Download Left ventricular ejection fraction during cardiac

THERAPY AND PREVENTION
SURGERY
Left ventricular ejection fraction during cardiac
surgery: a two-dimensional echocardiographic study
JEROME M. DUBROFF, M.D., MICHAEL B. CLARK, M.D.,
CALVIN Y. H. WONG, M.D., ALAN J. SPOTNITZ, M.D.,
ROBERT H. COLLINS, M.D., AND HENRY M. SPOTNITZ, M.D.
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ABSTRACT Although long-term effects have been studied, the immediate effect of surgery for
acquired heart disease on left ventricular function is not well defined. Accordingly, 44 adults with
acquired heart disease underwent intraoperative two-dimensional echocardiography with a gas-sterilized transducer before and immediately after cardiopulmonary bypass. Ejection fraction was measured
by short-axis area change at the maximum left ventricular cross section (SAAC-EF) and also by a
method using multiple sections. Correction of both mitral and aortic regurgitation produced a significant intraoperative decrease in ejection fraction from 0.49
19 (SD) to 0.32 + 0.16 (p < .02) and
from 0.41 + 0.13 to 0.30 + 0.17 (p < .0005), respectively. Relief of aortic stenosis and mitral
stenosis resulted in an intraoperative increase in ejection fraction from 0.45 + 0.10 to 0.55 + 0.09 (p
< .02) and from 0.41 + 0.05 to 0.50 + 0.07 (p < .05), respectively. Ejection fraction after coronary
artery bypass grafting was unchanged. Preload (end-diastolic area) was significantly decreased after
correction of aortic regurgitation (p < .02) but unchanged in other lesions. We conclude that (1)
correction of pure mitral and aortic valvular lesions produces characteristic alterations in ejection
fraction in the immediate postoperative period; (2) with the possible exception of patients with aortic
regurgitation, the observed change in ejection fraction does not appear to reflect changes in preload; (3)
noninvasive assessment of left ventricular function by two-dimensional echocardiography during
cardiac surgery appears feasible and could provide data important for clinical decision making in the
early postoperative period.
Circulation 68, No. 1, 95-103, 1983.
ALTHOUGH characteristic changes in left ventricular
function after surgery for acquired heart disease have
been reported,"X the immediate effects of surgery are
not well defined. Indeed, appropriate methods for
study of intraoperative or early postoperative ejection
fraction during thoracotomy have been developed only
recently.5 Accordingly, the present study was undertaken to further define short-term changes in ventricular performance before and after surgery in patients
undergoing correction of mitral or aortic valve disease
and in patients undergoing coronary bypass surgery.
From the Department of Surgery, Columbia University College of
Physicians and Surgeons and the Columbia-Presbyterian Medical Center, New York.
Supported in part by U.S.P.H.S. grant HL-22894.
Address for correspondence: H. M. Spotnitz, M.D., Columbia University College of Physicians and Surgeons, 630 West 168th St., New
York, NY 10032.
Received June 2, 1982; revision accepted March 24, 1983.
Performed in part during the tenure of an Established Investigatorship
of the American Heart Association (Dr. H. Spotnitz).
Vol. 68, No. 1, July 1983
Methods
Operative investigation. Forty-four patients undergoing
single-valve replacement or coronary artery bypass grafting
were studied (table 1). The patients suffered from acquired
single-valve disease or coronary artery disease. There were no
cases of significant coronary artery disease coexistent with the
valve lesions. No localized wall motion abnormalities were seen
in the patients with valvular disease. Of 14 patients, with coronary artery disease, 10 had no wall motion abnormalities detected by standard two-dimensional echocardiographic studies performed on the day before surgery. Localized wall motion
abnormalities were seen in four patients (Nos. 3, 4, 9, and 14).
Informed consent was obtained from all patients.
After general anesthesia with ketamine or morphine-nitrous
oxide, endotracheal intubation, and median sternotomy, patients were cannulated for cardiopulmonary bypass. Echocardiographic studies were obtained with a gas-sterilized hand-held
3.5 mHz transducer and were recorded on videotape (V-3000 or
V-3400 ultrasonograph; Diasonics, Salt Lake City). Use of intravenous vasopressors and vasodilators were generally avoided
during echocardiographic studies. Short-axis sections were recorded at four levels: (1) the base of the mitral valve, (2) the tip
of the mitral valve, (3) the maximum diameter of the left ventricle, and (4) the papillary muscles. Long-axis views, including
the cardiac apex, were also recorded. Patients underwent stan95
DUBROFF et al.
