Download Impact of valve prosthesis-patient mismatch on pulmonary

Journal of the American College of Cardiology
© 2005 by the American College of Cardiology Foundation
Published by Elsevier Inc.
Vol. 45, No. 7, 2005
ISSN 0735-1097/05/$30.00
doi:10.1016/j.jacc.2004.10.073
Impact of Valve Prosthesis-Patient
Mismatch on Pulmonary Arterial
Pressure After Mitral Valve Replacement
Mingzhou Li, MD, PHD, Jean G. Dumesnil, MD, FACC, Patrick Mathieu, MD,
Philippe Pibarot, DVM, PHD, FACC
Sainte-Foy, Quebec, Canada
We sought to determine the impact of valve prosthesis-patient mismatch (PPM) on
pulmonary arterial (PA) pressure after mitral valve replacement (MVR).
BACKGROUND Pulmonary arterial hypertension is a serious complication of mitral valve disease, and it is a
major risk factor for poor outcome after MVR. We hypothesized that valve PPM might be
a determinant of PA hypertension after MVR.
METHODS
Systolic PA pressure was measured by Doppler echocardiography in 56 patients with normally
functioning mitral prosthetic valves. Mitral valve effective orifice area (EOA) was determined
by the continuity equation and indexed for body surface area.
RESULTS
Thirty patients (54%) had PA hypertension defined as systolic PA pressure ⬎40 mm Hg,
whereas 40 patients (71%) had PPM defined as an indexed EOA ⱕ1.2 cm2/m2. There was
a significant correlation (r ⫽ 0.64) between systolic PA pressure and indexed EOA. The
average systolic PA pressure and prevalence of PA hypertension were 34 ⫾ 8 mm Hg and
19% in patients with no PPM versus 46 ⫾ 8 mm Hg and 68% in patients with PPM (p ⬍
0.001). In multivariate analysis, the indexed EOA was by far the strongest predictor of systolic
PA pressure.
CONCLUSIONS Persistent PA hypertension is frequent after MVR and strongly associated with the presence
of PPM. The clinical implications of these findings are important given that PPM can largely
be avoided by using a simple prospective strategy at the time of operation. (J Am Coll
Cardiol 2005;45:1034 – 40) © 2005 by the American College of Cardiology Foundation
OBJECTIVES
Pulmonary arterial (PA) hypertension is a frequent and
serious complication of mitral valve diseases, and it is a
major risk factor for poor outcome after surgery for mitral
stenosis (1) or mitral regurgitation (2– 4). Not surprisingly,
the impact of PA hypertension on morbidity and mortality
See page 1041
is highly dependent on its degree of severity. Severe PA
hypertension is associated with a high risk of perioperative
mortality (10% to 15%) in patients undergoing mitral valve
replacement (MVR) as well as with increased mortality in
the long term (1–3). Nonetheless, mild PA hypertension is
not necessarily benign because it is associated with significantly worse exercise capacity and higher morbidity and
mortality. Therefore, the normalization of PA pressure is a
crucial goal of MVR. Unfortunately, the regression of PA
hypertension after operation varies extensively from one
patient to the other and is often incomplete (5,6).
The effective orifice area (EOA) of prosthetic valves used
for MVR is often too small in relation to body size, thus
causing a mismatch between valve EOA and transvalvular
flow (7–10). As a consequence, normally functioning mitral
prostheses often have relatively high gradients that are
similar to those found in patients with mild/moderate mitral
stenosis (6,9 –11). Residual pressure gradients across mitral
prostheses may hinder or delay the regression of left atrial
and PA hypertension (7–9). We, therefore, hypothesized
that valve prosthesis-patient mismatch (PPM) might be an
important determinant of the persistence of PA hypertension after MVR. The main objective of this study was, thus,
to determine the impact of PPM on PA pressure after
MVR.
METHODS
From the Research Group in Valvular Heart Diseases, Research Center of Laval
Hospital/Quebec Heart Institute, Laval University, Sainte-Foy, Quebec, Canada.
