Download Left ventricular ejection fraction after acute coronary occlusion in

LABORATORY INVESTIGATION
VENTRICULAR PERFORMANCE
Left ventricular ejection fraction after acute
coronary occlusion in conscious dogs: relation to
the extent and site of myocardial infarction
RICKY M. SCHNEIDER, M.D., ALAN CHU, M.D., MAKOTO AKAISHI, M.D.,
WILLIAM S. WEINTRAUB, M.D., KENNETH G. MORRIS, M.D.,
AND FREDERICK R. COBB, M.D.
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ABSTRACT The change in left ventricular radionuclide ejection fraction after acute occlusion of the
left anterior descending (LAD) or circumflex (LC) coronary artery was compared with the ultimate
histologic extent of myocardial infarction in conscious dogs. The acute change in ejection fraction
correlated with size of infarction in 14 dogs with occlusions of the LAD coronary artery (r = .89, y =
1.12x + 14.2) and in 27 dogs with occlusions of the LC coronary artery (r = .71, y = 0.73x + 7.9);
the slope of the regression equation was greater (p < .05) for those with LAD than for those with LC
occlusions. Multivariate analysis revealed no independent contribution of left ventricular weight, the
subendocardial extent of infarction, or change in heart rate to the acute change in ejection fraction.
These data indicate that the decrease in ejection fraction after coronary occlusion is determined
primarily by the size of the ischemic area, which also determines size of infarction. In dogs instrumented over a long term, infarcts in the LAD myocardial distribution result in greater decreases in ejection
fraction than infarcts of comparable size in the LC distribution.
Circulation 72, No. 3, 632-638, 1985.
RESULTS OF A VARIETY of clinical studies support
the concept that left ventricular ejection fraction is a
measure of ventricular performance that is related to
the extent of myocardial infarction. 1-' In conscious dogs
linear relationships exist between changes in global and
regional ejection fraction measured by radionuclide angiography after acute coronary occlusion and the extent
of myocardium with reduced regional blood flow.6 Regional myocardial blood flow after coronary occlusion
correlates inversely with the extent of histologic necrosis.8' 9 Thus, the acute change in ejection fraction
would also be expected to correlate with ultimate infarct size.
Previous studies that have examined relationships
From the Department of Medicine, Division of Cardiology, Duke
University Medical Center and the Veterans Administration Medical
Center, Durham, and the Mid-Atlantic Heart and Vascular Institute,
Department of Medicine, Division of Cardiology, Presbyterian-University of Pennsylvania Medical Center, Philadelphia.
Supported by National Research Services Award grant HL07 101 and
Research grant HL 18537 from the National Institutes of Health, Bethesda, by the Medical Research Service of the Veterans Administration
Medical Center, Durham, and by a grant from the Mabel Pew Myrin
Trust.
Address for correspondence: Ricky M. Schneider, M.D., Mid-Atlantic Heart and Vascular Institute, Division of Cardiology, PresbyterianUniversity of Pennsylvania Medical Center, 51 N. 39th St., Philadelphia, PA 19104.
Received June 8, 1984; revision accepted May 23, 1985.
632
between measurements of left ventricular performance
and extent of infarction '-5 did not consider the influence of anatomic variables such as the location of the
infarct and its size relative to the left ventricular
weight. The goal of the present study was to assess the
relationship between acute changes in ejection fraction
after coronary occlusion and direct measurements of
the extent of infarction. Studies were performed in
awake animals instrumented over the long term to
avoid the confounding effects of anesthesia and surgery.
Methods
Experimental animals. Forty-one dogs weighing 20 to 30 kg
underwent permanent proximal occlusion of either the left
anterior descending (LAD) (14 dogs) or the left circumflex (LC)
(27 dogs) coronary artery. They were then maintained for at
least 3 days before being killed to permit histologic assessment
of infarct size, which was compared with acute changes in
radionuclide global and regional ejection fraction.
Surgical preparations. Dogs were anesthetized with sodium
thiamylal (30 to 40 mg/kg body weight) and underwent left
lateral thoracotomy. Either the LAD or the LC coronary artery
was freed by blunt dissection to permit placement of adjustable
occluders. Polyethylene loop, snare-type occluders were placed
loosely around the vessel and secured to the epicardium. A
pacing electrode was sutured to the right atrial appendage. All
dogs were allowed to recover for 7 to 14 days before being
studied.