TABLE 1
Patients studied by intraoperative echocardiography
Cardiac lesion
Aortic stenosis
Aortic
regurgitation
Mitral stenosis
Mitral
regurgitation
CAD
CAD
=
of the short axis at the level of the papillary muscles. In these
patients, only SAAC-EF determinations are reported.
Cross-
Total
clamp
bypass
Patients
Age
time
studied (mean yr) (min - SD)
time
(min)
8
67
69 19
100+31
10
5
52
59
99+27
78 22
132+32
115+34
9
14
50
55
79 + 20
101 25
132 + 33
166 43
coronary artery disease.
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dard surgical procedures. Myocardial protection was accomplished with topical hypothermia and/or potassium crystalloid
cardioplegia. After completion of procedures requiring cardiac
arrest, the aortic cross-clamp was removed and the heart was
defibrillated.8 The patient was then weaned from cardiopulmonary bypass and echocardiograms were repeated before decannulation. Postbypass echocardiographic studies were obtained
at similar heart rates and under similar hemodynamic conditions
to those of the prebypass studies. Echocardiograms were not
repeated after decannulation. No arrhythmias or other adverse
effects were observed that were attributable to the echocardiographic studies.
Calculation of ejection fraction with two-dimensional
echocardiography. Ejection fraction was calculated from
stopped-frame videotaped images planimetered with a light
pen. End-diastolic area (EDA) was measured coincident with
the peak of the R wave, and end-systolic area (ESA) at the
smallest cross section after the R wave. Outlines of the endocardial border "trailing edge" were planimetered by hand (see
figure 1). End-diastolic and end systolic images from three to
five cardiac cycles were planimetered and averaged for every
measurement.
The left ventricular ejection fraction was calculated by two
different methods. The short-axis area change (SAAC-EF) was
defined as
SAAC-EF = (EDA - ESA)/EDA
based on diastolic and systolic sections from level 3 (maximum
cross section). In addition, a multiple-section method was defined, modified after that of Quinones (M. Quinones, Houston,
TX, by permission) with the following formula:
EFQ = ef + L(l - ef)
where ef (EDA -ESA)/EDA and L is a correction factor for
apical shortening. The value for EDA used for calculation of
EFQ represented the average of short-axis sections 1, 2, and 4 in
diastole. Similarly, ESA represented the average of the shortaxis sections 1, 2, and 4 in systole; ef thus differs from SAACEF in that SAAC-EF is derived from a single short-axis section,
while the ef of the multiple-section method is determined with
averaged EDA and ESA values from short-axis sections at several levels of the left ventricle. The correction factor for apical
shortening is determined as follows: normal apical motion, L
0.15; hypokinetic apical motion, L - 0.05; akinetic apical
motion, L = -0.05; and dyskinetic apical motion, L -0.15.
In 12 patients, EFQ could not be determined because of
inadequate visualization of either the left ventricular long axis or
96
In one patient, SAAC-EF could not be calculated because of
inadequate visualization of the short axis at the level of the
ventricular maximal diameter. In this patient, only EFQ is
re-
ported.
Prebypass and postbypass ejection fractions were grouped by
lesion and compared by a paired t test. Prebypass and postbypass EDAs were similarly analyzed, All prebypass SAAC-EF
and EFQ values and all postbypass SAAC-EF and EFQ values
were pooled. F values were calculated comparing all prebypass
with all postbypass,ejection frations.
Validatlon of echocardiographic determination of ejection fraction. For validative purposes, ejection fraction as determined by our two-dimensional echocardiographic methods
was compared with that obtained by single-plane right anterior
oblique (RAO) cineangiography in a group of 21 patients with
documented coronary,disease who underwent cardiac catheterization and echocardiographic study within the same 24 hr period at Columbia-Presbyterian Medi,cal Center. Nine of these
patients were found to have localized wall motion abnormalities
by angiographic ventriculography. Single-plane left ventriculograms in the RAO position were traced by hand and planimetered to obtain the EDAs and ESAs. Ventricular volumes and
ejection fraction were calculated by the area-length method of
Dodge et al.9 as modified for the RAO position by Kennedy et
al. '0 A correction factor to account for magnification distortion
was determined by an imaged 1 cm grid positioned at the
approximate level of the left ventricle immediately after ventriculography. Standard echocardiographic short-axis and apical
views were obtained.