This work was supported by the Canadian Institutes of Health Research (MOP
67123), Ottawa, Ontario, Canada. Dr Pibarot is the Director of the Canada Research
Chair in Valvular Heart Diseases, Canadian Institutes of Health Research, Ottawa,
Ontario, Canada. Medtronic Inc., St-Jude Medical Inc., and Edwards Life Science
Inc. have provided financial support to the Departments of Cardiac Surgery and
Cardiology of the Quebec Heart Institute/Laval Hospital for the clinical and
echocardiographic follow-up of patients receiving Medtronic Intact, Medtronic
Mosaic, St. Jude bileaflet mechanical, and Carpentier-Edwards Perimount valves.
Drs. Pibarot and Dumesnil also received consultant and speaker fees from St. Jude
Medical and Medtronic Inc.
Manuscript received April 1, 2004; revised manuscript received July 16, 2004,
accepted October 14, 2004.
Patient population. We retrospectively analyzed the data
of patients with a mitral prosthesis who were consecutively
evaluated by Doppler echocardiography at the Quebec
Heart Institute between January 2003 and August 2003.
Exclusion criteria were as follows: 1) evidence of overt
prosthetic valve dysfunction; 2) presence of ⬎2⫹ aortic
valve regurgitation and/or ⬎ mild aortic stenosis. Seventytwo patients met these eligibility criteria. Measurement of
systolic PA pressure and/or mitral valve EOA could not be
obtained in 14 of these patients. The study group was,
Li et al.
Impact of Mitral Prosthesis-Patient Mismatch
JACC Vol. 45, No. 7, 2005
April 5, 2005:1034–40
Abbreviations and Acronyms
EOA ⫽ effective orifice area
MVR ⫽ mitral valve replacement
PA ⫽ pulmonary arterial
PPM ⫽ prosthesis-patient mismatch
therefore, composed of 56 patients with a mean age of 65 ⫾
12 years and a median follow-up time of 43 months (range
8 to 102 months).
Doppler-echocardiography. The systolic PA pressure was
calculated by adding the systolic right ventricular pressure
derived from the tricuspid regurgitation to the estimated
right atrial pressure (12–14). Right atrial pressure was
estimated from the diameter and the degree of collapse of
the inferior vena cava during inspiration (14 –16). Pulmonary arterial hypertension was defined as a systolic PA
pressure ⬎40 mm Hg (17).
Mitral valve EOA was determined by the continuity
equation using the stroke volume measured in the left
ventricular outflow tract divided by the integral of the mitral
valve transprosthetic velocity during diastole; PPM was
defined as an indexed EOA ⱕ1.2 cm2/m2 as suggested in
previous studies (9,10), and, on this basis, the patients were
arbitrarily divided into two subgroups (i.e., those with no
PPM and those with PPM).
Because atrioventricular compliance has been shown to
influence PA pressure in patients with mitral stenosis
(18,19), we also elected to calculate this parameter, such as
suggested by Flaschkampf et al. (18,19). Indeed, these
authors have presented analytical and numerical evidence
showing that net atrioventricular compliance (Cn), which is
the change in volume shift between left atrium and left
ventricle during diastole divided by the change in transmitral pressure gradient, can be determined noninvasively by
Doppler-echocardiography using the following equation:
Cn ⫽ 1,270 共EOA/E-wave downslope兲
[1]
whereby EOA is the mitral valve EOA determined by the
continuity equation in cm2, E-wave downslope is the mitral
velocity E-wave downslope measured in cm/s2, and the
result is expressed in ml/mm Hg. Schwammenthal et al.
(19) found that Cn as determined by this equation correlated
well (r ⫽ 0.79) with invasively determined values of the
same parameter in patients with mitral stenosis. It should be
emphasized that Cn is theoretically affected by both atrial
and ventricular chamber compliances but that these two
variables cannot be measured individually by noninvasive
methods. Nonetheless, the left atrium and left ventricle can
be seen as behaving like two capacitors in series, whereby
their compliances combine to yield net atrioventricular
compliance as follows:
Cn ⫽ 共1/Ca ⫹ 1/Cv兲⫺1
[2]
Statistical analysis. Differences between groups for preoperative, operative, and postoperative variables were tested for
1035
statistical significance by t test, chi-square test, or Fischer
exact test as appropriate. The Fischer exact test was used
instead of the chi-square test when over 20% of the expected
values in the contingency table were ⬍5. Statistical analysis
of the association of variables was performed with the
Pearson correlation coefficient. A forward stepwise regression analysis was used to identify the independent determinants of systolic PA pressure. Age and gender were forced
into the multivariate model, whereas other variables were
entered in the model when the p value was ⬍0.1 in
univariate analysis.
