Published online before print March 5, 2007, doi: 10.1161/CIRCULATIONAHA.106.631549
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(Circulation. 2007;115:1417-1425.)
© 2007 American Heart Association, Inc.
Valvular Heart Disease |
Impact of Prosthesis-Patient Mismatch on Survival After Mitral Valve Replacement
From the Laval Hospital Research Center/Québec Heart Institute, Faculty of Medicine, Laval University, Québec, Canada (J.M., P.M., J.G.D., D.T., F.D., D.D., P.P.), and Cardiovascular Biomechanics Team (IRPHE-CNRS), Université de la Méditerranée, Marseilles, France (D.T.).
Correspondence to Dr Philippe Pibarot, Laval Hospital Research Center, 2725 Chemin Sainte-Foy, Sainte-Foy, Quebec, Canada, G1V-4G5. E-mail philippe.pibarot{at}med.ulaval.ca
Received April 7, 2006; accepted December 21, 2006.
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Abstract |
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Background— We recently reported that valve prosthesis-patient mismatch (PPM) is associated with persisting pulmonary hypertension after mitral valve replacement. Thus, the objective of this study was to evaluate the impact of PPM on mortality in patients undergoing mitral valve replacement.
Methods and Results— The indexed valve effective orifice area was estimated for each type and size of prosthesis being implanted in 929 consecutive patients and used to define PPM as not clinically significant if >1.2 cm2/m2, as moderate if >0.9 and 
1.2 cm2/m2, and as severe if 0.9 cm2/m2. Moderate PPM was present in 69% of patients; severe PPM was seen in 9%. For patients with severe PPM, 6-year survival (74±5%) and 12-year survival (63±7%) were significantly less than for patients with moderate PPM (84±1% and 76±2%; P=0.027) or nonsignificant PPM (90±2% and 82±4%; P=0.002). On multivariate analysis, severe PPM was associated with higher mortality (hazard ratio, 3.2; 95% confidence interval, 1.5 to 6.8; P=0.003).
Conclusions— Severe PPM is an independent predictor of mortality after mitral valve replacement. As opposed to other independent risk factors, PPM may be avoided or its severity may be reduced with the use of a prospective strategy at the time of operation. For patients identified as being at risk for severe PPM, every effort should be made to implant a prosthesis with a larger effective orifice area.
Key Words: heart valve prosthesis • hemodynamics • mitral valve • mortality • surgery • valves
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Introduction |
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Mitral valve replacement (MVR) has higher short- and long-term mortality than aortic valve replacement or mitral valve repair.1 The suboptimal results of MVR underline the importance of identifying and, when possible, preventing prosthesis- and patient- related factors associated with negative postoperative outcomes.
Editorial p 1336
Clinical Perspective p 1425
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.2–5 As a consequence, normally functioning mitral prostheses often have relatively high gradients that are similar to those found in patients with mild to moderate mitral stenosis.3–7 Residual pressure gradients across mitral prostheses may hinder or delay the regression of left atrial and pulmonary arterial hypertension.3,8,9 The persistence of high left atrial pressures also may predispose to atrial dilatation and consequently atrial fibrillation. This arrhythmia may compromise cardiac output and increase the incidence of thromboembolic complications. In a recent study, we found that mitral valve prosthesis-patient mismatch (PPM), defined as an indexed EOA 1.2 cm2/m2, is a frequent occurrence (71%) after MVR and that it is associated with persisting pulmonary hypertension.8 Pulmonary hypertension may cause right-sided failure and is an important risk factor for morbidity and mortality in patients with cardiovascular diseases.
From these results, we therefore hypothesized that PPM might increase the risk of mortality after MVR. Thus, the objective of this study was to determine the impact of PPM on survival after MVR.
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Methods |
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Eligibility Criteria
Baseline clinical data and postoperative mortality were analyzed in 929 patients undergoing MVR at the Quebec Heart Institute between November 1986 and June 2005. Patients were excluded from the study if they had concomitant valve (aortic, pulmonary, or tricuspid) replacement or repair. Patients were not excluded if they had concomitant procedures such as coronary artery bypass graft (CABG) or if they had prior cardiac surgery, including CABG or mitral valve surgery.
