(Circulation. 1995;92:2496-2503.)
© 1995 American Heart Association, Inc.
Articles |
From the Division of Cardiovascular Diseases and Internal Medicine (M.E.-S., A.J.T., R.L.F.), Section of Cardiovascular Surgery (H.V.S., T.A.O.), and Section of Biostatistics (K.R.B.), Mayo Clinic and Mayo Foundation, Rochester, Minn.
| Abstract |
|---|
|
|
|---|
Methods and Results The long-term outcome of 576 operative survivors of surgical correction of pure mitral regurgitation performed between 1980 and 1989 was analyzed. Survival was 77±2% and 56±3% at 5 and 10 years, respectively. Cumulative incidence of congestive heart failure was 23±2%, 33±3%, and 37±3% at 5, 10, and 14 years, respectively. Survival after the first episode of congestive heart failure was dismal, 44±4% at 5 years. Cause of congestive heart failure was left ventricular dysfunction in two thirds of the patients and valvular dysfunction in the other third. With multivariate analysis, the independent predictors of postoperative heart failure were preoperative ejection fraction (P=.0001), coronary artery disease (P=.0017), and New York Heart Association functional class (P=.012), with borderline value for atrial fibrillation (P=.10). The performance of valve repair was independently predictive of a lower incidence of the combined end point of death and heart failure (P=.001), compared with valve replacement.
Conclusions Congestive heart failure frequently occurs late after surgical correction of mitral regurgitation and portends dismal prognosis. This complication is due most often to left ventricular dysfunction; its main determinant is decreased left ventricular function preoperatively. These data should lead to earlier indication of surgical correction of mitral regurgitation, before left ventricular dysfunction occurs.
Key Words: follow-up studies heart failure mitral valve prognosis surgery
| Introduction |
|---|
|
|
|---|
Therefore, we examined our experience with the outcome of patients operated on between January 1, 1980, and December 31, 1989, for pure mitral regurgitation and hypothesized that congestive heart failure after surgical correction (1) is frequent and of poor prognosis, (2) is due more often to left ventricular dysfunction than to valvular failure, and (3) can be predicted by the preoperative status of the patient and should have major implications on the clinical decision-making process.
| Methods |
|---|
|
|
|---|
The inclusion criteria were (1) surgical correction (repair or replacement) of mitral regurgitation performed between January 1, 1980, and December 31, 1989; (2) acquired pure mitral regurgitation as defined by echocardiographic and surgical assessment; and (3) immediate postoperative survival allowing for observation of long-term outcome.
Patients with associated coronary artery bypass graft surgery were included.
The exclusion criteria were (1) previous operation for mitral regurgitation; (2) previous or associated aortic or tricuspid valve replacement (tricuspid valve repair was not excluded); (3) operative death, defined as occurring during the first postoperative month or within the same hospitalization; and (4) mitral regurgitation due to dilated cardiomyopathy.
During the study period, 2183 patients had mitral valve operations. Of these, 654 had surgical correction for pure mitral regurgitation; 577 were operative survivors, of whom 576 (99.8%) had complete follow-up to death or 1994, and these 576 patients represent our study population. Some data on part of this patient population have been published previously.15 16 17
Of the 576 patients, the mean age was 64±12 years, 352 (61%) were men, and 242 (42%) were in atrial fibrillation. The cause of mitral regurgitation was defined as (1) ischemic, if it was documented to be due to coronary artery disease (120 patients) and (2) organic, if intrinsic disease of the mitral valve was documented (456 patients: rheumatic, 47; endocarditic, 40; degenerative with prolapse, 353; and miscellaneous, 16). Preoperatively, within 1 month of surgical correction, New York Heart Association (NYHA) dyspnea class III was noted in 276 patients (48%) and class IV in 94 (16%).
The surgical procedure performed was valve repair in 288 patients and valve replacement in 288 (bioprosthesis in 137 patients and mechanical prosthesis in 151). Coronary artery bypass graft surgery was performed in 211 patients. Perioperative myocardial infarction (new Q waves) occurred in 6 patients.