RESULTS
The patients demographic, preoperative, and operative
data are presented in Table 1. For the whole group, the
predominant mitral valve lesion at the time of operation was mitral regurgitation in 43% of patients, mitral
stenosis in 41%, and mixed mitral valve disease in 16%,
whereas evidence of PA hypertension defined as a preoperative systolic PA pressure measured by Dopplerechocardiography and/or catheter ⬎40 mm Hg was present
in 67% of patients. A mechanical prosthesis was inserted in
84% of patients, whereas 16% received a bioprosthesis. The
model of prosthetic valve was Standard St. Jude Medical
(St. Jude Medical, Minneapolis, Minnesota) in 34 (61%)
patients; On-X (MCRI, Austin, Texas) in 5 (9%); Advantage (Medtronic) in 4 (7%); Medtronic-Hall (Medtronic) in
4 (7%); Mosaic (Medtronic) in 4 (7%); Hancock
(Medtronic) in 2 (3.5%); Intact (Medtronic,) in 2 (3.5%);
and homograft (Cryolife, Kennesaw, Georgia) in 1 (2%).
The mitral valve leaflets and chordae were totally or partially
(posterior) preserved in 41% of patients. Concomitant
procedures included left atrial appendage obliteration in
23%, Maze procedure in 9%, and coronary artery bypass
graft surgery in 16%. The proportion of small (ⱕ27 mm)
valves was 52%, which is comparable with that reported in
previous recent series (20 –24). There was no significant
difference between patients having total, partial, or no
preservation of the valve leaflets and chordae with regard to
prosthesis size.
Based on an indexed EOA ⱕ1.2 cm2/m2, 40 of the 56
patients (71%) were classified as having PPM. In comparison to patients with no PPM, patients with PPM had a
significantly larger body surface area, a higher prevalence of
systemic hypertension, and a higher proportion of smaller
prostheses; indeed, prosthesis size was ⱕ27 mm in 66% of
patients with PPM as compared to only 19% of patients
without PPM. The other preoperative and operative data
were similar in both groups.
The postoperative Doppler-echocardiographic data are
presented in Table 2. The mean systolic PA pressure for the
whole group after operation was 42 ⫾ 10 mm Hg (range 22
to 61 mm Hg), whereas evidence of PA hypertension
defined as a systolic PA pressure ⬎40 mm Hg was found in
30 of the 56 patients (54%).
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Li et al.
Impact of Mitral Prosthesis-Patient Mismatch
JACC Vol. 45, No. 7, 2005
April 5, 2005:1034–40
Table 1. Demographic, Preoperative, and Operative Data
Variables
Demographic data
Gender
Female
Male
Age (yrs)
Body surface area (m2)
Preoperative data
Predominant valvular dysfunction
Mitral stenosis
Mitral regurgitation
Mixed mitral valve dysfunction
Coronary artery disease
Diabetes
Systemic arterial hypertension
Pulmonary arterial hypertension
Operative data
Type of prosthesis
Mechanical prosthesis
Bioprosthesis
Prosthesis size (mm)
25
27
29
31
33
Total chordal preservation
Posterior chordal preservation
Left atrial appendage obliteration
Maze procedure
Coronary artery bypass graft
All Patients
(n ⴝ 56)
No PPM
(n ⴝ 16)
PPM
(n ⴝ 40)
36 (64%)
20 (36%)
65 ⫾ 12
1.72 ⫾ 0.17
10 (63%)
6 (38%)
63 ⫾ 14
1.64 ⫾ 0.18
26 (65%)
14 (35%)
66 ⫾ 11
1.75 ⫾ 0.16
23 (41%)
24 (43%)
9 (16%)
12 (21%)
4 (7%)
17 (30%)
32/48 (67%)
8 (47%)
5 (33%)
3 (20%)
2 (13%)
1 (6%)
1 (6%)
11/16 (69%)
15 (36%)
19 (48%)
6 (15%)
10 (25%)
3 (8%)
16 (40%)
21/32 (66%)
47 (84%)
9 (16%)
14 (88%)
2 (13%)
7 (13%)
22 (39%)
15 (27%)
10 (18%)
2 (4%)
5 (9%)
18 (32%)
13 (23%)
5 (9%)
11 (20%)
2 (13%)
1 (6%)
7 (44%)
5 (31%)
1 (6%)
2 (13%)
3 (19%)
4 (25%)
2 (13%)
1 (6%)
33 (83%)
7 (18%)
*
5 (13%)
21 (53%)
8 (20%)
5 (13%)
1 (2%)
3 (8%)
13 (33%)
9 (23%)
3 (8%)
10 (24%)
p
Value*
NS
NS
0.03
NS†
NS†
NS†
0.02†
NS
NS†
0.001†
NS
NS
NS†
NS†
NS†
*p value for the difference between PPM and no PPM groups; †indicates when a Fischer exact test was used instead of the
chi-square test. The prosthesis sizes have been regrouped into two categories (25 to 27 mm category vs. 29 to 33 mm category)
to permit application of Fischer exact test.