Angiographic results were plotted
against ejection fraction as calculated by the short-axis area
change and multiple-section method (SAAC-EF and EFQ, see
above); linear regression correlative analysis was performed on
a PDP 11/70 computer.
Ejection fraction values as determined by the EFQ method
correlated well with those obtained by angiography (r = .91,
SEE = .06), with the resultant linear regression
EFQ = 0.87 ANGIO-EF + 0.04
Although not as accurate as the EFQ determination, the
SAAC-EF method also correlated fairly well with angiographic
=
values (r - .85, SEE
sion
.08), with the resulting linear regres-
SAAC-EF = 0.90 ANGIO-EF 0.02
Because of the close correlations observed, we chose to report our intraoperative ejection fraction results as directly measured rather than as values "corrected" by linear regression.
Results
Intraoperative investigation. Characteristics of the patients studied, including cross-clamp and bypass
times, are listed in table 1. Prebypass and postbypass
values for EDA, ESA, and ejection fraction by the two
methods used are presented in table 2 and figures 2 and
3. Summary data and statistics are presented in tables 3
and 4. All results are presented as mean + I SD.
Aortic stenosis. All six patients with aortic stenosis
demonstrated an increase in ejection fraction after bypass. Average SAAC-EF increased from 0.45 + 0. 10
before bypass to 0.55 + 0.09 after bypass (p < .02).
In five patients EFQ increased from 0.48 ± 0.06 to
CIRCULATION
THERAPY AND PREVENTION-SURGERY
0.54 + 0.04 (p < .04). Average prebypass EDA was
17.0 + 2.7 cm2; average postbypass EDA was 16.6 ±
3.4 cm2 (NS).
Aortic regurgitation. All 11 patients with aortic re-
gurgitation demonstrated a decrease in ejection fraction after bypass. The average SAAC-EF decreased
from 0.41 ± 0.13 before bypass to 0.30 + 0.17 after
bypass (p < .001). In nine patients EFQ decreased
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FIGURE 1. An intraoperative two-dimensional echocardiogranm of the left ventricle at maximum cross-sectional area is shown.
Top, Planimetered end-diastolic frame. Bottom. End-systolic frame. End-systolic and end-diastolic planimetered endocardial
outlines are superimposed.
Vol.
68, No. 1, July 1983
97
DUBROFF et al.
TABLE 2
Changes in intraoperative maximal diameter cross-sectional area and ejection fraction
Patient
No.
Prebypass area (cm2)
Postbypass area (cm2)
EDA
ESA
SAAC-EF
After
Before
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EDA
ESA
1
2
3
4
5
6
7
20.0
13.6
20.0
17.8
15.7
14.7
23.7
14.8
6.0
12.2
9.6
7.5
7.3
12.5
17.3
13.6
20.1
20.4
12.0
16.5
29.1
Aortic stenosis
9.2
5.5
11.8
9.7
4.2
6.2
14.4
5.4
2
3
4
S
6
7
8
9
10
11
12
13.2
22.5
14.8
39.6
10.0
18.5
23.5
29.2
38.6
39.8
39.7
42.6
16.0
7.7
22.5
3.8
9.9
18.6
19.4
20.9
25.8
26.8
21.3
13.9
17.8
8.4
39.0
10.7
16.8
23.1
23.8
36.3
30.2
35.5
42.3
Aortic insufficiency
7.8
14.8
4.5
28.7
4.1
9.5
18.8
18.8
26.5
26.7
30.2
27.5
0.59
0.29
0.48
0.43
0.62
0.46
0.21
0.34
0.46
0.35
