Download Hemodynamic Determinants of Prognosis of Aortic

Hemodynamic Determinants of Prognosis
of Aortic Valve Replacement in Critical Aortic
Stenosis and Advanced Congestive Heart Failure
BLASE A. CARABELLO, M.D., LAURENCE H. GREEN, M.D., WILLIAM GROSSMAN, M.D.,
LAWRENCE H. COHN, M.D., J. KENNETH KOSTER, M.D., AND JOHN J. COLLINS, JR., M.D.
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SUMMARY Fourteen patients with critical aortic stenosis (valve area 0.4 cm2/m2), a history of advanced
congestive heart failure, left ventricular ejection fraction less than 0.45 (mean 0.28 d 0.03) and no other
valvular lesions or obstructive coronary artery disease were studied to assess prognosis with aortic valve
replacement. Eleven of 14 (79%) survived surgery; 10 of these 11 showed major clinical improvement
postoperatively and form group 1. The three patients who died and the patient who did not improve form group
2. Although group 2 had higher preoperative values for aortic valve area and left ventricular end-diastolic
volume and lower ejection fraction and cardiac output than group 1, none of these factors alone reliably
predicted outcome. The mean systolic gradient was an important predictor of outcome: No patient with a mean
systolic gradient 30 mm Hg had a good outcome, irrespective of valve area or other hemodynamic variables.
Ejection fraction was plotted against left ventricular wall stress for both groups. For group 1, there was a
close linear relation that could be extrapolated back to normal wall stress and normal ejection fraction. This
suggested afterload mismatch as a major cause for this group's depressed ejection fraction. In group 2 ejection
fraction was lower for any given wall stress, suggesting depressed contractility, rather than afterload mismatch, as the cause of the left ventricular dysfunction. Thus, either afterload mismatch or depressed contractility may result in depressed ejection fraction in patients with aortic stenosis; which one predominates may
have major prognostic importance.
THE NATURAL HISTORY of critical aortic
stenosis is well defined.1 2 Patients with this disease
who have symptoms of congestive heart failure and remain untreated by aortic valve replacement have an
average life expectancy of approximately 2 years.
Although recent studies3-5 have shown that the majority of patients with critical stenosis and congestive
heart failure respond well to corrective surgery, some
patients with this condition are not helped by aortic
valve replacement. Patients with aortic stenosis and
congestive heart failure who responded well and those
who responded poorly to aortic valve replacement
may represent two distinct groups, rather than opposite ends of a spectrum. To test this hypothesis and
to identify the defining characteristics of these two
groups, we examined our experience at the Peter Bent
Brigham Hospital in patients with pure aortic stenosis
and severe congestive failure who underwent cardiac
catheterization and aortic valve replacement over a 5year period.
cm2/m2) who had no evidence of other hemodynamically significant valvular disease at catheterization were identified. Of this group, 28 patients (33%)
had an angiographically determined left ventricular
ejection fraction less than 0.45 and a clinical presentation of severe congestive heart failure (New York
Heart Association [NYHA] functional class LII or
IV). All 28 patients underwent coronary arteriography during catheterization. Ten patients had normal coronary arteriograms and four had minor, nonobstructive coronary narrowing (less than 40%
decrease in luminal diameter). These 14 patients
without significant coronary disease or other valvular
lesions, who had critical aortic stenosis, congestive
heart failure and depressed left ventricular ejection
fraction, constitute the study population.
Each patient underwent right- and retrograde leftheart catheterization, including left ventriculography
and coronary arteriography. Thirteen patients were in
sinus rhythm at catheterization, and one patient was
in atrial fibrillation. The left ventricle was entered
retrogradely via the brachial approach in all patients.
Systemic arterial pressure was measured by means of
a PE 160 catheter placed percutaneously in the right
femoral artery. Left ventricular pressure was
measured by standard fluid-filled angiographic
catheters in nine patients and by micromanometertipped, high-fidelity catheters in five. Left ventricular
pressure and systemic arterial pressure were recorded
simultaneously and mean systolic gradients were
measured by planimetry. All gradients were confirmed
by recording pressures during pullback of the catheter
from the left ventricle to the central aortic position.