Left Ventricular Function Analysis and
Coronary Angiography
Coronary angiography was performed in 477
patients and
showed significant (
70%) stenosis in 253 (in 120, or 100%,
of the patients with ischemic mitral
regurgitation and in 133, or 29%, of those with
organic mitral regurgitation). Preoperative left
ventricular function was analyzed with
echocardiography as previously
reported15 16 18 19 (453
patients) or left
ventricular angiography (354 patients) performed within 6
months of surgical correction. When both techniques were performed, the
ejection fraction was calculated as the average of the two reported
measurements. Therefore, preoperative ejection fraction (mean,
57±13%) was available for 545 patients.
After surgery, the ejection fraction was measured with echocardiography performed at our institution in 410 patients with a mean delay to surgery of 1.2±2.2 years.
Congestive Heart Failure
Congestive heart failure occurring
before or after surgical
correction was noted as diagnosed by the attending physician. In all
cases, class III or IV dyspnea and evidence of pulmonary edema
(clinical and/or radiological) and/or global heart failure were
present. The cause of heart failure was considered to be
valvular failure when, in addition to the signs of heart
failure, there was evidence of severe regurgitation or
stenosis (or both) of the mitral valve prosthesis or
repair. Conversely, heart failure was considered to be due to
myocardial failure in patients who were without signs of
valvular failure and in whom left ventricular
dysfunction was diagnosed. The cause of heart failure was confirmed in
93% of cases with echocardiography, radionuclide
angiography, catheterization, or autopsy.
Statistical Analysis
Group statistics were expressed as
mean±SD. Group comparisons
were based on standard t test or
2
test, as appropriate. The comparison of postoperative variables
between groups defined by the presence and cause of congestive heart
failure was performed by ANOVA and t test if appropriate.
Group survival was estimated with the Kaplan-Meier method and reported
as estimated survival±1 standard error. The observed survival of
patients was compared with the expected survival of age- and
sex-matched actuarial data from the 1980 US white population and
tested by the one-sample log-rank test.
The cumulative probability of congestive heart failure was estimated by the Kaplan-Meier method, with death (without heart failure) as a censoring event. The estimates of cumulative incidence of myocardial or valvular cause of heart failure were based on a Kaplan-Meier estimate, with the other cause as a noncensoring event. Unadjusted group comparison of the time to death or congestive heart failure was based on the two-sample log-rank test. The association of preoperative and intraoperative variables with the incidence of congestive heart failure both overall and by valvular or myocardial causes was estimated with the Cox proportional-hazards model. Multivariate analysis was performed in a sequential manner, starting with preoperative clinical variables (age, sex, cause of regurgitation, NYHA functional class, creatinine level, history of hypertension, history of congestive heart failure, and presence of coronary artery disease) and then adding left ventricular function (ejection fraction) and operative variables (valve repair or replacement and occurrence of myocardial infarction perioperatively). For the prediction of congestive heart failure of valvular origin, the presence of posterior leaflet prolapse was added to the model. To assess the possibility that the etiologic groups would have different predictive associations between these variables and the incidence of congestive heart failure, the set of interactions between the cause and each of the final model variables was added to the final model and tested for significance based on the F test. Survival after onset of congestive heart failure was calculated with the Kaplan-Meier method, with onset of heart failure as the starting time of the survival analysis of this subset of patients. The relative risk of death in patients with postoperative heart failure compared with those without heart failure was calculated by use of a time-dependent proportional-hazards model, with heart failure onset as the time-dependent variable. A value of P<.05 was considered significant.