0.32
0.50
2
3
4
5
11.9
17.0
16.3
13.4
17.6
6.1
10.3
10.4
6.5
10.9
19.5
22.3
Mitral stenosis
5.8
8.6
9.2
9.2
12.6
2
3
4
5
6
7
8
9
10.9
19.4
32.2
12.6
15.5
23.4
31.7
12.0
42.6
3.0
6.9
13.6
4.3
6.2
14.7
26.0
8.4
28.8
10.9
25.8
19.9
14.1
15.2
21.9
36.7
12.5
36.5
Mitral regurgitation
5.8
18.9
16.5
7.2
5.8
18.5
27.5
9.6
27.5
2
3
4
5
6
7
8
9
10
11
12
13
14
14.3
10.5
21.7
20.5
8.6
7.6
17.0
10.9
4.6
10.4
15.9
28.0
22.3
20.7
8.3
3.6
10.2
12.6
4.6
3.2
8.0
6.1
2.6
6.6
8.0
14.4
11.5
9.8
7.6
15.7
18.5
20.1
10.1
11.0
24.1
10.8
8.8
14.5
14.2
26.0
18.4
26.5
12.2
15.9
22.9
0.26
0.56
0.39
0.46
0.52
0.50
0.48
0.39
0.54
0.52
0.52
0.52
0.57
0.58
0.46
0.49
0.44
0.34
0.46
0.26
0.62
0.43
0.19
0.13A
0.27
0.12
0.1SA
0.35
0.52
0.43
0.34
0.42
0.31
0.35
0.55
0.58
0.37
0.45
0.32
0.59
0.48
0.26
0.29
0.16
0.39
0.21
0.49
0.39
0.36
0.42
0.38
0.52
0.46
0.60
0.51
0.43
0.39
0.33
0.42
0.39
0.46
0.46
0.47
0.49
0.72
0.64
0.58
0.66
0.60
0.37
0.18
0.30
0.50
0.47
0.27
0.17
0.49
0.42
0.16
0.25
0.23
0.35
0.40
0.53
0.25
0.16
0.50
0.34
0.23
0.41
0.45
0.15
0.12
0.37
0.40
0.42
0.46
0.55
0.51
0.50
0.49
0.64
0.56
0.50
0.58
0.52
0.54
0.46
0.52
0.43
0.56
0.42
0.52
0.40
Coronary artery disease
4.0
0.42
4.8
0.66
8.1
0.53
0.38
12.4
3.7
0.47
4.9
0.58
11.0
0.53
4.6
4.2
11.4
6.7
15.5
11.6
16.9
0.47
0.60
0.41
0.52
0.65
0.62
EFQ EF
Before
After
0.44
0.43
0.37
0.50
0.49
0.48
0.53
0.47
0.69
0.56
0.38
0.63
0.55
0.54
0.57
0.52
0.21
0.53
0.40
0.37
0.36
ASame patient (reoperation for repair of paravalvular leak).
98
CIRCULATION
THERAPY AND PREVENTION-SURGERY
80 r
70 F
60 H
P<02
z
0
cr
.50T
t
5 05
0
-oNS
o
FIGURE 2. Prebypass and postbypass values for
ejection fraction grouped by lesion. Data shown as
determined by the short-axis area change method.
Means are designated by open circles. Statistical significance is indicated.
40
z
0
H
30
Li
20
10
1-
0
POST
PRE
POST
PRE
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MS
POST
PRE
POST
PRE
POST
PRE
AR
CAD
AS
MR
before bypass to 0.25 ± 0.12 after bypass (p < .01).
Average prebypass EDA was 21.9 + 10.0 cm2; average postbypass EDA was 24.4 + 10.0 cm2 (NS).
Coronary artery disease. In the 13 patients in whom
it could be calculated, the average prebypass SAACEF was 0.48 ± 0.08; the average postbypass SAACEF was 0.49 ± 0.13 (NS). In the nine patients in
whom EFQ could be evaluated, the average prebypass
EFQ was 0.49 ± 0.05; the average postbypass EFQ
was 0.52 ± 0.08 (NS). The average prebypass EDA
was 15.2 ± 7.0 cm2; the average postbypass EDA was
16.2 ± 6.0 cm2 (NS).
from 0.45 + 0.09 before bypass to 0.34 + 0.10 after
bypass (p < .005). The average prebypass EDA was
25.0 ± 11.3 cm2; the average postbypass EDA was
22.0 ± 10 cm2 (p < .02).
Mitral stenosis. In five patients the average SAACEF increased from 0.41 + .05 before bypass to 0.50
+ 0.07 after bypass (p < .05). In three patients EFQ
increased from 0.41 + 0.06 before bypass to 0.44 ±
0.05 after bypass (NS). The average prebypass EDA
was 15.2 ± 2.3 cm2; the average postbypass EDA was
18.6 ± 4.5 cm2 (NS).
