Download Short-term Survival after Acute Myocardial Infarction Predicted by

Short-term Survival after Acute
Myocardial Infarction Predicted by
Hemodynamic Parameters
By PIETER D. VERDOUW, Ph.D., FRANS HAGEMEIJER, M.D.,
WILLEM G.
VAN
AND
DORP, B. S., ADRIE VAN DER VORM, R. N.,
PAUL G. HUGENHOLTZ, M.D.
SUMMARY
In the acute phase of myocardial infarction, short-term prediction of the likelihood of survival helps the
physician choose the appropriate therapy for individual patients. Of 122 patients admitted to the coronary
care unit of the Thoraxcenter, University Hospital, Rotterdam, with an acute myocardial infarction, 16 died
from pump failure. In these and the 106 survivors, the predictive value of peripheral systolic (SP) and
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diastolic (DP) blood pressure, pulmonary capillary wedge pressure (PCW), mixed venous oxygen saturation
(MVO2sat) in the pulmonary artery and heart rate (HR), both alone and in combination, was evaluated at
the time of admission and 24 hours later.
When, at admission, (DP X MVO2sat)/PCW exceeded 250%, 97/99 patients survived, whereas values
below 250% were associated with death in 14/23. All other parameters, taken alone or in other combinations, showed less discriminatory power. The mean value of this index in survivors (549%) was
statistically different (P < 0.001) from the mean value in nonsurvivors (183%). Twenty-four hours later all
survivors with admission values lower than 250% had an improved index. Of the 14 nonsurvivors with admission values lower than 250%, seven had already died, and in seven others the index had decreased still
further. Linear discriminant analysis showed that (0.024 SP 0.217 PCW + 0.234 MVO2sat) was the most
powerful prognostic index at the time of admission; its time course did not provide a more effective prediction of ultimate fatality than (DP X MVO2sat)/PCW.
Determination of (DP X MVO2sat)/PCW in patients hospitalized for acute myocardial infarction
provides a reliable prognosis for short-term patient survival. Its practical value in guiding patient management, more particularly for initiating mechanical circulatory assistance or for emergency surgery, must be
further assessed.
-
MYOCARDIAL INFARCTION (MI) in man leads
to death primarily by one of three mechanisms:
primary ventricular fibrillation, heart rupture, and
cardiogenic shock. Coronary care units (CCU) were
initiated primarily to prevent mortality due to electrical instability of the myocardium,1 2 and have been
extremely successful in this endeavor: primary ventricular arrhythmias are no longer a major cause of
death in the CCU. Cardiac ruptures are notoriously
unpredictable: the patient is usually well until his
sudden demise,3 and even emergency surgery comes
too late.4 Pump failure resulting from the loss of more
than 40% of the muscle mass of the left ventricle5' 6
may sometimes be reversed by timely institution of
circulatory assist,7' 8 and/or by emergency heart surgery.9 10 This last procedure, however, carries a
definite risk itself 1' and should be used only if phar-
macological therapy is unlikely to prevent a fatal outcome. A further reduction of mortality will therefore
be achieved only if choice of treatment in critically ill
patients is related to the likelihood of short-term survival.
Cardiogenic shock in MI is characterized by a low
systemic blood pressure, by sinus tachycardia, by high
left ventricular filling pressures and by a low pulmonary artery oxygen saturation.12-14 Continuous bedside monitoring of pulmonary artery pressures and of
mixed venous oxygen saturation has been possible
since the advent of balloon-tipped flow-directed
catheters,'1217 while rhythm monitoring and regular
measurement of arterial blood pressure have long
been standard procedures.
Any effective treatment for cardiogenic shock must
be done very early in order to salvage as much viable
myocardium as possible. The present study was
therefore undertaken to investigate whether appropriate hemodynamic monitoring could predict impending fatality in acute MI. To this end a prospective study was undertaken involving 122 patients
hospitalized for acute MI: 16 of these died in cardiogenic shock and 106 patients survived their stay in
From the Thoraxcenter, Erasmus University, Rotterdam, The
Netherlands.
Address for reprints: Thoraxcenter, Erasmus University, P.O. Box
1738, Rotterdam, The Netherlands.
Received September 16, 1974; revision accepted for publication
April 11, 1975
Circulation, Volume 52, September 1975
413
VERDOUW ET AL.
