpoints
in
AMI
the
prognostic
Problem Formulation
increase
value
for
of
osmolality
developing
have
Major
the
Adverse
Objectives
Research Authenticity
During
searching
of
previous
review
there
no
other
research.
is
Therefore,
it
studies
finding
is
and
literature
related
considered
to
this
that
this
research
Study Benefit
is
expected
to
bring
additional
to
This
investigate
research
further
will
also
about
plasma
answer
the
clinician
speculation
about
the
role
of
measuring
CHAPTER II
LITERATURE REVIEW
A.
1.
Literature Review
cardiovascular
disease
there
is
an
ischemic
artery
disease
(CAD)
and
acute
coronary
ST
segment
elevation
acute
myocardial
between
muscle.
condition,
such
oxygen
The
as
supply
factors
vigorous
decrease
perfusion
pressure
severely
decreased
in
anemia
(Lilly,
2011).
pathophysiology
of
ACS
blood
has
and
that
demand
underlying
exercise,
due
to
oxygen
The
of
the
this
stress,
and
hypotension,
and
content
due
understanding
undergone
to
of
remarkable
is
caused
by
the
development
of
culprit
coronary
of
AMI.
Thrombosis
occurs
because
of
two
endothelial
denudation
so
that
large
areas
of
surface.
disruption.
The
second
process
is
plaque
lipid
core
is
highly
thrombogenic;
consist
of
that
help
accelerate
coagulation
(Davies,
the
smaller
blood
vessel
stream
such
as
until
finally
coronary
artery
stop
and
in
the
forming
shows
mm
elevation
bundle
troponin
I,
branch
block
myoglobin,
and
in
more
than
lead
Cardiac
also
marker
increases
in
body
water
is
different
between
men
and
total
body
weight
is
water;
two-third
of
it
is
Osmoles
per
kilogram
osmolality;
osmoles
per
liter
osmolality.
physiological
of
of
water
is
solution
is
concentration
of
solute
and
osmolality
are
clinically
toward
cell
membrane.
The
difference
of
secretion
of
antidiuretic
hormone
(ADH).
Other
not
cause
fluid
shift
crossing
the
fluid
estimation
obtained
from
of
the
value
formula,i.e.
of
osmolality
osmolality
2Na
is
+
glucose
and
urea
nitrogen
level.
Therefore,
those
three
components,
whether
increasing
or
extracellular
out
to
and
fluid
entered
Na+/K+-ATPase
cation.
from
channel
in
Sodium
can
extracellular
the
cell
be
space
membrane.
>
is
defined
145mEq/l.
as
plasma
Hypernatremia
sodium
indicates
associated
total
body
with
sodium
plasma
content
hyperosmolality
may
be
normal,
bicarbonate
decrease
of
sodium
administration.
is
defined
Conversely,
as
the
hyponatremia.
osmolality.
Generally
hyponatremia
defined
as
sodium
loss
from
urine.
Hyponatremia
is
usually
serum
osmolality
(Guyton
&
Hall,
2011).
10
due
In
to
progression
some
research
of
previous
mention
that
underlying
hyponatremia
patient
with
heart
failure
(Goldberg
et
al.,
second
component
is
blood
glucose.
Blood
range
could
be
indicated
as
blood
glucose
and
long-term
associated
with
endothelial
prognosis.
Hyperglycemia
dysfunction,
platelets
11
use
of
shows
insulin
in
significant
treating
change
hyperglycemic
in
osmolality
there
was
no
significant
alteration
of
blood
alert.
Plasma
sodium
concentration
shows
no
of
insulin.
There
was
also
an
effect
to
Insulin
effect
was
the
electrolytes
significant
in
in
the
body
first
fluid.
30-60
minutes after administration and increasing during 6090 and 90-120 minutes collection period (DeFronzo et
al., 1974)
The third component is blood urea nitrogen. Blood
urea nitrogen normal range I s lie between 5 to 20
mg/dl, or 1.8 to 7.1 mmol/L, but normal range may vary
depending on the reference range used by the lab and
age (Hall et al., 1990). Generally, a high blood urea
nitrogen level related to kidney dysfunction. Another
factors causing elevation of blood urea nitrogen level
12
recent
dehydration,
heart
attack,
severe
gastrointestinal
burns,
and
high
bleeding,
protein
diet
throughout
the
follow
up
period.