Mitral regurgitation. In seven patients a decrease in
SAAC-EF was noted from the prebypass to the postbypass study. The ejection fraction in one patient increased and in one remained unchanged when calculated by the SAAC-EF method; both showed decreases
postoperatively by the EFQ method. The average
SAAC-EF decreased from 0.49 ± 0.19 before bypass
to 0.32 ± 0.16 after bypass (p < .02). In seven
patients the average EFQ decreased from 40.0 + 0.10
Discussion
Surgical intervention in the management of patients
with chronic valvular heart disease or ischemic heart
disease is primarily directed toward the amelioration of
symptoms and the preservation of left ventricular function. Using two-dimensional echocardiographic imaging, we have demonstrated characteristic changes in
soF
40 H
<I
30 _
FIGURE 3. Prebypass and postbypass values for
EDA grouped by lesion as measured at the maximum LV cross section. Means and statistics are as in
figure 2.
P<02
0
,i
,
20
a
0
Z
Lu
10
POST
PRE
PRE
MS
Vol. 68, No. 1, July 1983
AS
POST
PRE
POST
CAD
PRE
AR
POST
PRE
POST
MR
99
DUBROFF et al.
TABLE 3
Comparison of methods for measurement of preoperative and postoperative ejection fractions
Short-axis area change (mean
Aortic
Aortic
Mitral
Mitral
CAD
stenosis
regurgitation
stenosis
regurgitation
CAD
=
p
value
Preop.
EF
Postop.
EF
p
value
0.45 ± 0.1
0.41 +0.13
0.41+0.05
0.49 + 0.19
0.48±0.08
0.55 ±40.09
0.30+0.16
0.50+0.07
0.32 +0.16
0.49±0.13
.02
.001
.05
.02
.68
0.48 + 0.06
0.45 ± 0.09
0.41+0.06
0.40 + 0.1
0.49+0.05
0.54 ±0.03
0.34± 0.1
0.44+0.05
0.25 ±0.12
0.52±0.08
.04
.005
.02
.01
.12
coronary artery disease.
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echocardiographic determination of left ventricular dimensions and ejection indices allow for rapid assessment of changes in systolic and diastolic hemodynamic
parameters occurring during surgery. The SAAC-EF,
derived from a single echocardiographic image at the
level of the ventricular maximal diameter, is analogous
to an M mode-derived ejection fraction based on
changes in ventricular internal dimensions.'2 The
SAAC-EF correlated fairly well with angiographic determinations in our validative study (r = .85), but its
usefulness would be limited in the presence of postoperative paradoxic septal motion or other regional wall
motion abnormalities.'3 The use of multiple echocardiographic sections to determine ejection fraction, the
EFQ, provides a more representative sample of the
contracting ventricle and correlated well with angiography findings (r = .91), even in the presence of
localized asynergy or dyssynergy.
Aortic regurgitation. The present results demonstrate
statistically significant decreases in both ejection fraction and preload (measured as EDA) after correction of
aortic regurgitation. Reduction in left ventricular enddiastolic volume after correction of aortic regurgitation
had been shown previously in patients evaluated several weeks to months after surgery.' 14 15 Our data are
TABLE 4
Postoperative changes in cross-sectional area (mean
CAD
100
=
Modified Quinones formula (mean ± SD)
Postop.
EF
Intraoperative echocardiography. Our methods for
Aortic stenosis
Aortic regurgitation
Mitral stenosis
Mitral regurgitation
CAD
SD)
Preop.
EF
intraoperative left ventricular functional indices that
are closely related to the specific nature of the underlying heart disease.
Lesion
+
+
Preop. EDA
Postop. EDA
(cm2)
(cm2)
17.0 + 2.7
16.6+ 3.4
22.0+ 10.0
18.6+4.5
21.4+ 10.0
25.0+ 11.3
15.2 2.3
21.9+ 10.0
15.2+7.0
coronary artery disease.
16.2+6.0
SD)
p
value
NS
0.02
NS
NS
NS
consistent with these findings and suggest that preload
reduction occurs early after surgical correction of
chronic aortic regurgitation.