PPM ⫽ prosthesis-patient mismatch.
Impact of PPM on PA pressure. As expected, mitral valve
EOA and indexed mitral valve EOA were significantly
lower in patients with PPM as compared to patients with no
PPM. The former patients also had significantly higher
peak and mean transvalvular pressure gradients, PA pressure, and prevalence of PA hypertension, whereas their net
atrioventricular compliance was significantly lower (Table
2). The indexed EOA (i.e., the degree of PPM) correlated
well with postoperative PA pressures (r ⫽ 0.64; Fig. 1) and
to a lesser extent with peak (r ⫽ 0.50) and mean (r ⫽ 0.46)
gradients, and atrioventricular compliance (r ⫽ 0.37).
Hence, the average systolic PA pressure was significantly
higher (p ⬍ 0.001) in patients with PPM (46 ⫾ 8 mm Hg)
compared to patients with no PPM (34 ⫾ 8 mm Hg) (Table
Table 2. Postoperative Doppler Echocardiographic Data
Variables
All Patients
(n ⴝ 56)
No PPM
(n ⴝ 16)
PPM
(n ⴝ 40)
p Value
Atrial fibrillation
End-diastolic LV diameter (mm)
End-systolic LV diameter (mm)
End-diastolic interventricular septal thickness (mm)
End-diastolic LV posterior wall thickness (mm)
End-systolic LA diameter (mm)
Mitral valve EOA (cm2)
Indexed mitral valve EOA (cm2/m2)
Peak transmitral gradient (mm Hg)
Mean transmitral gradient (mm Hg)
Net atrioventricular compliance (ml/mm Hg)
Systolic PA pressure (mm Hg)
PA hypertension (systolic PA pressure ⬎40 mm Hg)
22 (39%)
49 ⫾ 7
34 ⫾ 9
10 ⫾ 2
10 ⫾ 2
51 ⫾ 11
1.8 ⫾ 0.4
1.1 ⫾ 0.3
11 ⫾ 4
4⫾2
4.1 ⫾ 1.7
42 ⫾ 10
30 (54%)
7 (44%)
50 ⫾ 7
34 ⫾ 9
10 ⫾ 1
10 ⫾ 3
52 ⫾ 14
2.3 ⫾ 0.3
1.4 ⫾ 0.1
8⫾2
3⫾1
5.3 ⫾ 1.6
34 ⫾ 8
3 (19%)
15 (38%)
49 ⫾ 7
33 ⫾ 8
10 ⫾ 2
11 ⫾ 2
50 ⫾ 10
1.7 ⫾ 0.3
1.0 ⫾ 0.2
12 ⫾ 4
4⫾2
3.6 ⫾ 1.6
46 ⫾ 8
27 (68%)
NS
NS
NS
NS
NS
NS
⬍0.001
⬍0.001
⬍0.001
0.001
0.001
⬍0.001
0.001†
Symbols as in Table 1.
EOA ⫽ effective orifice area; LA ⫽ left atrial; LV ⫽ left ventricular; PA ⫽ pulmonary arterial; PPM ⫽ prosthesis-patient mismatch.
JACC Vol. 45, No. 7, 2005
April 5, 2005:1034–40
Figure 1. Correlation between systolic pulmonary arterial (PA) pressure
and indexed mitral valve effective orifice area. An indexed mitral valve
effective orifice area ⱕ1.2 cm2/m2 afforded the best sensitivity and
specificity for the prediction of PA hypertension defined as a systolic PA
pressure ⬎40 mm Hg (thin lines).