414
the CCU. All patients included had sustained an acute
MI according to WHO criteria. In all 16 patients dying in cardiogenic shock, autopsy confirmed the
clinical diagnosis of extensive myocardial necrosis.
Materials and Methods
Patients
The present study was carried out on 122 consecutive
patients admitted to the CCU less than 24 hours after the
first symptoms of their acute MI. Patients who subsequently
died of cardiac rupture were excluded from this study.
Ninety-seven patients were male and 21 female; 11 men
and 5 women died; the mean age of the survivors was 58.5
and of the nonsurvivors 63.9; the difference was not
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statistically significant, and there was a marked overlap for
both groups.
There was no difference in admission delay (median: 4
hours) between survivors and nonsurvivors. Most patients
were first seen by a general practitioner and received pain
sedation with opiates and prophylactic lidocaine (100 mg
i.v. or i.m.) before being sent to the hospital. At home
bradyeardia was treated with atropine (0.25-0.50 mg i.v.);
no patient was given digitalis glycosides; furosemide 40 mg
i.v. was administered for pulmonary edema; maintenance
therapy prior to infarction was similar in both groups of
patients.
After admission to the CCU, management was identical
in all patients, except in cases of left ventricular failure
where ouabain and furosemide were given, guided by electrocardiographic monitoring, diuresis, and left ventricular
filling pressures. All patients received intravenous lidocaine
(2 mg/min). Cardiogenic shock was treated with a variety of
drugs. 'I
A typical history and an abnormal electrocardiogram were
considered sufficient indication for hemodynamic monitoring; this was initiated within 30 minutes after arrival in the
CCU. With the exception of lidocaine and oxygen, no
medication was given during this period of time. When
serial enzyme changes and the evolution of the electrocardiogram failed to confirm the admission diagnosis of MI, the
patient was excluded~from the study. No patient was on
respiratory assistance.
Survival
assessed during the usual four to five day
discharge from the CCU, patients
were followed until they went home two to three weeks after
their acute MI.
was
stay in the CCU; after
Technique
From an antecubital vein, a 5F Swan-Ganz catheter was
positioned in the pulmonary artery.'5 Pulmonary capillary
wedge pressure (PCW) was taken to reflect mean left ventricular filling pressure.13-17 Mixed venous oxygen saturation
(MVO2sat) was determined on a 3 ml blood sample taken
from the pulmonary artery and measured in vitro by
hemoreflectometry (American Optical). 19
Heart rate (HR) was counted from the electrocardiographic monitoring lead at the time of the hemodynamic
measurements, systolic and diastolic blood pressure (SP and
DP, respectively) were measured with a sphygmomanometer; in the presence of cardiogenic shock, systemic
arterial pressures were measured by means of an indwelling
arterial catheter connected to a Statham P23dB manometer
mounted at the bedside. In six patients all systemic arterial
pressures were thus measured invasively; in ten others early
measurements were made with a cuff and arterial catheterization carried out only upon hemodynamic deterioration.
Measurements were performed at four-hourly intervals.
Particular attention was paid to pulmonary artery pressure
recordings. Whenever the quality of the tracing was
technically inadequate this information was excluded from
the study. In critically ill patients where pulmonary artery
pressures were regarded as vitally important in guiding
patient therapy, unreliable pressure tracings were considered an indication for replacing the Swap-Ganz catheter
with a new one. This was not done in patients doing well
hemodynamically.
Measurements were performed at least 15 minutes after a
serious ventricular dysrhythmia. Oxygen administration was
also discontinued during at least 15 minutes prior to oxygen
saturation determinations.
Data Analysis
For this study a comparison was made between survivors
and nonsurvivors by utilizing only data for HR (min-'), SP
(mm Hg), DP (mm Hg), PCW (mm Hg) and MVO2sat (%),
compiled on admission and 24 hours later, although many
more data points were available. Various combinations of
these parameters were also evaluated: DP/PCW; MVO2sat/
PCW; (SP X MVO2sat)/PCW; (DP X MVO2sat)/PCW;
and (DP x MVO2sat)/(PCW X HR). Student's t-test was
used to compare the two groups. P values exceeding 0.05
were considered to be statistically not significant (NS). In
addition threshold values were determined below which survival was unlikely.