Reported changes in ejection fraction after surgical
correction of aortic regurgitation have been less consistent. Gaasch et al.,16 using M mode echocardiography, showed decreased wall thickening that reflected
decreased left ventricular performance 7 to 10 days
after surgery. Boucher et al.3 showed a significant decrease in ejection fraction measured by radionuclide
scanning 2 weeks after correction of aortic regurgitation. However, improvement in LV ejection fraction
several months to years after surgical correction has
also been reported." 14, 15 Changes in left ventricular
volume may explain some of these disparate findings.
If stroke volume remains constant, decreasing heart
size will result in an increase in measured ejection
fraction. The time at which left ventricular function is
evaluated is also likely to influence the results obtained
when assessing the apparent effects of surgical correction of aortic regurgitation. Differences between early
and late results may be affected by altered loading
conditions, by myocardial depression secondary to ischemic arrest during surgery and/or by anesthesia, or
by reversal of the prolonged effects of long-term volume overload.
Mitral regurgitation. In correction of mitral regurgitation, our data show a significant decrease in ejection
fraction after surgery without significant changes in
ventricular volume. These changes are similar to those
reported by others3'5' 17, 18 and support the view that
chronic mitral regurgitation causes latent left ventricular dysfunction, which is unmasked by surgical correction.5 However, the echocardiographic studies of
Schuler et al.'7 suggest that a long-term decrease in
ejection fraction persists only in the most severely impaired patients. We have performed serial echocardiographic ejection fraction determinations on our patients with mitral regurgitation, several of whom
demonstrate a significant and progressive improveCIRCULATION
THERAPY AND PREVENTION-SURGERY
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ment in systolic function in the first 10 to 14 days after
valve replacement. 19 More extensive follow-up investigation is planned to determine whether this subset of
patients can be identified through the use of intraoperative investigation.
Aortic stenosis. We have demonstrated that relief of
aortic stenosis results in a statistically significant increase in ejection fraction from the preoperative to the
postoperative study. Several investigators'5 20-22 have
demonstrated similar improvement in left ventricular
performance when measured weeks to months after
surgery. Our data suggest that left ventricular functional improvement occurs rapidly after valve replacement
in patients with aortic stenosis. In contrast with the
findings of Schwarz'5 but consistent with those of Kennedy et al.,21 there was no statistically significant
change in preload.
Mitral stenosis. After correction of mitral stenosis,
our data show a significant increase in ejection fraction. In contrast, Kennedy et al."8 found a significant
depression of ejection fraction in echocardiographic
studies performed postoperatively just before discharge. This apparent discrepancy may be explained
by differences in baseline left ventricular function.
Ejection fraction as determined by either EFQ or
SAAC-EF before surgical repair was depressed in four
of five of our patients with mitral stenosis. Reasons for
this are not entirely clear but may relate either to chronic rheumatic carditis or to immobilization of the inferobasal area by a rigid mitral valve complex.23 In contrast, most of the patients with mitral stenosis in the
report of Kennedy et al.'8 had normal preoperative
ejection indices. Other differences in myocardial preservation and operative technique may also play a role;
these intraoperative factors, however, are difficult to
assess quantitatively.
Coronary artery disease. We could demonstrate no
significant change in either ejection fraction or preload
after coronary artery bypass grafting. Newman et al.2
measuring scintigraphic ejection fraction 16 weeks
after coronary bypass surgery, could detect no change
in resting ejection indices. End-diastolic volume increased slightly only in those patients with postoperative symptoms.
Similar findings are reported in studies of ventricular function after bypass grafting as measured with
single plane or biplane contrast angiography24 25 several months after surgery. The patient populations
studied, however, differ in that preoperative left ventricular dysfunction (symptoms of congestive failure,
elevated end-diastolic pressure, and wall motion abnormalities) was present in most of the earlier studies.
Vol. 68, No. 1, July 1983
Using tantalum markers, Mintz et al.26 found a decrease in ejection fraction at 1 week when compared
with preoperative measurements. Ejection indices returned to preoperative levels by 2 months and remained stable over the year follow-up. Increases in
ejection indices in the early postoperative period have
been reported but may reflect catecholamine release
during surgery.26 27
Limitations: the intraoperative environment. Left ventricular function before and after cardiac surgery may
be influenced by a number of variables during the
perioperative period. Thus our observations concerning changes in ejection fraction must be assessed in
light of the known hemodynamic effects of (1) anesthesia, (2) myocardial preservation techniques, including
hypothermia and crystalloid cardioplegia, (3) cardiopulmonary bypass, and (4) changes in circulating hormone levels during and after surgery.