Data Collection
Baseline clinical data were prospectively collected in a computerized database. Survival data were obtained from the death certificates of the Registry Office of the Quebec Government (Registre de l’État Civil du Québec). To avoid misclassification of causes of death, all-cause mortality was selected as an objective end point.10
Of the 929 patients included in this cohort, 182 (20%) had a complete Doppler echocardiographic examination performed at our institution 1 year after MVR. The Doppler echocardiographic measurements were performed as previously described.4,8 Mitral valve EOA was determined by the continuity equation using stroke volume measured in the left ventricular outflow tract divided by the integral of the mitral valve transprosthetic velocity during diastole. The peak and mean transprosthetic pressure gradients were determined by the simplified Bernoulli equation. The systolic pulmonary arterial pressure was calculated by adding the systolic right ventricular pressure derived from the tricuspid regurgitation to the estimated right atrial pressure.
PPM Definition
Previous studies have shown that aortic PPM and its consequences on morbidity and mortality can be predicted at the time of operation by calculating the projected indexed EOA.11–15 In the present study, the projected indexed EOA was derived from the published normal in vivo EOA values for each model and size of prosthesis implanted in this cohort except for the MCRI On-X, Medtronic Advantage (Medtronic, Minneapolis, Minn), and Carpentier-Edwards Perimount valves (Table 1).4,16–19 Indeed, to the best of our knowledge, the normal in vivo EOA values for these 2 prosthesis models have not yet been reported or are not well documented in the literature. In their case, we used the normal EOA values established in our echocardiography laboratory from the data measured 1 year after operation (Table 1). PPM was defined as not clinically significant if the projected EOA indexed for body surface area was >1.2 cm2/m2, as moderate if it was >0.9 and 1.2 cm2/m2, and as severe if it was 0.9 cm2/m2. The selection of 1.2 cm2/m2 as the cutoff value for moderate PPM was based on the results of our previous studies.4,5,8 We selected a value of 0.9 cm2/m2 as the threshold for severe PPM because our previous numerical and clinical studies suggest that such a level of PPM is associated with moderate/severe pulmonary hypertension at rest and severe pulmonary hypertension on mild/moderate physical exercise.8,20
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Statistical Methods
Results are expressed as mean±SD or percentages unless otherwise specified. The cohort was divided into 3 groups according to PPM severity: nonsignificant, moderate, and severe. Preoperative data, operative data, and postoperative echocardiographic data were compared for statistical significance through the use of 1-way ANOVA, 
2, and Fisher exact test as appropriate. The statistical analyses were performed in the whole cohort (n=929) and in the subset of patients (n=655) who underwent isolated MVR (ie, without concomitant CABG).
The end point for this study was survival from the time of MVR. The survival function was obtained from the Nelson-Aalen estimator of the cumulative hazard rate, and differences among groups were compared with the log-rank test. The effect of the preoperative and operative variables on survival was assessed with the Cox proportional-hazards model. Variables with a value of P<0.25 on univariate analysis were incorporated into the model in a stepwise manner. The method used to test the proportionality assumption is described in Appendix I in the online Data Supplement.
To assess the effect of PPM on survival, we developed a first model with PPM entered as a nominal variable (nonsignificant, moderate, severe) and then a second model with indexed EOA entered as a continuous variable. We also entered into this model the indexed geometric orifice area (GOA) because this index has been used by other investigators to identify PPM.21–23 The GOA was calculated from the prosthesis internal orifice diameter, as provided by the manufacturer, assuming a circular orifice.21 All statistical analyses were performed with SAS statistical package software, version 9.1.3 (SAS Institute Inc, Cary, NC).
The authors had full access to and take full responsibility for the integrity of the data. All authors have read and agree to the manuscript as written.
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Results |
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Preoperative and Operative Data
Of the 929 patients of this cohort, 204 (22%) had nonsignificant PPM, 644 (69%) had moderate PPM, and 81 (9%) had severe PPM.