| Results |
|---|
|
|
|---|
|
Postoperative Survival
At the latest follow-up, 216 patients
had died and 360 were
alive. Overall survival rate was 77±2% at 5 years (93% of expected
survival), 56±3% at 10 years (84% of expected survival), and
44±4%
at 14 years (82% of expected survival) and was significantly decreased
in comparison with expected survival (P=.0001, Fig
1
). Patients with organic mitral
regurgitation had a better survival rate (62±3% at 10
years, 91% of expected rate) than those with ischemic mitral
regurgitation (36±6% at 10 years, 57% of expected
rate) (P=.0001) (Fig 2
). The determinants of
postoperative survival, and in particular the essential role of
preoperative ejection fraction, have been analyzed
elsewhere.16
|
|
Overall Congestive Heart Failure
Congestive heart failure was
diagnosed before surgery in 370
patients and after surgery in 152. The cumulative incidence of
postoperative congestive heart failure was 23±2% at 5 years,
33±3%
at 10 years, and 37±3% at 14 years (Fig 3
). The
survival rate after the occurrence of heart failure was dismal, 44±4%
and 18±5% at 5 and 10 years, respectively, after the first episode of
congestive heart failure (Fig 4
). The relative risk of
death after the occurrence of congestive heart failure compared with
those without heart failure was 5.2 (95% CI, 3.9 to 6.8). With
multivariate analysis, the independent clinical
predictors of congestive heart failure were presence of
coronary artery disease, cause of
regurgitation, preoperative symptoms, and atrial
fibrillation. Age, sex, preoperative creatinine level,
history of congestive heart failure, and hypertension were not
independently predictive of the occurrence of postoperative congestive
heart failure. When combined with preoperative ejection fraction and
the surgical variables, the only significant independent predictors
of congestive heart failure were ejection fraction
(P=.0001), coronary artery disease
(P=.0017), and NYHA class (P=.012), with a
borderline value for atrial fibrillation (P=.10) (Table
2
). The incidences of congestive heart failure at 10
years according to the level of preoperative ejection fraction were
19±3%, 29±5%, and 70±6% in patients with preoperative
ejection
fraction
60%, 50% to 59%, or <50%, respectively
(P=.0001) (Fig 5
). The risk ratio compared
with a preoperative ejection fraction
60% was 1.8 (95% CI, 1.1 to
2.9) for ejection fraction of 50% to 59% and 5.4 (3.6 to 8.2) for an
ejection fraction <50% regarding late occurrence of congestive heart
failure. The cumulative incidence of congestive heart failure according
to the preoperative symptoms and to the presence of coronary
artery disease is shown in Figs 6
and 7
,
respectively. The risk ratio for postoperative congestive heart failure
was 1.8 (95% CI, 1.2 to 2.6) for preoperative NYHA functional class
III or IV compared with class I or II. Compared with patients with
organic mitral regurgitation without coronary
artery disease, the risk ratio was 2.1 (95% CI, 1.4 to 3.2) in
patients with organic mitral regurgitation with
coronary artery disease and 4.5 (95% CI, 3.1 to 6.6) in
patients with ischemic mitral regurgitation.
Although preoperative congestive heart failure was not independently
predictive of postoperative heart failure in
multivariate analysis, it was
univariately associated with a risk ratio of 1.7 (95% CI,
1.2 to 2.4).
|
|
|
|
|
|
Cause of Congestive Heart Failure
The cause of heart failure
was diagnosed clinically and confirmed
with echocardiography, radionuclide angiography,
catheterization, or autopsy performed either at our
institution or outside in 142 of 152 patients (93%). The postoperative
echocardiographic variables obtained at our
institution in patients classified as without congestive heart failure
or with valvular or myocardial congestive heart failure are
presented in Table 3
. In patients with the
diagnosis of myocardial congestive heart failure, there was
considerable depression of left ventricular function with
left ventricular enlargement. In patients with
valvular congestive heart failure, left ventricular
function was not depressed, but there was residual enlargement of the
left atrium.
|
The cause of heart failure was valvular failure in 45
patients,
representing an incidence of 7±1% at 5 years and 11±2%
at 10 years. Valvular failure was observed in 24 repairs, 8
mechanical prostheses, and 13 bioprostheses, a distribution not
different from the patients without postoperative heart failure (224
repairs, 110 mechanical prostheses, and 90 bioprostheses;
P=.34). Reoperation was performed in 28 patients. The cause
of congestive heart failure was myocardial failure in 107 patients,
representing an incidence of 16±2% at 5 years and 23±2%
at 10 years (Fig 3
).