Patient
with
correlation
between
renal
failure
and
13
renal
disease
cause
(Schiffrin
(ESRD)
et
al.,
die
from
2007).
cardiovascular
The
relationship
been
shown
mostly
increasing
in
patients
with
in
correlation
with
CKD.
Another
related
of
atherosclerosis
formation.
Endothelial
present
2004).
Another
endothelial
mechanism
in
renal
disease
experimental
dysfunction
lead
(Endemann
to
give
study
Schiffrin,
showed
contribution
progression
&
of
renal
to
that
the
disease
14
Beside
endothelial
dysfunction,
hypertension
of
as
one
cardiovascular
circulating
protein
inflammatory
of
event.
serum
risk
The
inflammatory
(CRP),
the
markers
also
factors
increasing
markers
amyloid
A,
such
been
casing
level
as
of
C-reactive
interleukin-6,
and
adverse
are
atherogenesis
some
prognosis
(Libby
triggers
for
process
such
as
et
al.,
2002).
inflammations
oxidize
in
lipoproteins,
and
dyslipidaemia
associated
with
15
of
atherosclerosis
and
together
with
Indonesia,
the
management
of
AMI
patients
cardiovascular
events
(MACE)
emerging
even
and
effectiveness
approaches (Hollabaugh
by
Kern
et
coronary
procedural
al
myocardial
various
treatment
defined
intervention
with
MACE
(PCI)
following
include
infarction,
percutaneous
death,
emergent
peri-
coronary
16
et al., 2008).
vessel
revascularization
(Steinhubl
et
al.,
decreased
over
time
due
to
the
improvement
of
nonfatal
occasionally
myocardial
soft
revascularization
for
events
infarctions
such
progressive
as
but
also
angina
coronary
or
artery
17
as
clinical
and
procedural
factors.
Risk
insufficiency,
peripheral
vascular
disease),
as
thrombus,
lesion
characteristics
bifurcation),
(urgent/emergent),
and
(length,
procedural
intra-procedural
associated
circumstance
complication
B.
Basic Theory
2.
physiological
concentration
of
18
3.
osmolality
are
sodium,
glucose
and
urea
Major
adverse
clinical
end
hospital
or
including
cardiac
points
within
death,
events
that
7
MI,
occurring
days
or
(MACEs)
of
the
urgent
are
either
PCI.
target
a
in
MACEs
vessel
revascularization.
C.
1.
Null
hypothesis:
osmolality
Hypothesis
An
associate
elevation
with
of
major
on
admission
adverse
cardiac
Alternative
hypothesis:
An
elevation
of
on
19
D.
E.
Theoretical Framework
Conceptual Framework
20
CHAPTER III
METHODOLOGY
A.
previous
study
conducted
in
Department
of
was
done
in
Emergency
Unit
and
Intensive
Study Subjects
21
D.
Sample Size
since
this
sampling
method
is
easier
to
with
criteria
AMI,
both
for
the
STEMI
and
subjects
are:
(1)
whom
are
NSTEMI,
patients
thromboembolism,
(ketoacidosis
treated
and
diabetic
or
with
sepsis,
insulin,
venous
decompensated
diabetics
hyperglycemic
hyperosmolar
22
23
group
is
69
for
group
(subject
with
Study Instrument
that
are
used
in
the
research
clinical
laboratory
and
outcome
data,
(2)
Data
that
is
recorded
are
demographic
data
mellitus,
and
clinical
ischemic
data
heart
including
disease.
systolic
On
and
data
including
(1)
routine
blood
test:
chemical
nitrogen
(BUN)
examination:
and
random
creatinine,
glucose,
(3)
urea
electrolyte
24
hospitalization
cardiovascular
failure,
events
in
namely
cardiogenic
ICCU.