Although the catheter may contribute to the effective
stenosis in patients with aortic valve areas less than 0.6
cm2, 6 the degree of this contribution could not be
Materials and Methods
All catheterization reports from January 1, 1974 to
January 1, 1979 were examined. Eighty-six patients
with aortic stenosis (aortic valve areas less than 0.4
From the Departments of Medicine and Surgery, Harvard
Medical School and Peter Bent Brigham Hospital, Boston,
Massachusetts.
Supported in part by USPHS grant HL-19246.
Dr. Grossman is an Established Investigator of the American
Heart Association.
Address for correspondence: William Grossman, M.D., Department of Medicine, Peter Bent Brigham Hospital, 721 Huntington
Avenue, Boston, Massachusetts 02115.
Received July 19, 1979; revision accepted January 5, 1980.
Circulation 62, No. 1, 1980.
42
LV FAILURE IN AORTIC STENOSIS/Carabello
assessed, and therefore valve area was calculated using
the measured left ventricular and aortic pressures in
the manner described by Gorlin.7 Cardiac output was
measured by the Fick method, simultaneously with
the gradient recording. Left ventriculography was
done in single-plane right anterior oblique projection
and recorded on 35-mm cine film at 60 frames/second. Left ventricular volumes were determined by the
area-length method in 13 patients using a regression
equation derived in our laboratory from the study of
postmortem left ventricular casts.8 In the remaining
patient the absence of a grid for calculating the
angiographic magnification correction factor allowed
only for determination of ejection fraction. Left ventricular mass was calculated by methods previously
described.9' 10 The ratio of left ventricular wall
thickness (h) to the minor-axis radius (r) was also
calculated. Left ventricular circumferential midwall
stress (af) was calculated by methods described
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previously," using the formula of Mirsky12:
Pb
h __b2
(
h
2a2
2b
where P = left ventricular pressure, h = wall
thickness, a = midwall semimajor axis (L/2 + h/2)
and b = midwall semiminor axis (D/2 + h/2). Left
ventricular ejection fraction was calculated as
(EDV - ESV)/EDV, where EDV and ESV are left
ventricular end-diastolic and end-systolic volumes,
respectively.
Significant aortic regurgitation was ruled out by
aortography in two patients. In 11 other patients in
et
al.
43
sinus rhythm, the regurgitant flow was calculated as:
[(EDV - ESV) X AHR] - FCO
where EDV = angiographic end-diastolic volume,
ESV = angiographic end-systolic volume, AHR =
heart rate during angiography and FCO = cardiac
output determined by the Fick method. Regurgitant
flow was less than 3 1/min in all patients, suggesting
the absence of significant aortic or mitral
regurgitation.13' 14 In the last patient the presence of
atrial fibrillation precluded calculation of regurgitant
flow. In this patient the absence of a diastolic murmur,
widened pulse pressure and fluttering of the mitral
valve leaflet on the echocardiogram served to rule out
significant aortic regurgitation.
All patients underwent aortic valve replacement
within 1 month of catheterization. Eleven patients
received a porcine heterograft valve and three received
a Bjork-Shiley prosthesis. Follow-up information was
obtained from office records. Four patients underwent
radionuclide ventriculography postoperatively to
assess ejection fraction directly.
Statistical inference was made using the exact
probability method15 for attributes and the t test for
variables.
Results
The clinical data for all patients are shown in table
1. Thirteen patients were male, one was female. Eight
patients were in NYHA class III and six were in class
IV preoperatively. Of the eleven survivors, eight
became class I, two became class II and one remained
in class IV postoperatively (fig. 1). Patient follow-up
averaged 28 ± 5 months.