With multivariate analysis, there was no significant predictor of congestive heart failure due to valvular failure. Conversely, ejection fraction (P=.0001), coronary artery disease (P=.0008), atrial fibrillation (P=.006), and, of more borderline value, NYHA class (P=.06) were independent predictors of heart failure due to myocardial failure.
Cause of Regurgitation
In patients with ischemic mitral
regurgitation compared with those with organic mitral
regurgitation, the incidence of congestive heart
failure was higher (at 5 years, 45±5% versus 17±2% and at 10
years,
65±7% versus 25±3%; P=.0001). However, when
classified
according to the cause of heart failure, there was no significant
difference in congestive heart failure due to valvular
dysfunction between patients with ischemic mitral
regurgitation and those with organic mitral
regurgitation (at 10 years, 11±4% versus 11±2%;
P=NS), but patients with ischemic mitral
regurgitation had a higher incidence of congestive
heart failure of myocardial origin (at 8 years, 48±5% versus
14±2%;
P=.0001). However, in multivariate
analysis, the degree of left ventricular
dysfunction, but not the cause of regurgitation, was
independently predictive of postoperative congestive heart failure
(Table 3
). In addition, no interaction between the predictors
of
congestive heart failure and the cause of regurgitation
was noted. The survival rate after the first episode of congestive
heart failure was significantly but moderately worse in patients with
ischemic rather than organic mitral
regurgitation (at 7 years, 24±7% versus 36±6%;
P=.007). Overall, coronary artery disease was a
powerful predictor of postoperative congestive heart failure, and
specifically in patients with organic mitral
regurgitation, the incidence of congestive heart
failure was significantly higher in patients with associated
coronary artery disease than in those without overt
coronary artery disease (35±5% versus 21±3% at 10 years;
P=.0003).
Repair Versus Replacement
With univariate analysis, there was
a lower
incidence of postoperative congestive heart failure after valve repair
than after valve replacement (P=.04). However, such a
difference was not detectable in patients with ischemic mitral
regurgitation and was significant only in those with
organic mitral regurgitation (at 10 years, 17±3%
versus 33±4%; P=.04) and only for the myocardial
failure
cause (at 10 years, 9±2% versus 22±4%; P=.006).
However,
with multivariate analysis, valve repair was
not independently predictive of a decreased incidence of congestive
heart failure when stratified for the other predictors.
Nevertheless,
when a combined end point of death and congestive
heart failure was analyzed in patients with organic mitral
regurgitation, repair was an independent predictor of
improved outcome (P=.001) (Fig 8
). The
other independent predictors were ejection fraction
(P=.0001), age (P=.0001), coronary artery
disease (P=.0047), atrial fibrillation
(P=.08),
NYHA class (P=.025), and perioperative
myocardial infarction (P=.0001). The survival rate after the
first episode of congestive heart failure was not significantly
different in patients with valve repair or valve replacement (at 8
years after the episode of congestive heart failure, 17±7% in the
valve repair group versus 26±6% in the valve replacement group
[P=NS] were survivors).
|
| Discussion |
|---|
|
|
|---|
Congestive Heart Failure After Correction of Mitral
Regurgitation
The occurrence of congestive heart failure after
surgical
correction of mitral regurgitation is particularly
disturbing because the intent of the surgical intervention is to
eliminate preoperative congestive heart failure or to prevent
it.1 Indeed, marked improvement in symptoms after surgical
relief of mitral regurgitation is quite
common,2 3 4 5 6
with a very small percentage of patients
remaining in NYHA functional classes III and IV.20 Such an
early improvement may be misleading in terms of the true long-term
outcome as reflected in the present study. The incidence of
congestive heart failure and cardiac
death7 8 21 tends to
increase progressively with time, thus emphasizing the importance of
long-term follow-up for judging results. The prognosis of
postoperative congestive heart failure is dismal: More than one half of
the patients who had this complication died within 5 years after the
first episode, an incidence similar to nonvalvular causes
of heart failure.13 14 Such an impact on prognosis
underscores the importance of determining the cause of postoperative
heart failure and its predictors and considering how to prevent its
occurrence.