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Experimental protocols. Snares and electrodes were exteriorized from subcutaneous pouches immediately before each
study or 1 day earlier. Morphine sulfate, 5 to 10 mg, was
injected intravenously before control studies to provide mild
sedation and to minimize discomfort resulting from coronary
artery occlusion. Dogs were studied awake while lying loosely
restrained on their right sides.
Control hemodynamic measurements were made, and radionuclide angiography was performed in duplicate. The snare was
then tightened to occlude the artery permanently. Duplicate
radionuclide angiograms were acquired 30 to 60 min after occlusion. In the majority of experiments, to provide a regular
cardiac rhythm, rather than the sinus arrhythmia of the conscious dog, the heart was paced from the right atrial appendage
at a rate that slightly exceeded the sinus rate at rest; when
occlusion resulted in a sinus rate greater than approximately 120
beats/min, pacing was not performed.
Radionuclide angiography. Multigated equilibrium radionuclide angiography was performed after labeling of red blood
cells with 99'Tc in vivo. Care was taken to ensure that camera
position relative to the thorax remained constant between data
acquisitions. Weighted support pads were used to stabilize the
chest position.
Global left ventricular ejection fraction was measured in the
anterior or ventral projection with slight caudal tilt, a position
which provides optimal left ventricular separation from the right
ventricle and left atrium.6 10 Global ejection fraction measured
in this projection by radionuclide angiography correlates closely
with that obtained simultaneously with use of ultrasonic dimension crystals over a wide range of ventricular function. '0 Regional ejection fraction was determined in both the anterior and
60 degree left anterior oblique projections with the use of a
computer program that divided the left ventricle into quadrants
with a nongeometric or count-based center (figure 1).6 After
both LAD and LC coronary artery occlusions, the magnitude of
change in regional ejection fraction is significantly greater than
the magnitude of change in global ejection fraction, although
the quadrants analyzed do not assess left ventricular function in
anatomically or physiologically discrete myocardial zones.6
The mean difference ( + SD) between duplicate measurements
of global ejection fraction in conscious dogs is 0.02 + 0.02; the
mean difference between global ejection fraction determined by
different observers is 0.01 + 0.01.6 The mean difference be-
ANTERIOR
LAO
FIGURE 1. Regions assigned by the computer for the determination of
regional ejection fractions. Regions 1 to 4 were assigned in the anterior
projection and regions 5 to 8 were assigned in the 60 degree left anterior
oblique (LAO) projection. The background (BKG) area assigned in
each projection for global and regional analysis is indicated. AO =
aortic arch: LA = left atrium; LV = left ventricle; RV = right
ventricle.
Vol. 72, No. 3, September 1985
tween duplicate measurements of regional ejection fraction
ranges from 0.03 ± 0.02 to 0.04 ± 0.04; the mean interobserver variability in these values is 0.02 ± 0.02 to 0.05 ±
0.04.6
Quantitation of infarction. Dogs were killed a minimum of
3 days after coronary occlusion to allow sharp separation of
infarcted and noninfarcted myocardium by routine histologic
techniques.8, 9 The hearts were excised and placed in buffered
formalin for 3 days to permit fixation. The left ventricle was
sliced into four transverse rings from base to apex. The basal
and apical rings were cut into four circumferential regions:
anterior, septal, posterior, and lateral. The two middle rings
were cut into six circumferential regions: anterior, septal, posterior, posterior papillary muscle, lateral, and anterior papillary
muscle. Each circumferential region was cut into four transmural samples from subepicardium to subendocardium, each
weighing 1 to 2 g. The tissue samples were weighed, embedded
in paraffin, sectioned at two different depths, and stained with
hematoxylin and eosin.8 9 The samples were arranged so that
each histologic section demonstrated the transmural distribution
of infarction in the region. Infarcted myocardium was sharply
distinguished from intact mnyocardium and was characterized by
complete or partial cellular dissolution, inflammatory cell infiltration, and loss of normal cell architecture. Sketches of the
histologic extent of infarcted and of uninvolved myocardium in
each tissue sample were then quantitated by planimetry with a
graph pen ultrasonic digitizer and computer interface.', 9 Total
weight of the infarcted tissue was calculated as the sum of
weights of infarcted tissue in each individual sample. The
weight of infarcted tissue in the subendocardial half of the
myocardial wall was determined. Infarct weight was expressed
as a percentage of left ventricular weight.