TABLE 1. Clinical Characteristics of 14 Patients with Aortic Stenosis and Left Ventricular Failure
Age
Preoperative Postoperative Follow-up
NYHA class NYHA class (months)
Sex
Pt
(years)
Symptoms
Group 1
1
2
3
4
5
6
7
8
9
10
54
70
68
62
61
76
42
68
73
68
M
M
M
M
M
M
M
M
M
F
Angina, DOE
Syncope, DOE
DOE, PND
Angina, DOE, PND
DOE
Angina, DOE, edema
Syncope, DOE
DOE
Angina, DOE, PND, edema
Angina, syncope, DOE, PND
III
IV
III
III
III
III
III
III
IV
III
I
I
I
II
II
I
I
I
I
I
57
45
28
32
31
29
23
22
23
6
Group 2
OD
M
IV
DOE, PND
65
OD
M
IV
56
DOE, PND, edema
M
IV
PD
49
DOE, PND
M
edema
IV
IV
66
8
DOE, PND,
Abbreviations: DOE = dyspnea on exertion; PND = paroxysmal nocturnal dyspnea; OD = operative
death; PD = perioperative death; NYHA = New York Heart Association.
11
12
13
14
VOL 62, No 1, JULY 1980
CIRCULATION
44
NYHA
CLASSIFICATION
POST-OP
PRE-OP
8
11
111
IV
6
W
2x/
Lif6/
1~1
Iv
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FIGURE 1. Preoperative and postoperative New York
Heart Association (NYHA) classification of operative survivors who underwent aortic valve replacement for aortic
stenosis and left ventricular failure.
Three of 14 patients (2 1%) died in the operative or
perioperative period. This exceeds the overall mortality rate of 3.4% (five of 148 patients) for isolated
aortic valve replacement in patients with aortic
stenosis at our institution during the same period. Two
of the patients could not be weaned from cardiopulmonary bypass. The third patient died of a low
cardiac output state 9 days after operation. There
were no late deaths.
Ten patients who had a satisfactory result
(postoperative class I or II) were grouped together and
form group 1. The three patients who died at operation and the one patient who remained in class IV
postoperatively form group 2. The two groups were
compared to identify preoperative factors associated
with satisfactory or unsatisfactory outcome.
Preoperatively, all patients were receiving digoxin
and furosemide. All patients complained of at least
two-pillow orthopnea and dyspnea with minimal exertion or at rest. There was no statistical difference in
age between groups. Angina and syncope were more
frequent in group 1, while paroxysmal nocturnal
dyspnea and edema were more frequent in group 2
(table 1); neither of these differences was statistically
significant.
Two of 10 group 1 patients (20%) and all four
(100%) group 2 patients were in functional class IV
preoperatively (p < 0.05).
Hemodynamic and angiographic data are presented
in tables 2 and 3. The mean pulmonary capillary
wedge pressure was similar in both groups. The
average aortic valve area index for group 2 was
0.30 ± 0.02 cm2/m2, which was significantly larger
than for group 1 (0.21 ± 0.02 cm2/m2,p < 0.05). Cardiac index was significantly lower for group 2
(1.5 ± 0.3 1/min2) than for group 1 (2.1 ± 0.1
1/min/M2, p < 0.05). The average end-diastolic
volume index for group 2 was 174 ± 9 ml/m2, compared with 119 ± 9 ml/m2 for group 1 (p < 0.005).
The end-systolic volume index for group 2 was
140 ± 9 MIl/m2, compared with 80 ± 7 ml/m2 for
group 1 (p < 0.005). The average ejection fraction for
TABLE 2. Hemodynamic Data from Patients with Severe Aortic Stenosis and Left Ventricular Failure
Pt
Group 1
1
2
3
Left ventricular
end-diastolic pressure
(mm Hg)
Aortic valve
areaindex
(cm2/m2)
32
46
47
38
37
0.16
0.23
0.20
0.33
35
32
38
40
40
0.20
0.27
0.24
0.23
0.12
0.21 0.02
80 =19
0.25
0.31
0.39
0.26
40
18
20
32
4
5
6
7
8
9
10
Mean sEM
39
0.11
2
Peak systolic
gradient
(mm Hg)
Mean systolic
gradient
(mm Hg)
(1/min/M2)
90
38
66
46
60
80
42
46
48
93
2.4
1.7
2.4
2.5
1.4
1.6
1.8
2.0
2.4
2.3
110
60
76
51
87
97
55
50
74
138
61
Cardiac
index
6
2.1
1*
1.1
1.3
2.3
1.3
1.5 0.3*
0.1
Group 2
11
12
13
14
Mean - sEM
*p < 0.05.