2). Likewise, the prevalence of persistent PA hypertension
after MVR was 68% in patients with PPM versus 19% in
patients with no PPM (Fig. 2). An indexed mitral valve
EOA ⱕ1.2 cm2/m2 had a sensitivity of 68% and a specificity
of 81% to predict PA hypertension.
Impact of atrioventricular compliance on PA pressure. Systolic PA pressure also correlated (r ⫽ 0.53) with net
atrioventricular compliance (Fig. 3). On average, patients
with an atrioventricular compliance ⱕ4 ml/mm Hg had a
significantly higher (p ⬍ 0.001) postoperative systolic PA
pressure (46 ⫾ 8 mm Hg) compared to those with compliance ⬎4.0 ml/mm Hg (36 ⫾ 8 mm Hg).
Independent determinants of PA pressure. In multivariate analysis, the independent determinants of systolic PA
pressure were: indexed mitral valve EOA (p ⬍ 0.001), net
atrioventricular compliance (p ⬍ 0.001), and mean transvalvular flow rate (p ⫽ 0.04) (Table 3). Indexed EOA had
the most important contribution in the multivariate model
Li et al.
Impact of Mitral Prosthesis-Patient Mismatch
1037
Figure 3. Correlation between systolic pulmonary arterial (PA) pressure
and net atrioventricular compliance.
followed by atrioventricular compliance. Mean transvalvular
flow rate had a minimal contribution with borderline
significance. There was a weak (r ⫽ 0.35, p ⫽ 0.007)
correlation between time to follow-up and postoperative PA
pressure in univariate analysis, but this variable was not a
significant independent predictor of PA pressure in multivariate analysis.
In the subgroup of 48 patients in whom the preoperative
PA pressure was available, this variable did not come out as
a significant predictor of postoperative PA pressure in
multivariate analysis, and the only significant predictors
were the indexed MVA (⌬R2 ⫽ 0.39, p ⫽ 0.003) and the
net atrioventricular compliance (⌬R2 ⫽ 0.08, p ⫽ 0.01).
In Figure 4, the patients were separated into four subgroups depending on the presence of PPM and of low
atriocompliance defined as being ⱕ4.0 ml/mm Hg. The
systolic PA pressure and prevalence of PA hypertension
were 33 ⫾ 9 mm Hg and 23% in patients (n ⫽ 13) with no
PPM and normal compliance, 34 ⫾ 2 mm Hg and 0% in
patients (n ⫽ 3) with no PPM and low compliance, 40 ⫾ 5
mm Hg and 36% in patients (n ⫽ 11) with PPM and
normal compliance, and 48 ⫾ 7 mm Hg and 79% in
patients (n ⫽ 29) with PPM and low compliance.
Table 3. Independent Determinants of Postoperative Systolic
Pulmonary Arterial Pressure
Figure 2. Prevalence of pulmonary arterial (PA) hypertension before and
after mitral valve replacement in patients with prosthesis-patient mismatch
(PPM) versus those with no PPM. Open bars ⫽ preoperative; solid bars
⫽ postoperative.
Variables
Standardized
Coefficient
⌬R2
p
Value
Age
Gender
Indexed mitral valve EOA
Net atrioventricular compliance
Mean transvalvular flow rate
0.14
0.85
⫺0.52
⫺0.39
0.23
—
—
0.41
0.12
0.04
0.11
0.68
⬍0.001
⬍0.001
0.049
The ⌬R2 value represents the respective contribution of the variable to the variance of
the systolic pulmonary arterial pressure in the multivariate model.
EOA ⫽ effective orifice area.
1038
Li et al.
Impact of Mitral Prosthesis-Patient Mismatch
Figure 4. Systolic pulmonary arterial (PA) pressure according to valve
prosthesis-patient mismatch (PPM) and net atrioventricular compliance
(Cn). Low Cn is defined as Cn ⱕ4.0 ml/mm Hg.