Data analysis. The average of duplicate measurements of
global and regional ejection fraction was used in the analysis.
The left ventricular region manifesting the maximum change in
regional ejection fraction after acute coronary occlusion was
identified for each dog.6 The absolute acute decrease in ejection
fraction was divided by the control value, and expressed as a
percent of control. Similarly, the acute change in heart rate was
calculated as a percent decrease from control.
One-way analysis of variance was used to determine differences between dogs with LAD and those with LC coronary
artery occlusions with respect to multiple anatomic and physiologic variables. Linear regression analysis was performed to
examine the relationship between the change in global ejection
fraction and the percent of the left ventricle that was infarcted.
Multiple linear regression analysis was used to evaluate the
relative influence of the extent of infarction, the subendocardial
extent of infarction, the left ventricular weight, and the change
in heart rate in determining global ejection fraction. The criterion Mallows' Cpll was applied to all possible subsets regression'2 to select the "best" subset of variables correlating with the
change in global ejection fraction. The statistical importance of
an individual variable is expressed by its contribution to the r
value squared.
Results
Table 1 presents mean left ventricular weights, histologic infarct sizes, and heart rate and radionuclide
angiographic data for dogs subjected to LAD or LC
coronary artery occlusions. Mean left ventricular
weight and percent of left ventricle infarcted did not
differ between groups. Mean heart rate was greater at
control and after occlusion in the LAD group, but
633
SCHNEIDER et al.
TABLE 1
Infarct size and ejection fraction
Weight
Dog
No.
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=
Global EF
Regional EFA
% LV
(g)
Infarcted
Control
Occlusion
Control
Occlusion
Control
Occlusion
0.1
0
1.4
11.6
26.9
8.0
8.0
51.7
37.0
33.0
27.8
9.5
13.3
21.4
17.8
15.6
106
124
144
116
100
70
86
141
98
102
96
103
85
111
106
21
112
125
132
134
152
106
102
163
110
116
142
118
107
120
124
18
0.43
0.40
0.45
0.50
0.48
0.38
0.43
0.60
0.47
0.51
0.60
0.46
0.47
0.46
0.47
0.06
0.42
0.37
0.43
0.26
0.23
0.29
0.33
0.22
0.23
0.25
0.32
0.30
0.34
0.26
0.30
0.07
0.57
0.38
0.43
0.47
0.60
0.57
0.61
0.61
0.37
0.39
0.43
0.39
0.41
0.36
0.47
0.10
0.47
0.32
0.39
0.20
0.20
0.39
0.39
0.16
0.11
0.13
0.11
0.29
0.22
0.19
0.26
0.12
15.1
1.6
29.8
2.8
2.5
9.8
20.8
9.6
3.2
15.7
26.4
27.2
39.3
33.4
18.3
36.9
75
60
100
60
67
108
60
60
77
72
70
60
65
75
75
75
75
78
95
79
67
96
127
82
114
99
94
80
18
100
68
150
60
60
128
65
126
75
130
120
90
115
100
75
80
84
160
100
115
94
132
140
130
128
108
106
105
28
0.51
0.57
0.59
0.46
0.63
0.56
0.52
0.58
0.51
0.56
0.66
0.55
0.57
0.61
0.55
0.59
0.56
0.57
0.51
0.60
0.51
0.60
0.53
0.66
0.66
0.44
0.47
0.56
0.06
0.37
0.54
0.33
0.43
0.63
0.46
0.41
0.46
0.47
0.46
0.34
0.40
0.43
0.45
0.36
0.44
0.54
0.40
0.40
0.41
0.40
0.43
0.40
0.49
0.54
0.49
0.42
0.44
0.07
0.52
0.70
0.78
0.62
0.61
0.73
0.74
0.65
0.67
0.70
0.81
0.68
0.74
0.75
0.66
0.73
0.54
0.53
0.56
0.64
0.59
0.76
0.62
0.71
0.63
0.56
0.33
0.65
0.10
0.32
0.55
0.37
0.49
0.58
0.46
0.41
0.37
0.53
0.46
0.35
0.36
0.46
0.46
0.30
0.45
0.42
0.38
0.49
0.32
0.33
0.45
0.36
LAD artery occlusion
61.0
1
85.0
2
86.4
3
85.5
4
97.5
5
6
139.3
112.5
7
82.2
8
113.3
9
98.6
10
120.4
11
12
88.6
86.5
13
14
134.3
99.4
Mean
21.9
SD
LC artery occlusion
15
104.5
16
78.0
98.5
17
18
100.3
98.0
19
20
72.5
128.0
21
22
89.5
23
138.0
24
79.5
25
76.0
26
98.4
27
145.2
28
170.7
29
157.5
30
207.0
31
85.0
108.0
32
33
87.5
34
98.8
35
132.3
36
107.5
37
85.2
78.1
38
39
93.3
40
79.0
41
93.3
Mean
107.0
SD
32.7
.38
p value
EF
Heart rate (bpm)
of LV
ejection fraction; LV
1.9
26.1
1.4
29.1
36.9
26.9
28.1
26.9
17.0
4.2
17.7
18.8
12.4
.84
.11
.03
0.42
0.41
0.55
0.22
0.42
0.09
.13
left ventricle.