38
42
37
35
38 -1
0.30 0.20*
28
5*
20
21
23
25
22
LV FAILURE IN AORTIC STENOSIS/Carabello et al.
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TABLE 3. Angiographic Data from Patients with Severe Aortic
Stenosis and Left Ventricular Failure
LVEDVI
LVESVI
LVMI
Pt
(ml/rn2)
LVEF
(g/m2)
(ml/m2)
Group 1
1
132
74
0.44
302
2
0.17
3
154
110
0.29
239
4
94
58
0.38
253
5
157
118
0.25
207
6
88
54
0.39
191
7
105
74
0.29
176
8
125
75
0.40
202
9
93
74
0.21
139
10
123
81
0.34
211
Mean
119
80
0.32
213
16
9
SEM
0.03
;
=7
45
EF
Group 2
11
12
13
14
Mean
i SEM
189
174
150
183
174
162
137
116
156
140
a=9t
=9t
0.20
0.21
0.23
0.15
0.20
0.02*
231
207
217
347
251
-33
*p < 0.05.
tP < 0.005.
Abbreviations: LVEDVI = left ventricular end-diastolic
volume index; LVESVI = left ventricular end-systolic volume index; LVEF = left ventricular ejection fraction;
LVMI = left ventricular mass index.
FIGURE 2. Individual preoperative ejection fractions (EF)
for patients in groups 1 ( * ) and 2 (X). Although mean EF
was greater for group I than for group 2, three group 1
patients had EF similar to that of group 2. Thus, EF alone
was not a good predictor of outcome.
the left of the line developed from coordinates for
group 1 (fig. 5). Thus, for any given wall stress, ejection fraction was lower in group 2.
Left ventricular wall thickness/radius ratio (h/r)
was higher in group 1 patients (0.42 ± 0.03) than in
group 2 patients (0.35 ± 0.03), although the difference
was not statistically significant (p = 0.08).
group 2 was 0.20 ± 0.02, which was less than that for
group 1 (0.32 ± 0.03 p < 0.05) (fig. 2). The peak
systolic aortic valve gradient for group 2 was 28 ± 5
mm Hg, compared with 80 ± 9 mm Hg for group 1
(p < 0.005). A similar striking difference existed for
mean systolic gradient, which averaged 22 ± 1 mm
Hg for group 2 vs 61 ± 6 mm Hg for group 1
MEAN SYSTOLIC
GRADIENT
120
110
(p < 0.005) (fig. 3).
Four group 1 patients had postoperative determination of left ventricular ejection fraction by radionuclide ventriculography 6-13 months after surgery.
Because ejection fraction determined in this manner
correlates well with angiographically determined ejection fraction,'6' 17 we compared preoperative
angiographic ejection fraction with postoperative
radionuclide ejection fraction in these four group 1
patients. The preoperative ejection fraction was
0.33 ± 0.03, compared with 0.59 + 0.03 postoperatively (p < 0.001).
Mean circumferential wall stress was plotted
against ejection fraction for the five group 1 patients
not previously studied by this method, as well as for
the four previously analyzed"l (fig. 4). A linear
relationship (r = 0.93) similar to that reported by
Gunther and Grossman"l was found. Values for
preoperative wall stress in group 2 all fell below and to
100
mmHg
90
0
0
80
0
70
60
50
S
0
0
S.0
40
S
0
30
20
X
XXX
10
FIGURE 3. Mean systolic aortic pressure gradients for
patients in group 1 ( * ) and group 2 (X). Group 2 patients
had lower systolic gradients in every case.