Preoperative and operative data are shown in Tables 2 and 3
, respectively. Compared with patients with nonsignificant PPM, those with moderate or severe PPM had a larger body surface area and higher prevalence of male gender, mitral regurgitation, coronary artery disease, diabetes mellitus, renal failure, history of myocardial infarction, bioprosthesis implantation, small prosthesis (27 mm), and concomitant CABG. These patients also had lower preoperative left ventricular ejection fraction and longer cardiopulmonary bypass and aortic cross-clamp times. Conversely, they had lower prevalence of atrial fibrillation, concomitant Maze procedure, and left atrial appendage resection, and preoperative history of heart failure was less frequent in patients with severe PPM than in those with moderate PPM. The vast majority of the patients (78%) had chordal preservation, and no significant difference between groups existed with regard to the frequency of this procedure.
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In the subset of 655 patients with isolated MVR (ie, without CABG), the prevalence of coronary artery disease was low (9%), and no significant difference existed between the severe PPM group and the 2 other groups with regard to the prevalence of coronary artery disease, hypertension, renal failure, advanced New York Heart Association (NYHA) class, chronic lung disease, and left ventricular ejection fraction (Table AI, Appendix II, online Data Supplement). Nonetheless, the patients with severe PPM were significantly younger and had higher prevalence of male gender and diabetes mellitus but lower prevalence of history of heart failure and atrial fibrillation. Moreover, patients with moderate PPM had higher prevalence of chronic lung disease and renal failure but lower prevalence of coronary artery disease compared with those with nonsignificant PPM.
Postoperative Echocardiographic Data
The Doppler echocardiographic data obtained 1 year after MVR in a subset of 182 patients are shown in Table 4. Compared with patients with nonsignificant PPM, patients with moderate or severe PPM had significantly lower prosthetic valve EOA and indexed EOA and higher transprosthetic pressure gradients and systolic pulmonary arterial pressure. Patients with severe PPM also had significantly worse hemodynamics compared with those with moderate PPM. There was good agreement between the indexed EOA measured 1 year after MVR and the projected indexed EOA; the mean absolute difference between these 2 parameters was –0.008±0.21 cm2/m2.
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Impact of PPM on Mortality
The mean follow-up was 6.3±4.5 years (median, 5.7 years; maximum, 18.7 years). During follow-up, 169 patients died, and overall survival was 94.1±0.8%, 84.8±1.3%, and 76±1.9% at 30 days, 6 years, and 12 years, respectively. The cause of death was cardiovascular in 101 patients (60%), noncardiovascular in 42 patients (25%), and unknown in 26 patients (15%).
Thirty-day mortality was 4.9%, 7.4%, and 11% in the nonsignificant, moderate, and severe PPM groups, respectively. The differences among the 3 groups were not statistically significant, but there was a trend (P=0.1) for higher 30-day mortality in patients with severe PPM compared with those with nonsignificant PPM. For patients with severe PPM, 6-year survival (74±5%) and 12-year survival (63±7%) were significantly less than for patients with moderate PPM (84±1% and 76±2%; P=0.027) or nonsignificant PPM (90±2% and 82±4%; P=0.002) (Figure 1). Patients with moderate PPM had significantly lower survival compared with those with nonsignificant PPM (P=0.029) and higher survival compared with those with severe PPM (P=0.045). When operative mortality is excluded, patients with severe PPM still had significantly lower late survival compared with patients with nonsignificant PPM (70±7% versus 85±4% at 12 years; P=0.01).
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Likewise, survival (6 year, 77±7%; 12 year, 70±9%) remained significantly lower in patients with severe PPM than in those with nonsignificant PPM (92±2% and 85±5%; P=0.02) in the subset of patients with isolated MVR. Patients with moderate PPM had lower survival (6 year, 86±2%; 12 year, 80±2%; P=0.05) compared with those with nonsignificant PPM.
Independent Predictors of Mortality
Table 5 shows the predictors of postoperative mortality in univariate and multivariate analysis. Severe PPM was an independent predictor of mortality after MVR (hazard ratio [HR], 3.2; 95% confidence interval [CI], 1.5 to 6.8; P=0.003). Moderate PPM also tended to be associated with higher mortality on multivariate analysis (HR, 1.7; 95% CI, 0.97 to 2.8; P=0.06). When operative mortality is excluded, severe PPM remained an independent predictor of late mortality (HR, 2.3; 95% CI, 1.24 to 4.03; P=0.02). The other independent risk factors for mortality were preoperative NYHA functional class IV for the 2 first years after MVR, preoperative history of heart failure for the first 5 years after MVR, renal failure, diabetes mellitus, lower body surface area, and aortic cross-clamp time >80 minutes. In the subgroup of patients with moderate to severe PPM, there was a 1.7-fold (95% CI, 1.00 to 2.84; P=0.05) increase in mortality in patients with severe PPM compared with those with moderate PPM in multivariate analysis.