The anesthetics employed - ketamine, morphine,
and nitrous oxide - have each been shown to depress
myocardial contractility through a direct effect on heart
muscle.28230 However, alteration of vascular tone (morphine) or autonomic tone (ketamine) may serve to offset this direct effect to result in net improvement in
hemodynamic parameters, which is determined by the
specific combination of agents employed and the
amount of drug present in the circulation at any point in
time.3' The use of these agents was not controlled
during this investigation; there is thus no way to quantitatively assess their role in the changes in ventricular
performance that were observed in this study. However, the hemodynamic influence of anesthesia would be
expected to act fairly homogeneously, affecting patients within each subgroup studied, and thus would
not explain the significant drop in ejection fraction
seen only in patients with mitral or aortic regurgitation.
Studies in animals have consistently shown significant depression of left ventricular performance resulting from the use of topical hypothermia and cold crystalloid cardioplegia, the myocardial preservation
techniques used in this study. The clinical significance
of these observations is unclear; in patients undergoing
coronary bypass grafting, we and others2' 26 have
shown either no change or improvement in ventricular
functional parameters. Again, these effects would tend
to be distributed fairly evenly among all patient groups
and would not explain the significant decline in left
ventricular performance seen in our patients with mitral or aortic regurgitation. Studies to date have not
demonstrated increased sensitivity to global ischemia
resulting from long-term volume overload. Thus we
maintain32 that most structural and functional damage
101
DUBROFF et al.
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associated with long-term volume overload occurred
before surgical intervention and was "unmasked" by
correction of the valvular lesion.
It is possible that length of time on bypass or total
aortic cross-clamp time could affect the results of our
postbypass studies. However, we know of no data
relating ejection fraction to cross-clamp or bypass time
in the cardioplegic period. The quantitative significance of this variable is thus uncertain.
Changes in circulating levels of norepinephrine,
epinephrine, cortisol, antidiuretic hormone, and renin
have been well documented during and after surgery in
patients undergoing coronary bypass grafting.33" 4 The
relevance of these observations to our results was demonstrated by Wechsler et al. ,27 who, after identifying a
subset of patients with evidence of improved systolic
performance after coronary bypass grafting, demonstrated that this improvement could be reproduced in
all of their patients by catecholamine (isoproterenol)
infusion. These hormonal changes, however, would
tend to artificially elevate ejection indices and thus
could not account for the observed depression of ejection fraction in our patients with mitral or aortic regurgitation.
Conclusions
(1) Surgical correction of chronic mitral or aortic
valvular heart disease produces characteristic changes
in ejection fraction in the immediate postoperative period. These changes, similar in direction and magnitude to changes in ejection fraction shown by others to
be present weeks to months later, suggest that the
hemodynamic changes that occur after valve replacement occur rapidly and can be assessed easily during
the operative procedure itself.
(2) With the possible exception of patients with
aortic regurgitation, the observed change in ejection
fraction does not appear to reflect changes in preload.
(3) Noninvasive assessment of left ventricular
function by two-dimensional echocardiography during
cardiac surgery appears feasible, given the constraints
imposed by the intraoperative environment.
(4) Clinically, this new method may prove to be
valuable in the evaluation of the effects on ventricular
function of new surgical techniques. It may facilitate
assessment of possible intraoperative myocardial injury and thus could provide data important for clinical
decision making in the early postoperative period.
We thank Mr. Peter Bloom for technical assistance, Miss
Doris Costello for echocardiographic assistance, Robert
Sciacca, Eng.Sci.D, for statistical analysis, and Mrs. Rosemary
Marx for her secretarial work.
102
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Vol. 68, No. 1, July 1983
103
Left ventricular ejection fraction during cardiac surgery: a two-dimensional
echocardiographic study.
J M Dubroff, M B Clark, C Y Wong, A J Spotnitz, R H Collins and H M Spotnitz
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Circulation. 1983;68:95-103
doi: 10.1161/01.CIR.68.1.95
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