Whereas late occurrence of congestive heart failure may be due to primary failure of valve repair,9 mechanical prostheses,11 or bioprostheses,10 the most common cause of heart failure in the present study was left ventricular dysfunction. This complication is frequently present early after surgical correction of mitral regurgitation15 22 and has even been noted with intraoperative imaging techniques.23 The absence of symptoms early after suppression of the valvular regurgitation may be observed even in the presence of left ventricular dysfunction as a result of previously documented normalization of left atrial pressure24 25 and is similar to what is observed in nonvalvular ventricular dysfunction.26 However, with time, overt congestive heart failure occurs in a significant proportion of patients. After the signs of heart failure are present, the prognosis is poor, similar to that of patients with nonvalvular left ventricular dysfunction.13 14
Predictors of Postoperative Congestive Heart Failure
Postoperative congestive heart failure in most cases is due to
left ventricular dysfunction and rarely to failure of the
surgical procedure,27 which cannot be predicted from
preoperative variables. Intraoperative complications, such as
myocardial infarction, may lead to left ventricular
dysfunction, but these are rare.28 That preoperative left
ventricular ejection fraction is the most powerful
predictor of postoperative heart failure strongly suggests that left
ventricular dysfunction is present
preoperatively.29 30 This observation agrees with the
fact
that preoperative variables of left ventricular
function have frequently been noted to be predictors of postoperative
survival16 31 and postoperative left
ventricular
function.15 22 29 30 Judging
normalcy of ejection fraction is complicated in patients with mitral
regurgitation due to altered loading
conditions.32 33 34 However, it should be
noted that the
incidence of congestive heart failure is very high in patients with
severely depressed ventricular function (ejection fraction
<50%), but it is also increased in patients with borderline ejection
fraction (50% to 59%), which indicates that these patients already
have a significant degree of left ventricular dysfunction,
which may go unnoticed until the appearance of severe symptoms at a
late stage.1
Other preoperative predictors are also important. Severe symptoms (NYHA classes III and IV) and atrial fibrillation tend to be associated with an increased incidence of late congestive heart failure.35 The role of atrial fibrillation suggests the need for appropriate controlled studies to establish the need to intervene aggressively to maintain normal sinus rhythm. Associated coronary artery disease is a powerful predictor of an excess incidence of congestive heart failure and late death,16 36 independent of ejection fraction. Such an effect emphasizes the importance of detecting coronary artery stenosis before surgery, although the impaired prognosis occurred despite bypass operation being combined with valvular correction. The survival rate after correction of ischemic mitral regurgitation was mediocre, as noted previously,37 and the excess mortality was due primarily to the severe left ventricular dysfunction commonly present in that disease.38 The suggested advantage of mitral valve repair over valve replacement in this subset of patients39 was not observed in the present study.
Prevention of Congestive Heart Failure
Congestive heart
failure due to dysfunction of the surgical
correction of the mitral valve in most cases may be prevented by use of
intraoperative transesophageal
echocardiography.40 Prevention of
valve endocarditis and thrombosis is important in avoiding late
valvular complications that could result in congestive heart
failure.7 10 11 Prevention of
postoperative congestive
heart failure due to left ventricular dysfunction is more
difficult but of considerable clinical significance.
Early
Surgical Correction
Patients with a significant degree of left
ventricular
dysfunction (ejection fraction <60%) should have surgical correction
without waiting for further deterioration of their
condition.16 For patients in this category, surgical
correction of the regurgitation should not be denied
(despite a high incidence of postoperative congestive heart failure)
for two reasons: (1) in patients with an ejection fraction <50%,
surgical correction, in comparison with medical treatment, improves the
prognosis41 42 and (2) the occurrence of congestive
heart
failure is often delayed, and surgical correction may provide up to
several years of marked symptomatic improvement.