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In the subset of patients with isolated MVR, severe PPM remained an independent predictor of mortality (HR, 1.9; 95% CI, 1.2 to 3.0; P=0.01) and moderate PPM was of borderline significance (HR, 1.3; 95% CI, 0.99 to 1.9; P=0.06) after adjustment for age, coronary artery disease, diabetes mellitus, and other relevant risk factors (Table AII, Appendix II, on-line Data Supplement).
Moreover, we developed another model by incorporating into the multivariate model the indexed EOA instead of PPM as a continuous variable. In the model that included the data of the whole cohort, lower indexed EOA (ie, higher degree of PPM) was independently associated with increased mortality risk (HR, 1.2; 95% CI, 1.05 to 1.36 for 0.1-cm2/m2 reduction in indexed EOA; P=0.005). The other independent risk factors in this second model were preoperative NYHA functional class IV for the 2 first years after MVR, preoperative history of heart failure for the first 5 years after MVR, renal failure, aortic cross-clamp time >80 minutes, and history of myocardial infarction. As opposed to the indexed EOA, the indexed GOA and label prosthesis size were not significantly associated with higher mortality on univariate or multivariate analysis both in the whole cohort and in the subset of patients with isolated MVR. Multiple forward stepwise linear regression analysis including variables presented in Tables 2 and 3
and with the indexed EOA as dependent variable revealed that the independent contribution of label prosthesis size to the variance of the indexed EOA was 27% (
r2= 0.27, P<0.001), whereas that of the patient’s body surface area was 30% (r2= 0.30, P<0.001). Similar to what was reported for aortic prostheses, the GOA grossly overestimates the EOA but to a much larger extent for bioprostheses than for mechanical valves (Figure 2).15 In the present study, the indexed GOA varied from 1.9 to 3.7 cm2/m2 for an indexed EOA of 1.2 cm2/m2.
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Discussion |
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The major finding of the present study is that severe PPM is a strong and independent predictor of survival in patients undergoing MVR. Indeed, severe PPM was associated with a 3-fold increase in the risk of mortality compared with nonsignificant PPM. Moreover, although the difference in survival between patients with moderate PPM and those with nonsignificant PPM was not statistically significant, the survival curve of the former was nonetheless intermediate between the curves of patients with severe PPM and those with nonsignificant PPM. In addition, on multivariate analysis, there was a definite trend (P=0.06) for an association between moderate PPM and increased mortality (HR, 1.7; 95% CI, 0.98 to 2.8).
Mechanisms Responsible for the Adverse Effect of PPM
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.2,11,14,15,24–26 However, the hemodynamic and clinical impact of PPM after MVR has been relatively unexplored.3–5,8,9,23 Rahimtoola and Murphy3 were the first to describe the case of a patient with PPM in the mitral position. In subsequent studies, Dumesnil et al4 and Dumesnil and Yoganathan5 showed that the indexed EOA of mitral prostheses should ideally not be less than 1.2 to 1.3 cm2/m2 to avoid abnormally high residual transvalvular pressure gradients. Hence, PPM in the mitral position can be equated to residual mitral stenosis with similar consequences (ie, the persistence of abnormally high mitral gradients and increased left atrial and pulmonary arterial pressures). In turn, pulmonary arterial hypertension may cause right-sided failure, and the persistence of high left atrial pressures may predispose to atrial fibrillation. This arrhythmia may compromise cardiac output and increase the incidence of thromboembolic complications. The passive elevation in pulmonary capillary pressure caused by elevated left atrial pressure also may lead to the development of pulmonary edema.