Major
mortality,
shock,
adverse
acute
resuscitated
heart
lethal
Research Variable
variable
is
plasma
osmolality
on
Confounding
variables
in
variables
exclusion
(controllable)
criteria,
these
are
criterias
Confounding
Operational Definition
Plasma osmolality
Plasma
osmolality
is
concentration
measure
of
all
shock,
resuscitated
lethal
arrhythmia
25
shows
mm
elevation
bundle
troponin
I,
branch
block
myoglobin,
and
in
more
than
lead
Cardiac
also
marker
increases
in
26
Chronic
kidney
disease
is
determined
as
elevated
meet
the
needs
of
organ
and
tissue
for
activity
was
recorded.
Sign
of
congestion
is
of
right-sided
distention,
congestion
hepatomegaly,
and
are
jugular
peripheral
venous
edema.
right
upper
quadrant
discomfort
due
to
hepatic
mellitus
disorders
that
compromises
share
the
group
common
of
metabolic
phenotype
of
27
tricuspid
or
pulmonary.
The
confirmation
of
and
by
fibrosis,
vascular
disorganization
architecture,
and
of
the
regenerating
normal
potentially
sterile
life
parts
of
threatening
the
body.
It
complication
is
of
a
an
respiratory
rate
more
than
20
times
per
28
ketoacidosis
is
an
acute,
major,
life-
diabetes.
This
condition
is
complex
disorder
that
occurs
in
mellitus characterized by
plasma
osmolality
>
315
patients
with
diabetes
bicarbonate
>
15
cigarettes
(including
hand
rolled
cigarettes,
29
Malignancy
ability
refers
to
to
spread
cancerous
to
other
cell
that
sites
in
have
the
the
body
Malignant
cells
tend
to
have
fast,
Statistical Analysis
and
stratified
characteristics
by
are
cut
off
of
expressed
osmolality.
as
frequency
with
characteristics
the
are
chi-squared
expressed
as
test.
mean
Continuous
and
standard
multivariate
analysis
of
variables
with
p-value
30
J. Ethical Consideration
Ethical clearance for the research has been obtained
from Medical and Health Research Committee Faculty of
Medicine
research.
Universitas
Gadjah
Mada
for
the
current
31
CHAPTER IV
A. RESULT AND DISCUSSION
discharged.
population
without
This
control
research
only
population,
has
one
because
the
logistic
independent
regression
variable
(MACE)
was
used
represent
because
as
both
binominal
32
significance
0.013.
The
result
shown
in
in
predicting
MACE
occurrence.
After
Odd
Ratio
95% CI
Lower
Upper
2.69
1.21
5.99
p-value
0.015
33
is
good.
The
accepted,
final
which
result
means
that
concluded
with
that
the
the
H0
increase
of
baseline
characteristics
of
the
group
with
variable
to
osmolality
in
predicting
MACE,
to
the
result
of
the
correlation
between
34
Normoosmolal
N=137
Hyperosmolal
N=64
PValue
56.28.9
9.16.8
57.98.7
8.66.5
0.99
0.99
117(85.4)
12.4
61.3
10.2
47(73.4)
50.0
50.0
14.1
0.04
<0.001
0.13
0.43
130.623.5
129.123.6
0.99
80.814.6
78.513.4
0.99
54.7
7.3
2.2
40.6
17.2
0.0
0.06
0.03
0.23
0.06
77.4
22.6
37.1
25.5
82.8
17.2
13.2
29.7
34.3
34.4
7.3
78.1
10.9
3.6
99.3
100.0
100.0
100.0
83.9
53.3
0.0
0.0
0.0
75.514.6
7.8
84.8
4.7
3.1
100.0
100.0
100.0
100.0
76.6
50.0
1.6
1.6
1.6
77.319.1
0.49
N.A.
N.A.
N.A.
0.21
0.66
0.14
0.14
0.27
1.00
12.93.7
257.063.2
1.20.4
14.21.7
13.45.5
12.13.5
241.946.9
1.40.7
13.71.9
18.58.6
0.99
0.99
1.00
0.99
0.99
137.32.9
3.90.5
109.985.6
151.558.9
139.93.5
4.00.6
104.53.8
250.6132.1
0.99
0.99
0.99
0.99
0.06
0.54
0.99
0.56
35
Comparison through all groups was performed with the Chisquared test for the discrete data or the Kruskal-Wallis test for
the
continuous
characteristics.