Linear discriminant function analysis was used to find out
if any linear combination of two or three of the following
parameters would provide a better discrimination: age, HR,
SP, DP, PCW, and MVO,sat. The number of patients
wrongly classified by any of these combinations were computed.
Results
Observations on Admission to the CCU
All measurements are given in detail in tables 1 and
2. Heart rate and diastolic blood pressure did not
allow any discrimination between survivors and nonsurvivors. Mean SP was significantly higher in survivors than in nonsurvivors (P < 0.005), but overlap
was such that measuring SP on admission predicted
survival only when it was in excess of 150 mm Hg.
There was a significant difference (P < 0.001) in
PCW between survivors and nonsurvivors (fig. 1),
although there was a considerable overlap as eight out
of 18 patients with a PCW > 20 mm Hg survived. No
deaths occurred in the 66 patients with a PCW < 15
mm Hg at the time of admission (table 2).
Similarly, the difference in MVO2sat between survivors and nonsurvivors was significant (P < 0.001).
When MVO2sat > 70%, 58 out of 58 patients survived, while in eight out of the nine with a
MVO2sat < 55% there was a fatal outcome. When
MVO2sat was between 55 and 70% at the time of admission death occurred in eight of 55 patients.
A combination of parameters improved the accuracy of prognosis. DP/PCW > 4.25 suggested surCirculation, Volume 52, September 1975
SHORT-TERM SURVIVAL AFTER MI
415
Table 1
Values of Individual Hemodynamic Parameters for Survivors and Nonsurvivors at Admissior
Survivors
(N = 106)
Nonsurvivors
(N = 16)
Mean
SD
Parameters
Mean
SD
DP/PCW
(SP X MVO2sat)/PCW (%)
(DP X MVO2sat)/PCW (%)
(DP X MVO2sat)/(PCW X HR) (%/min.)
0.024 SP - 0.217 PCW + 0.234 MVO2sat -13.1
84.2
134.7
84.9
13.0
68.1
8.47
910
549
6.31
3.31
18.2
26.6
16.6
5.4
6.2
6.76
680
334
3.79
2.34
HR (beats/min)
SP (mm Hg)
DP (mm Hg)
PCW (mm Hg)
MVO2sat (%)
90.8
107.8
73.1
22.4
51.4
3.39
270
183
2.07
-3.31
P
17.4
23.9
16.1
6.0
12.9
i 0.99
128
90.0
0.98
3.86
NS
<0.005
NS
<0.001
<0.001
<0.005
<0.001
<0.005
<0.001
<0.001
Abbreviations: HR = heart rate; SP = systolic pressure; DP = diastolic pressure; PCW = pulmonary
capillary wedge pressure; MVO2sat = mixed venous oxygen saturation; SD = standard deviation; NS =
not significant.
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vival in 94/95 observations, and MVO2sat/PCW
greater than 3.75%/mm Hg predicted survival in
89/91. The same was true for (DP MVO2sat)/ PCW
greater than 250%, as survival took place in 97/99,
and (SP MVO2sat)/PCW > 400%, where survival
occurred in 94/96. When all four parameters were
combined, (DP
MVO2sat)/(PCW x HR) >
3.2%/min correctly predicted survival in 96/97.
Linear discriminant analysis showed that the most
powerful combination of parameters was 0.024SP
0.217 PCW + 0.234 MVO2sat (tables 1 and 2), which
predicted survival in 96/99.
Barring reinfarction and heart rupture, initial
hemodynamic observations above the threshold levels
suggested ultimate survival. In critically ill patients
these threshold values, measured at the time of admission, defined a group in which a roughly 50%
probability of fatal outcome existed.
therefore discarded as being unreliable.
Analysis of the trends for HR, DP, SP, and MVO2sat
showed that none of these had changed significantly
since admission in patients still alive at that moment.
Only PCW had decreased significantly (P < 0.001).
Moreover in the group of 66 survivors, ten had an admission PCW > 20 mm Hg, while 24 hours later only
one patient still presented this elevated left ventricular filling pressure.
When the parameters were combined, mortality
could be forecasted more precisely. The most powerful prognostic index for immediate survival was the
trend of (DP X MVO2sat)/PCW of the 23 patients at
risk when its value was 250% or less at admission (fig.