We recently demonstrated that mitral PPM defined as an indexed EOA 1.2 cm2/m2 is a strong independent risk factor for the persistence of pulmonary hypertension after MVR.8 In this previous series, the prevalence of pulmonary hypertension indeed decreased from 69% before operation to 19% after operation in patients with no PPM, whereas it remained unchanged in those with PPM (66% before versus 68% after MVR). Consistently, in the present study, patients with PPM had higher postoperative pulmonary arterial pressures (Table 4). The major consequence of pulmonary hypertension is right ventricular failure, which generally results from chronic pressure overload and associated volume overload with the development of tricuspid regurgitation. Hence, the persistence of left atrial and pulmonary hypertension associated with PPM is likely the main factor responsible for the increased mortality observed in the patients with severe PPM. In fact, there was a strong coherence between the differences in mortality rates (Figure 1) and the differences in hemodynamics (Table 4) observed among the nonsignificant, moderate, and severe PPM groups. Nonetheless, further studies are necessary to better understand the mechanisms responsible for the association between PPM and mortality after MVR.
Comparison With Previous Studies
Previous studies27–29 have identified several independent predictors of survival in patients undergoing MVR; most of them also were found to be present in this study: older age and preoperative history of NYHA functional class IV, diabetes mellitus, renal failure, and heart failure. However, it must be emphasized that the influence of PPM was not analyzed in theses studies.
Indeed, very few studies have attempted to examine the impact of mitral prosthesis size and hemodynamics on postoperative outcomes.30,23 In a recent study that included 708 patients undergoing MVR, Ruel et al30 found no significant association between labeled prosthesis size and postoperative mortality. In another series of 428 patients undergoing MVR with 1 type of mechanical valve, Yazdanbakhsh et al23 defined PPM as an indexed GOA 1.9 cm2/m2 and found a significant impact on 30-day mortality but not on long-term mortality. This result, however, cannot be applied to other types of prosthesis because, as evidenced by Figure 2, for a similar value of indexed EOA, the values for indexed GOA will vary widely from 1 type of prosthesis to the other. Hence, it is not surprising that, in the present study in which multiple types of valves were used, only the indexed EOA could be related to postoperative outcomes, whereas no such relation was found for labeled prosthesis size or indexed GOA. To this effect, it should be emphasized that the labeled prosthesis size and the indexed GOA have similarly been shown to have no relevance to hemodynamics or outcomes in patients undergoing aortic valve replacement.12,15,21,22,25,26 Hence, it would appear that, as for the aortic valve, the indexed EOA is the only valid parameter that can be used to identify PPM. To the best of our knowledge, the present study is the first to examine postoperative outcomes in these terms.
Clinical Implications
The practical implications of these findings are important given that PPM does not appear to be a rare phenomenon in patients undergoing MVR. Indeed, the prevalence of moderate PPM was 69% and that of severe PPM was 9% in the present study. Moreover, among the risk factors identified to be independently associated with higher postoperative mortality, PPM is the only one that can potentially be avoided by the use of 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 position11,12,26,31: The projected indexed EOA of the prosthesis to be implanted is calculated, and if PPM is anticipated, potential alternatives include aortic root enlargement to accommodate a larger prosthesis and use of another type of prosthesis with better hemodynamic performance (ie, with a larger EOA).
Obviously, the best way to avoid PPM in the mitral position would be to repair rather than to replace the valve. Nonetheless, a significant proportion of mitral valves cannot be repaired and need to be replaced. Given the results of the present study, it would thus appear appropriate in such cases to calculate the projected indexed EOA of the prosthesis to be implanted before operation, as is done for the aortic valve,26 and to consider alternative options if PPM, especially severe PPM, is anticipated. Unfortunately, the options for preventing PPM in the mitral position are much more limited than in the aortic position. In particular, no alternative technique exists to implant a larger prosthesis, and the implantation of a homograft or of a stentless prosthesis is technically more demanding and associated with poor long-term durability.32,33 Hence, the preventive strategy can be oriented only toward the implantation of a prosthesis having a larger EOA for a given annulus size. In this context, our findings provide further impetus for developing better-performing mitral prostheses and for acquiring the ability to perform mitral valve repair in as many patients as possible.
Study Limitations
The study is retrospective in design, and it is always possible that a selection bias or unidentified confounders might have influenced the results.34
The incidence of coronary artery disease was higher in the patients with severe PPM. Although an effort was made to adjust for the effect of coronary artery disease in multivariate analysis, it is possible that this confounding factor might have resulted in an overestimation of the impact of severe PPM on mortality. Nonetheless, in the subset of patients with isolated MVR in whom the incidence of coronary artery disease in the severe PPM group was low and similar to that in the no PPM group, severe PPM remained an independent predictor of mortality.