Patients with
apparently preserved left ventricular
function who have an ejection fraction
60% have a relatively low
incidence of postoperative congestive heart failure. These patients
have been shown to have an excellent late survival,16 with
a low incidence of postoperative left ventricular
dysfunction.15 22 Thus, that stage of preserved left
ventricular function represents the ideal
indication for surgical correction of mitral
regurgitation. Even at that stage, severe symptoms
(NYHA class III or IV) are associated with increased incidence of heart
failure and increased mortality,16 suggesting that
correction of mitral regurgitation in patients in NYHA
class I or II with an ejection fraction
60% may be a reasonable
approach under certain conditions. Such an aggressive approach is
defensible only in patients at low operative risk and in those medical
centers with documented high rates of success in repairing the mitral
valve with low operative mortality.
Valve Repair as the
Preferred Surgical Procedure
Although valve repair does not reduce the
incidence of valve
failure, it is univariately associated with a lower
incidence of postoperative congestive heart failure due to myocardial
failure. It is an independent predictor of a lower incidence of the
combined end point of congestive heart failure and death in patients
with organic mitral regurgitation. Valve repair also
has been reported to result in decreased operative mortality and better
long-term survival17 43 as well as better left
ventricular function.17 23 44 Valve
repair
should be discussed in all surgical cases of mitral
regurgitation.45 The low operative risk is
another incentive to perform early surgical correction of mitral
regurgitation. However, valve repair does not eliminate
the risk of congestive heart failure or the need for surgical
correction of mitral regurgitation before the
occurrence of left ventricular dysfunction.
Pharmacological
Prevention of Congestive Heart
Failure
In the present series, medical treatment of heart failure was
adapted to the clinical circumstances, and its effect on outcome cannot
be analyzed. Angiotensin-converting enzyme
inhibitors have been used successfully to prolong survival
in patients with congestive heart failure13 14 and to
improve the outcome of those with asymptomatic left
ventricular dysfunction.26 Although no
randomized trial has studied the use of these medications for the
prevention of congestive heart failure after surgical correction of
mitral regurgitation, their use in patients in whom
left ventricular dysfunction has been diagnosed early after
surgical correction appears worthy of consideration and future
analysis.
Limitations of the Study
Although heavy reliance on
echocardiographic
estimates of left ventricular ejection fraction may be a
cause of concern, the use of echocardiography in
this setting is standard practice, and previous studies from our
institution have documented the acceptable correlations to angiography
and, most importantly, the high prognostic value of these
estimates.15 16 However, the importance of careful
attention to quality control issues in laboratories that perform such
studies needs to be emphasized.
Although all the patients in the present series were considered to have severe mitral regurgitation, an important limitation is the lack of quantitation of the severity. This is another important measurement that needs to be integrated in the assessment of left ventricular function and perhaps may be of value in selecting patients for early intervention. Within the time frame of the present study, such quantitation was not routinely available. However, methods that can be used in routine clinical practice are now available for quantifying not only the regurgitant volume46 but also the effective regurgitant orifice.47 48 Further studies are necessary to delineate the natural history of mitral regurgitation classified according to these variables so as to better define the indications for early surgical intervention.
Conclusions
Congestive heart failure is a frequent
postoperative complication
of surgical correction of mitral regurgitation. It is
rarely due to valvular failure but rather is caused most often
by left ventricular dysfunction present before surgery.
The poor prognosis of this complication justifies an aggressive
detection of left ventricular dysfunction and prevention of
heart failure, particularly through the use of early valvular
repair.
| Acknowledgments |
|---|
| Footnotes |
|---|
Received February 27, 1995; revision received May 15, 1995; accepted May 30, 1995.