ARegion demonstrating the maximum acute decrease in EF following coronary occlusion.
p values reflect results of analysis of variance comparing LAD occlusions to LC occlusions. For heart rate, global EF and
regional EF, percent change from control to occlusion was compared in the two groups.
634
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increased to a similar extent (p = . 1 1) in both groups.
Mean global and regional ejection fractions were lower
in the control state and after occlusion in the LAD
group. Percent change in global ejection fraction was
greater (p = .03) in dogs with LAD coronary artery
occlusion than in those with occlusion of the LC artery
(34.2 + 19.7 vs 20.7 + 13.1, mean + SD). Changes
in regional ejection fraction were greater than those in
global ejection fraction after both LAD and LC artery
occlusions; however, the percent change in regional
ejection fraction did not differ significantly (p = . 13)
between groups (45.6 + 23.1 vs 34.9 ± 14.2).
In figure 2 the percent change in global ejection
fraction measured within 1 hr after occlusion of the
LAD or LC coronary artery is plotted against the percent of the left ventricle that ultimately infarcted. After
LAD artery occlusion, histologic infarct size ranged
from 0 to 51.7% of the left ventricular weight and
correlated linearly (r = .89) with percent change in
global ejection fraction (y = 1.12x + 14.2). After
occlusion of the LC artery, infarct size ranged from
1.4% to 36.9% of the left ventricular weight and correlated modestly (r = .71) with change in ejection fraction (y = 0.73x + 7.9). The slope of this relationship
was significantly greater (p < .05) for dogs with LAD
(1.12) than for those with LC (0.73) artery occlusions,
indicating that for comparable ultimate infarct size,
acute LAD artery occlusion decreased global ejection
fraction to a greater degree than did acute LC artery
occlusion. In addition, y axis intercepts were signifi-
cantly greater than 0 after occlusion of both the LAD (p
< .003) and LC (p < .02) arteries, suggesting that
after acute coronary occlusion, the reduction in global
ejection fraction was influenced by dysfunction in
myocardium that did not become irreversibly injured.
Multivariate analysis revealed that the left ventricular weight and the subendocardial extent of infarction
did not independently influence the change in ejection
fraction after coronary occlusion. After occlusion of
the LC, but not after that of the LAD, there was a
modest inverse correlation between the change in heart
rate and the change in global ejection fraction (r =
- .49): that is, increases in heart rate were associated
with decreases in ejection fraction. Neither the control
value for global ejection fraction, regional ejection
fraction, nor heart rate influenced the change in global
ejection fraction after coronary occlusion in either
group. Thus, although there were baseline differences
between the LAD and LC groups with respect to heart
rate and global ejection fraction (table 1), these variables were not independently predictive of the change in
ejection fraction after occlusion.
Discussion
The major new findings of the present study are that
(1) the acute reduction in global ejection fraction that
follows coronary artery occlusion is directly related to
the extent of final myocardial infarction, and (2) infarction occurring in the LAD as compared with the
LC region of the dog left ventricle results in dispropor-
LAD Occlusions
LC Occlusions
50
LL.
c
-c
30
y=1.12X+14.2
10
0
r = .89
,
% LV infarcted
FIGURE 2. Relationships between percent change in global ejection fraction and percent of the left ventricle that infarcted after
LAD (left) and LC (right) artery occlusions. The slope was significantly greater (p < .05) for the LAD than for the LC group. The
y intercepts were significantly greater than 0 for both LAD (p < .003) and LC (p < .02) artery occlusions.