2). All nine survivors had an improvement in this index, whereas all nonsurvivors showed a deterioration,
except for two who evidenced transient signs of
amelioration. Two of 57 survivors with an index exceeding 250% at the time of admission showed a fall
in index to less than 250% by 24 hours. In both instances this reflected a slight drop in diastolic blood
pressure. The trend of (SP
MVO2sat)/PCW (table
3) was only slightly less effective in predicting im-
X
X
X
Observations 24 Hours after Admission
By 24 hours after admission 7/16 in the nonsurvivor
had died. The PCW tracings were no longer of
sufficient quality in 40 survivors and these data were
group
X
,able 2
Threshold Values of Various Hemodynamic Parameters Providing Prognosis of Survival or Fatality at the Time of Admission
Parameters
SP (mm Hg)
PCW (mm Hg)
MVO2sat (%)
Threshold for
survival
>150
< 15
> 70
> 4.25
> 3.75
DP/PCW (mm Hg/mm Hg)
MVO2sat/PCW (%/mm Hg)
(SP X MVO2sat)/PCW (%)
_400
.250
(DP X MVO2sat)/PCW (%)
> 3.2
(DP X MVO2sat)/(PCW X HR) (%/min)
0
0.024SP - 0.217PCW + 0.234MVO2sat -13.1
S
(N
=
29
66
58
94
89
94
97
96
96
NS
106)
(N = 16)
1
0
0
1
2
2
2
1
3
Threshold for
fatality
<100
> 20
< 55
4.25
3.75
<400
<250
< 3.2
< 0
<
<
S
(N
=
NS
106)
7
8
1
12
17
12
9
10
10
(N = 16)
5
10
8
15
14
14
14
15
13
Abbreviations: S = survivors; NS = nonsurvivors; HR = heart rate; SP = systolic pressure; DP = diastolic pressure; PCW
= pulmonary capillary wedge pressure; MVO2 = mixed venous oxygen saturation.
Circulation, Volume 52, September 1975
VERDOUW ET AL.
416
E:E
admission
E
admission
after
admission
after
24 hours
a f ter
adm iss ion
24 hours
24 hours
o
C-,
of ter
24 hours
*---l
*0
40 -
1250
35-
-
3025-
* @
1000-
:-
:
20-
11
9
0
15
--
a
750105
..
-
00
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*- *
0
500-
non-survivors
survivors
to
*.
Figure 1
.1*.
Admission values for PCW of 106 survivors (first column) and 16
nonsurvivors (third column). The difference in PCW for both
groups is statistically significant (P < 0.001). However, the most
significant feature is that none of the 66 patients with admission
PCW < 15 mm Hg died. The second and fourth column give the
PCW for the patients from whom these values could still be obtained 24 hours later (66 survivors and 9 nonsurvivors). Only 1/12
survivors with an admission PCW > 20 mm Hg still showed such a
high value 24 hours later.
250-
a
.9
survivors
non- survivors
Figure 2
mediate survival: 10/12 increased but only 6/12
reached the threshold level of 400%.
The most powerful index obtained by linear discriminant analysis (0.024 SP - 0.217 PCW + 0.234
MVO2sat) was as effective as the two others (table 3).
These indices showed transient increases in some
patients who ultimately died. On the other hand, a
decrease in either (DP x MVO2sat)/PCW or (0.024
SP - 0.217 PCW + 0.234 MVO2sat), despite therapy,
correctly indicated imminent patient demise.
The trends in all other combined indices showed no
greater discriminatory power.
Table 3
Trend of Hemodynamic Prognostic Indices in Wrongly
Classified Survivors and Nonsurvivors 24 Hours after Admission
(DP x MVO2sat)/PCW at admission for 106 survivors and 16
nonsurvivors (first and third column respectively). There is a significant difference between the two groups (P < 0.005). The threshold
values above which survival is very likely is at 250% (97 of 99
patients). For all patients with an index < 250% at the time of admission and still alive 24 hours later the trend of
(DP x MVO2sat)/PCW is indicated by a straight line. All survivors
show increased values, whereas the index had deteriorated
further in 4/6 nonsurvivors.
even
Patient Survival
All 106 MI patients surviving their stay in the CCU
discharged from the hospital two to three weeks
after their heart attack. Death from cardiogenic shock
occurred in seven patients within 24 hours, in eight
others on the second day and in one on the third day.
were
Discussion
Index
#
(SP X MVO2sat)/PCW
(DP X MVO2sat)/PCW
0.024 SP - 0.217 PCW +
0.234 MVO2sat- 13.1
12
S
f
NS*
9
10
9
0
9
9
3
2
6
7
10
10
0
9
3
6
2
*Still alive 24 hours after admission.