ACE,
angiotensin-converting
enzyme;BUN;CABG,
coronary
artery
bypass grafting, ischemic heart disease;LMWH, low molecular weight
heparin; NSTEACS, non-segment T elevation acute coronary syndrome;
PCI,
percutaneous
coronary
intervention;
STEMI,
segment
T
elevation myocardial infarction;UFH, unfractionated heparin.
multinominal
comparison
in
regression
table
1,
because
several
from
the
variables
data
show
al.,
2006).
Table
shows
the
comparison
of
36
Hyperosmolal
123
49
15
14
MACE
Non-MACE
37
With MACE
N= 29
60.88.2
8.55.9
Without MACE
N= 172
56.18.8
8.96.8
PValue
0.01
0.02
0.86
24(11.9)
5.0
9.0
1.0
140(69.7)
19.4
48.8
10.4
6.5
1.5
0.0
43.8
9.0
1.5
12.9
1.5
5.5
8.2
66.2
19.4
21.4
42.1
6.0
28.4
1.0
10.9
2.0
0.5
14.4
14.4
14.4
14.4
10.9
6.5
0.5
0.5
0.0
14.11.8
124.524.7
6.5
69.2
7.0
3.0
85.1
85.6
85.6
85.6
70.6
45.8
0.0
0.0
0.5
14.11.8
131.023.2
0.86
<0.001
<0.001
<0.001
0.39
0.39
0.15
0.14
0.27
0.04
0.52
78.215.0
80.414.2
0.98
82.121.4
13.43.9
238.152.5
1.61.0
20.610.4
137.64.0
4.20.8
103.24.2
238.5139.2
70.114.8
12.63.5
254.659.7
1.20.4
14.15.8
138.23.2
3.90.5
109.176.4
173.788.9
0.20
0.09
0.15
0.55
0.02
0.34
0.70
0.97
0.41
0.18
0.61
0.41
0.53
0.99
0.48
0.97
0.15
0.98
0.39
0.81
38
From
comparison
table
above
there
are
some
analyse
those
variables
since
they
may
have
Odd
Ratio
95% CI
Lower
Upper
1.06
1.02
1.11
p-value
0.009
Odd
Ratio
95% CI
Lower
Upper
0.99
0.93
1.05
p-value
0.732
Odd
Ratio
95% CI
Lower
Upper
1.01
0.81
1.26
p-value
0.91
Odd
Ratio
95% CI
Lower
Upper
1.11
1.06
1.17
p-value
0.00
39
Table 8. Binary logistic analysis of variables with pvalue less than 0.05
Variable
Odd
Ratio
Lower
Upper
BUN
1.13
1.06
1.19
0.00
Age
1.07
1.01
1.13
0.01
Onset
0.95
0.88
1.03
0.19
Osmolality
2.69
1.21
5.99
0.01
Hemoglobin
1.25
0.98
1.61
0.07
The
main
95% CI
finding
of
this
p-value
logistic
regression
adjusting
inclusion
and
exclusion
criteria.
with
the
result
of
strong
association
between
there
are
to
MACE,
dyslipidemia.
cardiovascular
There
also
some
such
is
outcomes
a
in
as
variables
sex
and
research
patients
that
show
history
analyzing
with
of
about
type
40
about
the
relation
between
metabolic
intolerance,
arterial
obesity,
dyslipidemia,
and
size
the
of
and
infarction
hypertension,
central
microalbuminuria;
gender,
stated
that
the
female
MACE
(Kranjcec
&
Altabas,
2012).
From
this
haemoglobin,
and
BUN
have
significance
under
41
cardiac
related
disease,
age
is
an
important
predictor
based
on
analysis
result
from
MACE,
the
average
time
from
onset
until
the
long
the
patient
delayed
will
increase
last
variable
that
may
influence
MACE
42
is
also
study
predicting
patient.
discussing
survival
Patients
hypotension
that
rate
with
needs
about
in
BUN
chronic
high
serum
intervention
independently
heart
failure
BUN
develop
(Klein
et
al.,
mg/dl
was
associated
with
long-term
mortality
43
CHAPTER V
CONCLUSION AND SUGGESTION
A.