| References |
|---|
|
|
|---|
This article has been cited by other articles:
![]() |
T. G. Neilan, T.-T. Ton-Nu, Y. Kawase, R. Yoneyama, K. Hoshino, F. del Monte, R. J. Hajjar, M. H. Picard, R. A. Levine, and J. Hung Progressive nature of chronic mitral regurgitation and the role of tissue Doppler-derived indexes Am J Physiol Heart Circ Physiol, May 1, 2008; 294(5): H2106 - H2111. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. I. Fann, N. B. Ingels Jr., and D. C. Miller Pathophysiology of Mitral Valve Disease Card. Surg. Adult, January 1, 2008; 3(2008): 973 - 1012. [Full Text] |
||||
![]() |
A. Marciniak, P. Claus, G. R. Sutherland, M. Marciniak, T. Karu, A. Baltabaeva, E. Merli, B. Bijnens, and M. Jahangiri Changes in systolic left ventricular function in isolated mitral regurgitation. A strain rate imaging study Eur. Heart J., November 1, 2007; 28(21): 2627 - 2636. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. L. Ngaage, H. V. Schaff, C. J. Mullany, S. Barnes, J. A. Dearani, R. C. Daly, T. A. Orszulak, and T. M. Sundt III Influence of Preoperative Atrial Fibrillation on Late Results of Mitral Repair: Is Concomitant Ablation Justified? Ann. Thorac. Surg., August 1, 2007; 84(2): 434 - 443. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Lee and T. H. Marwick Assessment of subclinical left ventricular dysfunction in asymptomatic mitral regurgitation Eur J Echocardiogr, June 1, 2007; 8(3): 175 - 184. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. M. Suri, H. V. Schaff, J. A. Dearani, T. M. Sundt III, R. C. Daly, C. J. Mullany, M. Enriquez-Sarano, and T. A. Orszulak Survival advantage and improved durability of mitral repair for leaflet prolapse subsets in the current era. Ann. Thorac. Surg., September 1, 2006; 82(3): 819 - 826. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Rosenhek, F. Rader, U. Klaar, H. Gabriel, M. Krejc, D. Kalbeck, M. Schemper, G. Maurer, and H. Baumgartner Outcome of Watchful Waiting in Asymptomatic Severe Mitral Regurgitation Circulation, May 9, 2006; 113(18): 2238 - 2244. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Kouris, I. Ikonomidis, D. Kontogianni, P. Smith, and P. Nihoyannopoulos Mitral valve repair versus replacement for isolated non-ischemic mitral regurgitation in patients with preoperative left ventricular dysfunction. A long-term follow-up echocardiography study Eur J Echocardiogr, December 1, 2005; 6(6): 435 - 442. [Abstract] [Full Text] [PDF] |
||||
![]() |
R Lee, B Haluska, D Y Leung, C Case, J Mundy, and T H Marwick Functional and prognostic implications of left ventricular contractile reserve in patients with asymptomatic severe mitral regurgitation Heart, November 1, 2005; 91(11): 1407 - 1412. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. S. Shah, S. A. Hannish, C. A. Milano, and D. D. Glower Isolated Mitral Valve Repair in Patients With Depressed Left Ventricular Function Ann. Thorac. Surg., October 1, 2005; 80(4): 1309 - 1314. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Eguchi, E. Ohtaki, T. Matsumura, K. Tanaka, T. Tohbaru, N. Iguchi, K. Misu, R. Asano, M. Nagayama, T. Sumiyoshi, et al. Pre-operative atrial fibrillation as the key determinant of outcome of mitral valve repair for degenerative mitral regurgitation Eur. Heart J., September 2, 2005; 26(18): 1866 - 1872. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. Detaint, D. Messika-Zeitoun, J.-F. Avierinos, C. Scott, H. Chen, J. C. Burnett Jr, and M. Enriquez-Sarano B-Type Natriuretic Peptide in Organic Mitral Regurgitation: Determinants and Impact on Outcome Circulation, May 10, 2005; 111(18): 2391 - 2397. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Zamorano, L. P. de Isla, L. Oliveros, C. Almeria, J. L. Rodrigo, A. Aubele, J. Banchs, and C. Macaya Prognostic influence of mitral regurgitation prior to a first myocardial infarction Eur. Heart J., February 2, 2005; 26(4): 343 - 349. [Abstract] [Full Text] [PDF] |
||||
|
|