Abbreviations: S = wrongly classified survivors; NS wrongly classified nonsurvivors; T = increase; T = decrease.
Many indices have been proposed to predict
survival after acute myocardial infarction.2126 Most
parameters used in calculating these indices such as
age, sex, location of the infarct, etc. are factors which
cannot be influenced by therapy. Heart rate and
hemodynamic parameters, on the contrary, are variables reflecting pump function, and improvement or
deterioration during medical or surgical intervention
Circulation, Volume 52, September 1975
SHORT-TERM SURVIVAL AFTER MI
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are measurements of the degree of left ventricular
failure and the likelihood of a fatal outcome. The predictive value of these measurements is implied in all
the aforementioned indices.2 24
Hemodynamic parameters are relatively easy to
measure, and routine determinations possess sufficient
accuracy; any combination of parameters can be
calculated rapidly and used in patient management,
as they immediately reflect changes of left ventricular
function.
Sphygmomanometric determinations of systemic
blood pressure are reasonably accurate in normotensive and hypertensive patients; in shock, however, an
indwelling arterial catheter must be used, positioned
in the aorta because vasoconstriction renders
peripheral blood pressure determinations unreliable,
not reflecting the true performance of the left ventricle. No complications were encountered in the limited
experience presented here; however, few patients in
this group survived. Very few complications were
reported from an intensive care unit where radial
artery catheterization was performed routinely.26 In
the gray area, where patient survival is not a certainty,
accurate determination of systemic blood pressure
with an indwelling catheter is to be recommended.
Only invasive techniques can be used for measuring
pulmonary artery pressures and mixed venous oxygen
saturation. At the site of incision inflammation is usual
and after a few days the indwelling catheter produces
sterile phlebitis. Infections due to the procedure are
very rare and reflect poor technique, as does the occurrence of ventricular dysrhythmias during the
passage of the catheter tip through the right ventricle.
A more worrisome complication is the occurrence of
fan-shaped pulmonary shadows in 10% of 200 consecutive patients monitored with the Swan-Ganz
catheter,27 probably caused by pulmonary emboli or
by thrombosis of the pulmonary artery; similar complications have been described by others.28 29 Since we
started using systematic anticoagulation with heparin,
a prospective monitoring of this complication shows
that incidence decreased dramatically, thereby indicating that clotting, and not prolonged positioning
of the catheter in wedge position, is the cause.
Hemodynamic monitoring of the critically ill is not
a novelty. Various on-line bedside computerized
monitoring systems have been described in order to
assess patient response to therapy.30' 31 In cardiogenic
shock due to myocardial infarction a combination of
arterial diastolic pressure, stroke index and central
blood volume was found to be a reliable indicator of
the severity of shock31 and could be used in patient
management. A further refinement of this method32
takes into account not only hemodynamic parameters
but also metabolic factors such as blood gasses'2' 13 and
Circulation, Volume 52, September 1975
417
arterial lactate concentrations reflecting tissue perfusion deficits.
Quite a different approach consists in calculating
left ventricular contractility without left ventricular
catheterization. This was done33 by measuring
systemic diastolic blood pressure, left ventricular filling pressure, and the pre-ejection period measured
from the phonocardiogram, the electrocardiogram,
and carotid artery pulse tracings. A careful analysis34
of these data showed that the pre-ejection period
added very little to the prognostic significance of this
index, so that when omitted the method was reduced
to a simple determination of two factors, reflecting
mainly preload and afterload.
This was the starting point of the present investigation: estimating left ventricular function by
measuring preload and afterload, taking into account
heart rate and mixed venous oxygen saturation,12
which reflects the adequacy of systemic blood flow in
relation to tissue oxygen need.
