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J Thorac Cardiovasc Surg 2007;133:1464-1473
© 2007 The American Association for Thoracic Surgery
Surgery for Acquired Cardiovascular Disease |
Division of Cardiac Surgery, University of Ottawa Heart Institute, Ottawa, Ontario, Canada.
Read at the Eighty-sixth Annual Meeting of The American Association for Thoracic Surgery, April 29–May 2, 2006, Philadelphia, Pa.
Received for publication May 29, 2006; revisions received November 28, 2006; accepted for publication December 12, 2006. * Address for reprints: Buu-Khanh Lam, MDCM, Division of Cardiac Surgery, University of Ottawa Heart Institute, 40 Ruskin St, H3404, Ontario, Canada K1Y 4W7. (Email: bklam{at}ottawaheart.ca).
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Abstract |
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Methods: Between 1985 and 2005, 884 patients, with a mean age 63 ± 12 years, underwent mitral valve replacement (657 mechanical, 227 bioprosthesis) with contemporary prostheses. Mean clinical and echocardiographic follow-up was 5.1 ± 4.1 years (4344 patient-years). Patient–prosthesis mismatch was defined as an indexed effective orifice area of 1.25 cm2/m2 or less. Parametric and nonparametric analyses were used to determine predictors of outcomes.
Results: The incidence of patient–prosthesis mismatch was 32%. Predictors of recurrent congestive heart failure included low indexed effective orifice area, low ejection fraction, elevated postoperative mean mitral gradient, and use of a bioprosthesis (P 
.05). Postoperative pulmonary hypertension was associated with small mitral size, elevated mean mitral gradient, low ejection fraction, and atrial fibrillation (P .05); indexed effective orifice area did not predict postoperative pulmonary hypertension (P = .89). Poor late survival was predicted by low indexed effective orifice area (1.25 cm2/m2), New York Heart Association class 3 or 4, elevated right ventricular pressure, stroke, older age, coronary artery disease, and bioprosthesis use (P .05). Survival for patients with patient–prosthesis mismatch versus those without patient–prosthesis mismatch at 1, 3, 5, and 10 years was 91% versus 95%, 85% versus 90%, 78% versus 86%, and 65% versus 75%, respectively (P = .05).
Conclusions: Patient–prosthesis mismatch after mitral valve replacement is not uncommon; it is associated with recurrence of congestive heart failure and postoperative pulmonary hypertension and independently affected late survival. This study emphasizes the importance of implanting a sufficiently large prosthesis in adult patients undergoing mitral valve replacement.
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Introduction |
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The concept of patient–prosthesis mismatch (PPM) was first described by Rahimtoola1 more than a quarter of a century ago. Since that time, the deleterious effects of PPM on left ventricular remodeling, functional status, and early and late survivals after aortic valve replacement have been extensively reported.2-9
Recently, there has been increasing interest in mitral valve patient–prosthesis mismatch (MVPPM), which has been described less often in adults but is commonly encountered in the pediatric population.10-12 MVPPM was identified in case report13 but has subsequently been more clearly defined using echocardiographic parameters as an indexed effective orifice area (IEOA) of 1.2 to 1.3 cm2/m2 or less.14,15 The clinical problems associated with adult MVPPM have not been detailed but seem to include postoperative pulmonary hypertension (PHTN) and increased early mortality, although the latter has been disputed.16-18
The objectives of this study were to determine (1) the incidence of MVPPM and (2) the impact MVPPM on recurrent congestive heart failure (CHF), postoperative PHTN, and late survival.
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Materials and Methods |
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The mean follow-up was 5.1 ± 4.1 years (4344 patient-years, median 3.8 years, maximum 19 years) and complete.
In addition, 746 patients (84%) underwent a complete M-mode, 2-dimensional, and Doppler transthoracic echocardiogram at their first annual follow-up appointment and subsequently as clinically indicated per the recommendations of the American College of Cardiology/American Heart Association/American Society of Echocardiography 2003 Guideline Update for the Clinical Application of Echocardiography.20 Postoperative follow-up transthoracic echocardiographic recordings of systolic pulmonary artery pressure (SPAP) were available on a subset of 518 patients (59%). Cardiac dimensions, gradients, and estimation of right ventricular systolic pressure (RVSP) and SPAP were assessed with continuous-wave Doppler. For SPAP, the maximum peak TR velocity (V) recorded from any view was used to determine the RVSP with the simplified Bernoulli equation (RVSP = 4V2 + radial artery pressure), with radial artery pressure assumed to be 10 mm Hg. SPAP was assumed to equate the RVSP in the absence of pulmonary stenosis and right ventricular outflow tract obstruction. The mean interval to the follow-up echocardiograms was 5.2 ± 3.7 years (range 0.5-19 years, median 5.1 years).