There
is
strong
Conclusion
and
independent
association
Further
test
with
Suggestion
adding
more
subjects
is
Analysis
in
correlation
from
each
aspect
of
multi
variation
analysis
for
predictor
is
44
REFERENCES
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Cardiovascular
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viewed
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30
2014,
http://www.who.int/mediacentre/factsheets/fs317/en/
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Arora,
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2013,
Intensive
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Hariawan
H,
Puspitawati
buruk
kardiovaskular
sindroma
koroner
selama
akut.
perawatan
Laporan
47
Problem
With
Composite
End
Points
in
DM,
Braundwald,
E,
Fauci,
AS,
Hauser,
SL,
H,
Kakefuda,
Y,
Ishibashi,
M,
Abe,
D,
for
long-term
risk
stratification
in
48
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Board
Review
Book,
Mortality
Syndrome
Among
and
Filtration
Patient
Normal
to
Rates,
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Journal
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of
the
or
Changes
In
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Function
During
Glucose
and
Mortality
In
Elderly
49
Patients
Hospitalized
Infarction:
Without
Implication
Recognized
With
Acute
for
Patients
Diabetes,
Myocardial
With
Circulation,
and
vol.
D,
Influencing
Altabas,
Infarct
2012,
Size
in
Metabolic
Patients
Syndrome
With
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of
Disease,
9thedn,
Elsevier,
Canada.
Levin, A, Singer, J, Thompson, CR, Ross, H, Lewis M
1996, Prevalent LVH in the Predialysis Population:
Identifying
Opportunities
for
Intervention,
50
LS
2011,
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of
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Disease,
&
Wilkins,
Philadelphia.
Longo, D, Fauci, A, Kasper, D, Hauser, S, Jameson, J
&Loscalzo,
2008,
Harrisons
Principles
of
SJ,
Papadaski,
M,
Rabow,
MW
2014,
CURRENT
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Ready
for
Prime
Time?,
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for
Cardiopulmonary
51
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RM.
2005,
Hyponatremia
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Huber,
K,
Wiess,
TW,
2014,
Plasma
acute
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Pourmoghaddas,
M,
Hadizadeh,
M,
2013,
Factors
percutaneous
affecting
coronary
outcome
intervention
of
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primary
acute
52
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Effects
on
the
Cardiovascular
Measured
Correlates
Cardiac
With
Event
Intervention.
Platelet
Reduced
After
Results
Risk
Inhibition
of
an
Percutaneous
of
the
GOLD
Adverse
Coronary
(AU-Assessing
RM
Species
&
Schiffrin,
in
Hypertension,
EL
Vascular
2004,
Biology:
Histochemistry
Reactive
and
Oxygen
Implication
Cell
in
Biology,
APPENDIX
Table 9
MACE * Osmolable Cross tabulation
Osmolable
Hyper
MACE
No
Count
62
83
Expected Count
24,1
58,9
83,0
% within MACE
25,3%
74,7%
100,0%
% within Osmolable
72,4%
87,3%
83,0%
% of Total
21,0%
62,0%
83,0%
-,6
,4
17
Expected Count
4,9
12,1
17,0
% within MACE
47,1%
52,9%
100,0%
% within Osmolable
27,6%
12,7%
17,0%
8,0%
9,0%
17,0%
Std. Residual
1,4
-,9
Count
29
71
100
Expected Count
29,0
71,0
100,0
% within MACE
29,0%
71,0%
100,0%
100,0%
100,0%
100,0%
29,0%
71,0%
100,0%
Count
% of Total
Total
Total
21
Std. Residual
Yes
Normo
% within Osmolable
% of Total
Table 10
Tests of Normality
a
Kolmogorov-Smirnov
osmol
MACE
Shapiro-Wilk
Statistic
Df
Sig.
Statistic
df
Sig.
,529
137
,000
,346
137
,000
,474
64
,000
,525
64
,000
N
Included in Analysis
Missing Cases
Total
Percent
201
100,0
,0
201
100,0
53
Unselected Cases
Total
,0
201
100,0
Table 11
Dependent Variable Encoding
Original Value
Internal Value
Experiencing MACE
Table 12
Categorical Variables Codings
Parameter
coding
Frequency
osmol
(1)
137
1,000
64
,000
Table 13
a,b,c
Iteration History
Coefficients
Iteration
Step 0
-2LL
Constant
169,332
-1,423
165,924
-1,742
165,887
-1,780
165,887
-1,780
Table 14
54
Classification Table
a,b
Predicted
MACE
Not
experiencing
Experiencing
Percentage
MACE
MACE
Correct
Observed
Step 0
MACE
172
100,0
29
,0
Overall Percentage
85,6
Table 15
Variables in the Equation
B
Step 0
Constant
-1,780
S.E.