Early results3" of this investigation showed that
hemodynamic measurements at the time of admission
did not provide sufficient information on patient
prognosis. Different combinations of preload, afterload, and MVO2sat correctly reflect the hemodynamic state of the patient at that moment. A poor
pump function was found in a group with a 50% mortality; a more precise prognosis was not possible at the
time of admission because the effectiveness of patient
therapy could not be foreseen. An improvement of
hemodynamic parameters should precede obvious
clinical amelioration and this was observed in the
present investigation.
Linear discriminant analysis heavily weighted
MVO2sat over either SP or PCW; however, all three
were needed to evaluate hemodynamic improvement
or deterioration. MVO2sat and PCW are independent
variables;12 the importance of MVO2sat indicates the
usefulness of its on-line monitoring by means of
fiberoptic catheters.13
The question remains whether invasive monitoring
is required in these patients or whether a clinician at
the bedside using auscultation and chest radiography
would not be just as effective. Auscultation alone is insufficient as it does not permit detection of interstitial
edema and must be associated with frequent chest
roentgenograms if the evolution of this stage of
pulmonary edema is to be evaluated. Furthermore,
radiological changes are much slower in their onset or
disappearance than changes in left ventricular filling
pressure, or even changes in P terminal forces.36
Pulmonary capillary wedge pressure must remain
significantly elevated for prolonged periods of time
before alveolar flooding occurs, manifesting clinically
as moist rales. Conversely, rales may still be present
VERDOUW ET AL.
418
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even though PCW has returned to normal. This
apparent discrepancy between auscultation, radiography, and hemodynamic monitoring merely reflects the time required for the reabsorption of excess extravascular lung fluids, a process that may take
12 to 24 hours, even when left ventricular filling
pressure has returned to normal as the result of
treatment. 36
Hemodynamic monitoring therefore is a jump from
a qualitative evaluation to a quantitative measurement of left ventricular function; furthermore, the
effectiveness of therapeutic interventions can be
determined immediately. Our data suggest that when
pump function remains good during the first few
hours after infarction, cardiogenic shock is unlikely to
develop unless a new coronary event supervenes.
Early therapy may however prevent the onset of the
vicious cycle of cardiogenic shock and the loss of
ischemic myocardium. The failure to observe instances of pump-failure late after the acute episode
favors this interpretation.
The severity of pump failure is clearly related to the
extent of the necrotic area.5`7 Serial enzyme determinations,25' 37 radionuclide imaging of the heart3' 39
and precordial ST-segment mapping40 can be used to
measure infarct size. Recently evidence has been accumulating40-42 that medical intervention may influence the extent of myocardial necrosis. Of these
techniques, only ST-segment mapping may be used
directly in patient management to measure the degree
of ischemia rather than pump function. The information obtained by this method, measuring degree of
ischemia, may complement the findings derived from
hemodynamic monitoring, which measures pump
function.
All nonsurvivors ultimately died in class IV cardiogenic shock according to the classification used by
the myocardial infarction research units (MIRU).14
This classification is based on clinical symptoms and
hemodynamic parameters, including the cardiac output. The index presented here combines quantitative
information required to make this classification (except the cardiac output) and in addition takes into account MVO2sat. The aim is for a trend-analysis of an
index combining significant and independent
variables for assessing left ventricular pump function;
in the future, this should include the cardiac output,
urine production, plasma colloidosmotic pressure43
reflecting changes in blood volume, and arterial lactate content.32 The clinical usefulness of this or similar
indices will have to be assessed in critically ill patients.
Carefully controlled studies should determine when
mechanical circulatory assist and emergency surgery
should be initiated. Conversely the findings from such
studies should provide the clinician with evidence
when to desist from further massive support therapy
since the remaining viable muscle mass cannot support life either on a short or on a long term basis.
Acknowledgment
We wish to thank the nursing staff of the coronary care unit of the
Thoraxcenter, Academic Hospital Dijkzigt, Rotterdam: without
their active cooperation in accurately recording this important information day and night, the present investigation could not have
been brought to fruition.
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Short-term survival after acute myocardial infarction predicted by hemodynamic
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P D Verdouw, F Hagemeijer, W G Dorp, A V Vrom and P G Hugenholtz
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Circulation. 1975;52:413-419
doi: 10.1161/01.CIR.52.3.413
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