The proportion of smaller prostheses (<27 mm) in this study might also appear high compared with other series. However, it must be emphasized that it is not prosthesis size per se that matters but rather its relation to body surface area and that larger prosthesis sizes cannot necessarily be equated with larger indexed EOAs.
Conclusions
Severe PPM is an independent predictor of mortality after MVR. As opposed to other independent risk factors, PPM may be avoided or its severity may be reduced with the use of prospective strategy at the time of operation. To this effect, the projected indexed EOA should be systematically calculated at the time of operation to estimate the risk of PPM, and if anticipating severe PPM, the surgeon should attempt to implant another type of prosthesis with a larger EOA. These findings also provide impetus for the development of better-performing mitral prostheses.
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Acknowledgments |
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We thank Paul Cartier, MD; Richard Baillot, MD; Richard Bauset, MD; Éric Charbonneau, MD; Denis Desaulniers, MD; Éric Dumont, MD; Michel Lemieux, MD; Jacques Métras, MD; Jean Perron, MD; Gilles Raymond, MD; and Pierre Voisine, MD, for implanting the prostheses and for participating in this study. We also thank Brigitte Dionne, Stéphanie Dionne, and Martine Fleury for the data collection and validation of clinical data, as well as Serge Simard, MS, and Jean-Marc Daigle, MS, for their support in the statistical analyses.
Sources of Funding
This work was supported by a grant from the Canadian Institutes of Health Research (MOP 57745), Ottawa, Canada. Dr Pibarot holds the Canada Research Chair in Valvular Heart Diseases, Canadian Institutes of Health Research, Ottawa, Ontario, Canada. Dr Mathieu is a research scholar from the Fonds de Recherche en Santé du Québec, Montréal, Canada.
Disclosures
Dr Mathieu, Dr Dagenais, and Dr Doyle have received research grants from Edwards Life Sciences, Sorin, and Medtronic. Dr Dumesnil has received research grants from Medtronic and has held consultancies and/or is on the speaker’s bureau of Medtronic, St Jude Medical, and MCRI. Dr Pibarot has received research grants from St Jude Medical, Medtronic, Edwards Life Sciences, and Sorin. He also has held consultancies and/or is on the speaker’s bureau of St Jude Medical, Edwards Life Sciences, Medtronic, and Sorin. J. Magne and D. Tanné report no conflicts.
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CLINICAL PERSPECTIVE
We recently reported that prosthesis-patient mismatch (PPM) is associated with persisting pulmonary arterial hypertension after mitral valve replacement. In the present study, which included 929 consecutive patients undergoing mitral valve replacement, severe PPM was associated with a 3-fold increase in postoperative mortality after adjustment for other risk factors. The clinical implications of this study are important given that PPM is frequent (prevalence, 69% for moderate PPM and 9% for severe PPM), and in contrast to most other risk factors for mortality, it can theoretically be prevented or its severity can be reduced by the use of a prospective strategy at the time of operation. In this regard, mitral valve repair would appear to be the best option when feasible. In the remaining cases and as has been demonstrated for the aortic valve, the strategy is based on implanting a prosthesis providing a sufficiently large effective orifice area in relation to body surface area (ie, >0.9 cm2/m2 to avoid severe PPM and >1.2 cm2/m2 to avoid moderate PPM). In contrast to aortic valve surgery, however, mitral valve surgery does not allow annular enlargement, and the implantation of a homograft or a stentless prosthesis is technically more demanding and associated with poor long-term durability. Hence, the only alternative at present is to implant a prosthesis with a larger effective orifice area for a given annulus size, which unfortunately may not be sufficient to completely avoid PPM in some cases. In this sense, our findings also provide the impetus for developing better-performing prostheses and alternative techniques allowing more frequent repair or implantation of better-performing prostheses.
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The online-only Data Supplement, consisting of supplemental Methods and tables, is available with this article at http://circ.ahajournals.org/cgi/content/full/CIRCULATIONAHA.106.631549/DC1.
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