Wald
,201
df
Sig.
78,644
,000
Exp(B)
,169
Table 16
Variables not in the Equation
Score
Step 0
Variables
osmol(1)
Overall Statistics
df
Sig.
6,174
,013
6,174
,013
55
Table 17
a,b,c,d
Iteration History
Coefficients
Iteration
Step 1
-2LL
Constant
osmol(1)
165,218
-1,063
-,529
160,224
-1,180
-,888
160,081
-1,184
-,985
160,081
-1,184
-,989
160,081
-1,184
-,989
Table 18
Omnibus Tests of Model Coefficients
Chi-square
Step 1
df
Sig.
Step
5,806
,016
Block
5,806
,016
Model
5,806
,016
Table 19
Model Summary
Step
1
Nagelkerke R
Square
Square
-2 Log likelihood
160,081
,028
,051
Table 20
Hosmer and Lemeshow Test
Step
1
Chi-square
,000
df
Sig.
0
56
Table 21
Classification Table
Predicted
MACE
Not
experiencing
Experiencing
Percentage
MACE
MACE
Correct
Observed
Step 1
MACE
Not experiencing
MACE
172
100,0
29
,0
Experiencing MACE
Overall Percentage
85,6
Table 22
Variables in the Equation
95% C.I.for
EXP(B)
B
Step
1
osmolal
Constan
t
S.E.
Wald
df
Sig.
Exp(B)
,989
,408
5,874
,015
2,690
-2,173
,282
59,358
,000
,114
Lower
1,208
Upper
5,986
57
Table 23
Variables in the Equation
95% C.I.for
EXP(B)
B
Step
1
S.E.
Wald
df
Sig.
Exp(B)
Lower
Upper
Umur
,002
,020
,008
,928
1,002
,963
1,042
Onset
-,036
,027
1,798
,180
,964
,915
1,017
HB
-,080
,098
,666
,415
,923
,762
1,119
,108
,030
13,272
,000
1,114
1,051
1,181
-,442
,466
,901
,343
,643
,258
1,601
-,720
2,218
,105
,745
,487
BUN
MACE(1
)
Constan
t
Table 24
Variables in the Equation
95% C.I.for
EXP(B)
B
Step
1
BUN
Consta
nt
S.E.
Wald
df
Sig.
Exp(B)
,102
,026
15,464
,000
1,108
-3,478
,504
47,598
,000
,031
Lower
1,053
Upper
1,166
Table 25
Variables in the Equation
95% C.I.for
EXP(B)
B
Step
1
HB
Constan
t
S.E.
Wald
df
Sig.
Exp(B)
,013
,112
,014
,905
1,013
-1,968
1,589
1,533
,216
,140
Lower
,814
Upper
1,262
58
Table 26
Variables in the Equation
95% C.I.for
EXP(B)
B
Step
1
Onset
Constan
t
S.E.
Wald
df
Sig.
Exp(B)
-,011
,031
,117
,732
,989
-1,687
,334
25,431
,000
,185
Lower
Upper
,931
1,052
Table 27
Variables in the Equation
95% C.I.for
EXP(B)
B
Step
1
Umur
Constan
t
S.E.
Wald
df
Sig.
Exp(B)
Lower
,062
,024
6,730
,009
1,064
-5,386
1,442
13,950
,000
,005
Upper
1,015
1,114
Table 28
Variables in the Equation
95% C.I.for
EXP(B)
B
Step
1
S.E.
Wald
df
Sig.
Exp(B)
Lower
Upper
BUN
,121
,030
16,127
,000
1,129
1,064
1,198
Umur
,068
,027
6,159
,013
1,070
1,014
1,128
Onset
-,051
,039
1,724
,189
,950
,881
1,025
,227
,128
3,133
,077
1,255
,976
1,613
-10,532
2,917
13,039
,000
,000
HB
Consta
nt
59