Vol. 72, No. 3, September 1985
635
SCHNEIDER et al.
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tionately greater reduction in global left ventricular
function as measured by the radionuclide angiographic
technique.
Occlusion of the LAD or LC artery produced a wide
range of infarct sizes. The variability resulted in part
from the modification of the site of occlusion and in
part from inherent variability in the extent of ischemia
and subsequent infarction resulting from proximal
coronary occlusion in conscious dogs.8, 9 The entire
left ventricle was sectioned into 1 to 2 g samples for
direct histologic quantitation of size of infarction. In
previous studies of acute coronary occlusion6'7 we
used similar techniques for tissue sectioning, but analyzed regional myocardial blood flow rather than histologic infarction. In the earlier experiments the size of
the ischemic zone was estimated as the percent of the
left ventricular weight in which myocardial blood flow
was reduced more than 25% from normal zone flow.
The acute change in global ejection fraction correlated
with size of the ischemic zone in 13 dogs with LAD
artery occlusions (r = .84, y = 0.96x + 1.7) and in
13 dogs with occlusions of the LC artery (r = .75, y =
0.53x + 2.0)67
It is of interest that the slopes of the relationships
between decrease in ejection fraction and infarct size
tended to be greater than the slopes of the relationships
between decrease in ejection fraction and extent of
ischemia for both LAD (1.12 vs 0.96) and LC artery
occlusions (0.73 vs 0.53). The y axis (change in ejection fraction) intercepts were greater than 0 for the
relationships of infarct size to change in ejection fraction, whereas the y intercepts were close to 0 for the
relationships of the extent of ischemia to change in
ejection fraction. These data indicate that the global
ejection fraction is sensitive to mild reductions in regional blood flow; consequently, acute reductions in
global ejection fraction are influenced both by the
amount of myocardium that infarcts and by the amount
that does not infarct after permanent coronary occlusion. It is not surprising that both the extent of acute
ischemia after coronary occlusion and the extent of
subsequent infarction are directly related to the
changes in global ejection fraction, since several studies have demonstrated direct relationships between
myocardial ischemia and infarction. 8 9
Multivariate analysis demonstrated no consistent relationships between left ventricular weight, the subendocardial extent of infarction, or the change in heart
rate and acute changes in global ejection fraction. In
our previous examination6 7of the relationship between the size of the ischemic zone and the change in
ejection fraction, a more extensive analysis was per636
formed to assess the influence of acute changes in heart
rate, aortic blood pressure, and the left ventricular enddiastolic count rate, a radionuclide index of relative
left ventricular volume. None of these variables correlated independently with the change in ejection fraction. However, it should be noted that neither the present protocol nor the previous one6'7 was designed to
assess long-term effects of loading conditions or effects of deliberately altering loading conditions on
changes in global ejection fraction. It is likely that
certain of these and other unanalyzed variables contributed to the significant scatter in the linear correlations.
A significant finding of this study was that for similar degrees of left ventricular infarction, occlusion of
the LAD artery produced greater decreases in global
ejection fraction than did occlusion of the LC artery. It
is of interest that the decreases in regional ejection
fraction after the two occlusions were not significantly
different, suggesting that the disproportionate effects
of LAD vs LC regional ischemia on left ventricular
function were more apparent at a global than at a regional level. Our previous work6 has indicated a modest linear relationship between acute decreases in regional ejection fraction and size of the ischemic zone
after occlusion of both the LAD and LC. This makes it
unlikely that the radionuclide angiographic technique
preferentially evaluated regional function in dogs that
had LAD vs LC artery occlusions in the present study.