Mitral Valve Patient–Prosthesis Mismatch Definition
The calculation of the indexed valve area has been somewhat controversial. Some reports have used the geometric orifice area (GOA)17,18 provided by the manufacturer as a base value, whereas other reports have used the effective orifice area (EOA) measured in vivo.14,15 To avoid confusion, the indexed valve area will be referred to specifically as indexed GOA (IGOA) or IEOA. In this study, we used the latter method because of its known clinical correlation with clinical outcomes and more accurate estimation of postoperative gradients.21 The IEOA was obtained by dividing the valve’s in vivo EOA (centimeters squared), provided by the manufacturer or obtained from the literature, by the patient’s calculated body surface area (meters squared). When more than 1 EOA was available, the mean value was used in the calculation of IEOA. By using these criteria and the work by Li and colleagues,16 in which MVPPM was defined as an IEOA of 1.2 to 1.3 cm2/m2 or less, we defined MVPPM as any IEOA of 1.25 cm2/m2 or less. The selection of this value was also based on the lack of clinical effect in our statistical modeling with IEOA values of 1.5 cm2/m2, 1.4 cm2/m2, and 1.3 cm2/m2.
Definition of Outcomes
Primary outcomes in this study included (1) the recurrence of CHF as defined by New York Heart Association functional class 3 or 4 for more than 4 consecutive weeks or death where the primary contributing diagnosis was CHF; (2) postoperative PHTN as an SPAP greater than 40 mm Hg as measured by echocardiography;22 and (3) late survival as a patient censored at a minimum of 30 days after surgery.
Data Analysis
Descriptive statistics were used to summarize data. Categoric data were described using frequencies and percentages; comparisons were made using the chi-square test or the Fisher exact test when the frequency was less than 5. Continuous variables were presented as mean ± standard deviation, and comparisons of continuous variables were performed using the Student t test for normally distributed data and the Wilcoxon rank-sum test when values were skewed. Exploratory correlation analyses were performed using the Spearman (rs) correlation coefficient.
The Kaplan–Meier method was used to assess time-related outcomes (freedom from CHF, freedom from postoperative PHTN, and survival). Predictors of outcomes were identified using a semiparametric multivariable Cox proportional hazard model; variables screening ensured that an adequate (n = 10) number of events were associated with a potential risk factor and that the scales of ordinal and continuous variables were calibrated with respect to outcome. Variable selection proceeded in a forward stepwise manner with a liberal entry criterion of P less than .1 and a stay criterion of P equal to or less than .05. Logistic regression was applied to determine the effect of valve type (mechanical, bioprosthesis), valve size criteria (manufacturer size, calculated IEAO), and echocardiographic parameters (mean and peak mitral gradients, SPAP) on the cumulative rate of recurrent CHF and postoperative PHTN. All time-related estimates are considered reliable to 10 years. All analyses were performed using the SAS statistical software (SAS v9.1; SAS, Cary, NC).
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Results |
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Outcomes
Recurrence of congestive heart failure
The overall freedom from recurrence of CHF at 1, 3, 5, and 10 years was 98%, 96%, 94%, and 85%, respectively (Figure E1). In patients with MVPPM, 1, 3, 5, and 10-year rates were significantly less than patients without MVPPM (P < .0001) (Figure 1, A). Predictors of recurrent CHF included low IEOA (1.0 and 1.5 cm2/m2, hazard ratio [HR] 4.0, 1.6-10.4, and 3.5, 1.9-6.3), worse left ventricular function (HR 1.01, 1.0-1.03), elevated mean mitral gradient on follow-up echocardiography (HR 2.0, 1.1-3.3), and prolonged cardiopulmonary bypass (HR 1.1, 1.01-1.1) (Table E1). Coronary artery disease, age, and peak mitral gradients on follow-up did not predict the return of CHF (P>.05). There was a linear effect of MVPPM (odds ratio [OR] 3.9), postoperative mitral gradients (OR 1.8), use of a bioprosthesis (OR 2.7), and elevated SPAP (OR 1.02) on the recurrence of CHF (Appendix E1).
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1.25 cm2/m2), there was no correlation between IEOA and mean and peak gradients, or with SPAP; however, a strong correlation was observed between peak mitral gradient and SPAP. In patients with an IEOA of 1.0 cm2/m2 or less, IEOA correlated well with mean and peak mitral gradients but not with SPAP. In general, elevated postoperative mean and peak mitral gradients were closely related to SPAP. In patients with bioprostheses, a linear relationship was seen between IEAO and mean mitral gradients, but not peak mitral gradients or SPAP.
Freedom from PHTN at 1, 3, 5, and 10 years was 99%, 96%, 93%, and 78%, respectively (Figure E2). Freedom from postoperative PHTN in patients with MVPPM at 1, 3, 5, and 10 years was similar to that of patients without MVPPM (98% vs 99%, 97% vs 96%, 96% vs 92%, and 69% vs 78%, respectively, P = .6); however, patients with smaller sized valves ( 27) had higher rates of postoperative PHTN when compared with patients with valve sizes 29 or larger (P = .005) (Figure 1, B).