VOL 62, No 1, JULY 1980
CIRCULATION
46
.6
.6
z .5
0
O .5
H
(-)
z
U-
lL
z .4
.4
U0
H
u3
0
0
Li.3
0
0
0
x
0
.2
.2
x
x
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x
I
15J
200
25U
or
(dynes
300
x
35U
400
450
11
150
1
103/cm2)
FIGURE 4. Ejection fraction plotted against mean circumferential left ventricular wall stress (a) for nine group I
patients. A linear relationship (r = 0.93) that could be extrapolated back to normal ejection fraction and a wasfound.
Open circles represent patients previously presented,"
closed circles represent newly evaluated patients.
t
-1 I
300
250
350
aJ dynes x 103/cm2
200
400
450
FIGURE 5. Ejection fraction (EF) plotted against mean
circumferential left ventricular wall stress (a) for group I
(0, * ) and group 2 (X). Open circles represent patients
previously presented,.' closed circles and crosses (X) represent newly evaluated patients. Group 2 patients fell below
and to the left of group 1 patients, indicating lower ejection
fraction despite less This is consistent with the concept
that left ventricular performance (EF) was depressed in
group I patients due to afterload mismatch and in group 2
patients due to myocardial failure.
a.
Discussion
The main finding of this study is that patients with
critical aortic stenosis and advanced congestive heart
failure apparently fall into two distinct subgroups.
One subgroup (group 1) had left ventricular failure apparently on the basis of excessively high wall stress
and afterload mismatch."8 This group uniformly had a
good surgical result. A second subgroup (group 2) had
more severe left ventricular failure despite less severe
aortic stenosis (larger valve area) and a lesser
afterload, suggesting depressed myocardial contractility as a major contributing factor producing left
ventricular failure. These patients had a poor
prognosis.
Cohn and associates'9 stressed the importance of
preoperative left ventricular function as a prognostic
guide to both valvular and coronary artery bypass surgery. Forty percent of their patients with an ejection
fraction less than 0.50 died at surgery. However, recent studies by Croake et al.,3 Smith et al.4 and
Thompson et al.5 suggest that this relationship may
not hold true for patients with severe aortic stenosis
and depressed left ventricular function. These studies,
however, did not identify preoperative factors that
predicted outcome, possibly because many patients in
these studies had coronary artery disease. Because
coronary artery disease is believed to be a strong
negative prognostic factor,20-23 it may have obscured
other prognostic factors. Our series of patients,
although not large, only included patients with severe
aortic stenosis and no obstructive coronary disease.
That patients with aortic stenosis and depressed left
ventricular function should do well after surgery is not
altogether surprising. Many studies have shown
postoperative improvement in left ventricular function
after aortic valve replacement in patients with aortic
stenosis and depressed preoperative ejection fraction.4 5, 24-27 Gunther and Grossman"l recently
presented evidence supporting the concept that some
patients with aortic stenosis and depressed left ventricular performance may have this depression on the
basis of excessive wall stress (afterload mismatch)
rather than on the basis of depressed contractile state.
Relief of this excessive afterload by aortic valve
replacement allows for immediate improvement of
ventricular performance; hence, even patients with
severely depressed preoperative left ventricular function may have an excellent surgical result. Further
support for this concept comes from the elegant
studies of Strauer,28 29 who reported that in patients
with left ventricular pressure-overload hypertrophy
from hypertension, as well as aortic stenosis and
regurgitation, left ventricular ejection fraction and
peak systolic wall stress correlate inversely.
Our study confirms that many patients with
LV FAILURE IN AORTIC STENOSIS/Carabello et al.
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depressed left ventricular function and aortic stenosis
have a good prognosis with aortic valve replacement.