The present findings with regard to global function are
consistent with observations made in experiments in
which size of the ischemic zone rather than size of
infarction was estimated.6 7 In the earlier study the
slope of the relationship between the change in global
ejection fraction and size of the ischemic zone was also
greater for LAD than for LC artery occlusions (0.96 vs
0.53; p < .01). While global ejection fraction decreased to a greater extent after LAD than after LC
artery occlusions (27.7% vs 13.4%; p = .004), regional ejection fraction decreased to a similar extent in
the two groups.6'7
The mechanisms or factors responsible for the disproportionate effects of LAD vs LC artery occlusion
on global function are not clear. The anatomic distributions of infarction or ischemia were different with occlusion of the LAD artery than with that of the LC, and
consequently may have influenced global ejection
fraction in different ways. Occlusion of the LAD coronary artery induced infarction of the anterior-apical
region, with variable extension toward the base,
whereas occlusion of the LC artery induced infarction
of the inferior-basal region, with variable extension
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toward the apex. Larger LAD artery infarcts tended to
involve more of the anterior and lateral walls and extended toward the base, whereas larger LC artery infarcts tended to extend more medially and laterally
than toward the apex. It has not been determined in
studies in the dog to what extent LAD as compared
with LC artery occlusions preferentially affect minoror major-axis shortening, although as noted above the
larger infarct regions with LAD artery occlusion may
be expected to involve shortening in both the major
and minor axes. Previous investigations have indicated
that myocardial segment shortening in the dog is greater at the apex than at the base of the left ventricle, 13 and
infarction of a left ventricular region that shortens to a
greater degree than the remainder of the ventricle may
be expected to alter global function disproportionately.
On the other hand, shortening of the left ventricular
minor axis contributes approximately 87% to generation of the stroke volume.'4
Studies have suggested that hypofunction may extend for a variable distance outside the ischemic zone,
possibly as a result of tethering.'5 It is not known
whether the adjacent hypofunctional nonischemic region influences global function or whether the hypofunctional nonischemic region is larger after LAD than
after LC artery occlusion. Global left ventricular contraction represents the sum of shortening in the nonischemic and ischemic regions. Although the present
studies indicate that hyperfunction in the nonischemic
region rarely compensates completely for acute ischemic region hypofunction, in certain studies it has been
observed that there is less hypercontraction in nonischemic myocardium remote from the ischemic region
after LAD than after LC occlusion in the dog. 16 17 Such
a regional difference would contribute to disproportionate effects of LAD and LC artery occlusion on
global ejection fraction.
Finally, in phantom heart studies performed to simulate results of radionuclide angiography during regional left ventricular dysfunction, there was greater
attenuation of counts from hypofunctional regions that
were distant from the detector and consequently true
volume changes from simulated posterior and anterior
hypokinesis were underestimated and overestimated,
respectively. 18 This theoretical problem, however, had
only a minor effect on measurements of ejection fraction in experiments in conscious dogs. 19 It is of interest
that in several clinical studies it has been observed that
anterior infarction causes greater decreases in left ventricular function than does inferior infarction,20' 21 but it
is not clear from these studies whether the differential
effects on global function resulted from different sizes
Vol. 72, No. 3, September 1985
of infarction or different physiologic effects of infarcts
of comparable size.5' 22
This study demonstrates a major influence of the
extent of acute infarction on changes in left ventricular
ejection fraction and relatively minor influences of
other parameters. The results presented are consistent
with those of an earlier experiment6' in which the size
of the ischemic zone was correlated with acute changes
in ejection fraction. In both studies anterior ischemia
produced greater reduction in global ejection fraction
than did inferior ischemia of a similar extent. Although
the precise mechanisms responsible for this disproportionate effect have not been determined, the observation is pertinent to the angiographic evaluation of global function in the setting of acute infarction.
We are grateful to Joseph C. Greenfield, Jr., M.D., and
Richard H. Helfant, M.D., for support, to Cynthia Silvaggi
Baker, R.N., and James A. Stanfield, N.M.T., for assistance in
performing the radionuclide studies, to Marjorie Grubb and
Robert Murdock, Jr. for technical support, to Kirby Cooper and
Eric Fields for surgical preparations, to Michael Taylor and staff
for animal care, and to Kathy Tuppeny for secretarial assistance.
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CIRCULATION
Left ventricular ejection fraction after acute coronary occlusion in conscious dogs:
relation to the extent and site of myocardial infarction.
R M Schneider, A Chu, M Akaishi, W S Weintraub, K G Morris and F R Cobb
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Circulation. 1985;72:632-638
doi: 10.1161/01.CIR.72.3.632
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