DISCUSSION
An increase in PA pressure can result from elevation of
pulmonary blood flow, pulmonary venous pressure, and/or
vascular resistance (25–27). The major consequence of PA
hypertension is right ventricular failure, which generally
results from chronic pressure overload and associated volume overload with the development of tricuspid regurgitation (26); PA hypertension is an important risk factor for
morbidity and mortality in patients with cardiovascular
diseases (28 –33). The clinical course of patients with PA
hypertension can be highly variable depending on the
underlying disease. However, with the onset of right ventricular failure, patient survival is generally limited to approximately six months (26); PA hypertension is frequently
(30% to 70%) observed in patients with mitral valve disease
(2– 6,34). The passive elevation of PA pressure due to
elevated left atrial pressure is the main mechanism leading
to PA hypertension in these patients. In addition to this
passive elevation of PA pressure, there is often a reactive
vasoconstriction of the pulmonary arterioles that causes an
increase in pulmonary vascular resistance and, thus, contributes to the elevation of PA pressure. Moreover, in patients
with longstanding disease, potentially irreversible structural
changes may occur in the pulmonary vasculature.
Given that PA hypertension is quite prevalent in patients
with severe mitral valve disease and that it is associated with
poor functional capacity and dismal prognosis (1–3,35),
normalization of PA pressure, therefore, constitutes a crucial goal of MVR. Successful surgical relief of the mechanical cause of pulmonary venous hypertension generally
reduces PA pressure and promotes regression of the reversible components of pulmonary vascular changes (25,26).
Unfortunately, the relief of the passive elevation of left atrial
pressure and, thus, of PA pressure is often incomplete, (5,6)
likely due to the interaction of prosthesis- and/or patientrelated factors. Zielinski et al. (5) reported PA pressure data
obtained by catheterization before and one year after MVR.
In 14 patients with PA hypertension (defined as systolic PA
pressure ⬎40 mm Hg) before operation, PA hypertension
was still present in seven patients (50%) one year after
JACC Vol. 45, No. 7, 2005
April 5, 2005:1034–40
operation. Furthermore, among the eight patients who had
normal PA pressure before MVR, three (38%) developed
PA hypertension after MVR. In addition, all patients except
two had PA pressure ⬎50 mm Hg when they were
submitted to mild exercise (25 W workload). Of the 56
patients included in the present study, 30 (54%) still had PA
hypertension after MVR.
Impact of PPM on PA pressure. Previous studies have
demonstrated that PPM is associated with inferior hemodynamics, less regression of left ventricular hypertrophy,
more cardiac events, and higher mortality rates after aortic
valve replacement (7,10,36 – 44). However, the hemodynamic and clinical impact of PPM after MVR is relatively
unexplored (8 –10). In the first published report of mitral
PPM, Rahimtoola and Murphy (8) described the case of a
patient who remained symptomatic and had persistent PA
hypertension and progressive right-sided failure after MVR.
Accordingly, the major finding of the present study is that
PPM is a strong risk factor for the persistence of PA
hypertension after MVR. Hence, the prevalence of PA
hypertension decreased from 69% to 19% after operation in
patients with no PPM, whereas it remained unchanged in
patients with PPM (66% before operation vs. 68% after
operation) (Fig. 2).
In patients with an aortic prosthesis, previous studies also
consistently found a strong correlation between the indexed
EOA and the postoperative transprosthetic gradients measured at rest or during exercise (36,40,45). However, as
reported in the present study as well as in the previous study
by Dumesnil et al. (9), the correlation between the indexed
EOA and the mean transprosthetic pressure gradients is
lower in patients with mitral prostheses (r ⬍ 0.50) than in
patients with aortic prostheses (r ⬎ 0.75). In this context, it
should be emphasized that the hemodynamics of the mitral
valve are much more sensitive to the chronotropic conditions than that of the aortic valve. Indeed, for similar
indexed EOA, the pressure gradients across the mitral valve
are highly influenced by the transvalvular flow rate, which is
essentially determined by two factors: the diastolic filling
volume and the diastolic filling time. In turn, diastolic time
is highly dependent on heart rate. A change in heart rate has
a much greater impact on the diastolic duration than on the
systolic duration. This difference may contribute to the
explanation of the lower correlation between indexed EOA
and pressure gradients that is observed in mitral prostheses.
In this context, it is also interesting to note that the indexed
mitral EOA correlated better with systolic PA pressure than
with transprosthetic pressure gradients; this finding is consistent with the fact that PA pressure is probably less
influenced by chronotropic conditions than are pressure
gradients.