Ten of 14 such patients (72%) returned to class I or
II postoperatively. When we analyzed preoperative
factors we thought might have had prognostic
importance, we found a significant difference in
preoperative left ventricular function between the
patients who had a satisfactory surgical result (group
1) and those who did not (group 2). Group 2 patients
had more advanced clinical class, lower cardiac index,
higher end-diastolic volume index and lower ejection
fraction than group 1 patients. However, none of these
factors alone was highly predictive of outcome. Twenty percent of group 1 patients were in class IV and
returned to class I postoperatively. Twenty percent
had a cardiac index less than 1.6 1/min/m2, 20% had
an end-diastolic volume index greater than 150 ml/m2
and 30% had an ejection fraction less than 0.25.
However, when ejection fraction was plotted against
mean wall stress (u) for both groups, major differences
were found. The linear relationship between ejection
fraction and wall stress could be extrapolated to a normal ejection fraction and normal wall stress for group
1 patients, suggesting that the major factor in the
decreased left ventricular performance in group 1
patients preoperatively was excessive wall stress. In
contrast, group 2 patients had a lower ejection fraction at a given wall stress than group 1 patients. Group
2 also had a larger aortic valve area index than group
1. Thus, group 2 had poorer left ventricular performance despite less wall stress and less obstruction to
outflow. This suggests that group 2, unlike group 1,
had depressed myocardial contractility as a significant
component of their left ventricular failure, rather than
excessive wall stress.
The etiology of this depressed contractility is uncertain. One possibility is that group 2 patients with
depressed contractility represent the end stage of a
natural progression of the disease. However, this
seems unlikely because there was actually less severe
aortic stenosis in group 2 patients. A second explanation is that a concomitant cardiomyopathy of unknown etiology was also present in group 2. As our
study was not designed to evaluate this question, data
for or against this supposition are lacking. Third,
some ventricles simply may not tolerate excessive wall
stress as well as others. High wall stress, if produced
acutely, may cause myocardial injury in experimental
animals.30, 31 However, the variability in response to
chronically elevated wall stress is not known.
The relatively low wall stress in group 2 patients can
readily be translated into the low transvalvular
gradients and lower left ventricular systolic pressures
(less than 150 mm Hg in every case). Thus, a peak
systolic gradient less than 30 mm Hg across the aortic
valve when associated with congestive failure may
identify patients with a significant component of intrinsic myocardial contractile depression. These
patients have greater depression of ventricular performance even though afterload is relatively less, and
may not be fully identified on the basis of preoperative
symptoms, functional class, cardiac output, end-
47
diastolic volume or ejection fraction, because patients
with aortic stenosis may have a severe abnormality in
any one of these variables and still have a good
prognosis. A low transvalvular gradient indicative of a
low cardiac output and larger orifice area suggest
severe left ventricular dysfunction but less obstruction
to outflow. When this is coupled with decreased ejection fraction, despite normal or only slightly increased
LV wall stress, the implication is that significant cardiomyopathy is present and the prognosis is poor.
Aortic valve replacement in this group carries an extraordinarily high risk.
We found encouraging results for aortic valve
replacement in patients with severe aortic stenosis and
depressed preoperative left ventricular function. The
majority of patients in this series had left ventricular
failure because of excessive afterload imposed by the
stenotic valve. This group of patients has a good
prognosis, because aortic valve replacement decreases
afterload and allows for improved ventricular performance. The explanation for the afterload excess or
"afterload mismatch" in these patients is uncertain,
because many patients encountered in our laboratory
during the same years had identical degrees of
obstruction (as judged by valve area) but normal left
ventricular wall stress and ejection fraction. Because
concentric hypertrophy usually develops in aortic
stenosis in such a fashion as to maintain normal wall
stress,32 we have speculated that inadequate hypertrophy of the left ventricular myocardium may explain
the high wall stress and depressed fiber shortening in
this subset of patients.`' The lower h/r ratio in group 2
is consistent with this concept, but the number of subjects is too small to permit any firm conclusion to be
drawn.
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Hemodynamic determinants of prognosis of aortic valve replacement in critical aortic
stenosis and advanced congestive heart failure.
B A Carabello, L H Green, W Grossman, L H Cohn, J K Koster and J J Collins, Jr
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Circulation. 1980;62:42-48
doi: 10.1161/01.CIR.62.1.42
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