Atrioventricular compliance, a physiological modulator
of PA pressure. Patients with chronic mitral valve disease
often have an abnormally low atrial compliance due to left
atrial remodeling and hypertrophy. In turn, a reduction in
atrial compliance will necessarily result in a decrease in net
JACC Vol. 45, No. 7, 2005
April 5, 2005:1034–40
atrioventricular compliance because, according to equation
2, the latter is always lower than either of its two components (i.e., left ventricular and left atrial compliances). In
patients with native mitral valve stenosis, Schwammenthal
et al. (19) demonstrated that atrioventricular compliance is
an important physiological modulator of left atrial and PA
pressures. In the context of MVR, it, however, becomes
evident that compliance is also influenced by PPM. This
observation appears to be confirmed by the results of
univariate and multivariate analysis (Table 3), whereby, in
univariate analysis, PPM (i.e., indexed EOA) accounts for
41% of the variance of PA pressure compared to 28% for
compliance, whereas, in multivariate analysis, the independent contribution of PPM remains at 41%, but that of
compliance decreases to 10%, suggesting that compliance is
indeed influenced by PPM. Also consistent with this
observation is the fact that reduced atrioventricular compliance had a minimal effect on PA pressure in the absence of
PPM, whereas the combination of PPM and low atrioventricular compliance was associated with a dramatic increase
in the prevalence of PA hypertension (Fig. 4). Hence, it
would appear that a decrease in atrial compliance may be
relatively well tolerated in patients with a prosthetic valve
with a large EOA and no PPM but that the same condition
may be much less well tolerated in patients with a relative
obstruction to flow due to the prosthesis.
Clinical implication. The clinical implications of these
results are important given that PPM is frequent in patients
undergoing MVR. Moreover, as opposed to most other risk
factors for PA hypertension, PPM may eventually be
avoided by using a prospective strategy at the time of
operation. Such a strategy has been well described and
validated for the prevention of PPM in the aortic position
(40,43,46,47). Suggested options to avoid PPM in the aortic
position are either to perform an aortic root enlargement to
accommodate a larger prosthesis or to use another type of
prosthesis with a better hemodynamic profile (i.e., with a
larger EOA; e.g., a stentless bioprosthesis or a mechanical
valve).
In the mitral position, there is no alternative technique
allowing implantation of a larger prosthesis size. The
preventive strategy should, therefore, be focused on the
implantation of the prosthesis having the largest EOA for a
given size. The objective would be to obtain a postoperative
indexed EOA ⬎1.2 to 1.3 cm2/m2. To this effect, the
bileaflet mechanical valves of new generation may be an
interesting option given that their hemodynamics are generally superior to that of other prostheses (48).
Study limitations. The main limitation of this study is its
retrospective design. This may have introduced some selection bias. Also, the preoperative values of systolic PA
pressure could not be obtained in several patients. Further
prospective studies are, thus, necessary to determine the
impact of PPM on the regression or progression of PA
hypertension.
Beyond PPM and atrioventricular compliance, other
Li et al.
Impact of Mitral Prosthesis-Patient Mismatch
1039
factors, such as pulmonary vascular resistance or PA compliance, may also influence the normalization of PA pressure after MVR. However, these factors are difficult to
estimate by Doppler-echocardiography, and they were indeed not measured in this study. Nonetheless, it should also
be considered that, as opposed to PPM, these factors are
hardly preventable or modifiable. Hence, although this
information could be used to evaluate postoperative outcome, it could not contribute to the development of a
prospective strategy that would optimize the regression of
PA hypertension after MVR.
Conclusions. Persistent PA hypertension is frequent after
MVR and strongly associated with the presence of valve
PPM. The clinical implications of these findings are important given that PPM may be avoided by using a simple
prospective strategy at the time of operation.
Acknowledgments
The authors thank Isabelle Laforest, Dominique Labrèche,
Julie Martin, Brigitte Dionne, and Julien Magne for their
technical assistance in the realization of the study.
Reprint requests and correspondence: Dr. Philippe Pibarot,
Laval Hospital, 2725 Chemin Sainte-Foy, Sainte-Foy, Quebec,
Canada, G1V 4G5. E-mail: [email protected].
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