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Survival
Overall 1, 3, 5, and 10-year survivals were 95%, 90%, 85%, and 73%, respectively (Figure E3). Patients with MVPPM had worse 1, 3, 5, and 10-year survivals (91% vs 95%, 85% vs 90%, 78% vs 86%, and 65% vs 75%, respectively, P = .05) (Figure 1, C). Survival in patients with elevated SPAP (>40 mm Hg) was less than their counterparts with SPAP in the normal range (P = .02) (Figure E4).
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Discussion |
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The concept of residual obstruction with persistent elevated transprosthetic gradients postaortic valve replacement was first reported by Rahimtoola in 1978.1 Since then, many significant contributions have led to the establishment of precise diagnostic criteria and to the development of preventative strategies to avoid PPM in the context of aortic valve replacement.21,23 The negative effects of aortic valve PPM on left ventricular remodeling, functional status, early mortality, and late survival have been extensively corroborated.2-9 What remains uncertain is whether clinically deleterious effects of PPM could be encountered after MVR.
Mitral Valve Patient–Prosthesis Mismatch
There has been a recent mounting interest in MVPPM, which has been well documented in the pediatric population. In the latter, mitral valve re-replacement rates upward of 27% have been reported because somatic growth has led many children to outgrow their mitral valve prosthesis.10,12 A variety of factors have been used in an attempt to define the concept of clinical MVPPM in childre: These have included size/weight ratios, Z scores, maximum transprosthesis velocity (Vmax), and 2.5 times increase in body weight from the time of implant. In all instances, these factors have been correlated with outcomes (early mortality, survival, and PHTN).10-12
Adult MVPPM was the subject of an original case report in 1981;13 it has subsequently been theorized, through in vitro pulse duplicator analysis, that an IGOA less than 1.3 to 1.5 cm2/m2 could potentially leave the patient with high postoperative transprosthetic gradients unrelated to structural dysfunction.14 In a clinical study, a good correlation between elevated transprosthetic mitral gradient and in vivo IEOA was demonstrated by the use of the continuity equation during echocardiographic assessment of porcine mitral prostheses.15 In this report, an IEOA of 1.3 to 1.5 cm2/m2 or less at rest was associated with a mean mitral gradient of 4 mm Hg; with every 10% increase in stroke volume (maximum 50%), there was a proportional increase of the mean mitral gradient (eg, IEOA 1.0 cm2/m2, +50%, mean mitral gradient of 14 mm Hg). In our study, we had an incidence of MVPPM (IEOA 1.25 cm2/m2) of 32% with 5% of patients having an IEOA less than 1.0 cm2/m2.
Mitral Valve Patient–Prosthesis Mismatch and Congestive Heart Failure Recurrence
The unadjusted 1, 5, and 10-year cumulative incidence of recurrent CHF post-MVR was 2%, 6%, and 15%, respectively; the rates were significantly higher (5%, 15%, and 38%, respectively) when adjusted for MVPPM criteria. These results are similar to those we previously reported and take into further consideration the indexed in vivo EOA rather than only prosthesis size.24 CHF was 3.5 and 4 times more likely to develop postoperatively in patients with an IEAO of 1.0 cm2/m2 or less and an IEAO of 1.25 cm2/m2 or less, respectively. Elevated mean mitral gradients were associated with recurrence of CHF. Although an IEOA of 1.25 cm2/m2 or less and elevated mean mitral gradients predicted the recurrence of CHF, no direct significant correlation was established between these 2 variables (rs = –0.12, P = .1). This finding was in contrast with work from Dumesnil and colleagues15 and Li and colleagues16 that described a moderate level of correlation between IEOA and transprosthetic gradients (r = 0.46-0.63). This weaker correlation could be due to the smaller proportion of patients with prostheses less than 27 mm (26% vs 52%16 and 69%15) observed in our study; this could considerably decrease the risk of elevated transprosthetic gradients developing in patients and thereby impacting the establishment of a correlation. A second potential reason for this would be the dependency of transprosthetic gradients on transvalvular flow rate, a dependent factor of diastolic filling time, which is in return sensitive to the effect of chronotropy. In this context, the establishment of good correlations between IEOA and transprosthetic gradients is more difficult post-MVR than aortic valve replacement.
In our study, in view of the high proportion of patients (76%) with class I and II left ventricular function preoperatively, the effect of left ventricular function on recurrence of CHF was noted as marginal (HR 1.01). As in patients with aortic valve PPM, we must not discount the potential impact of left ventricular function on outcomes post-MVR.3,25
Postoperative PHTN was weakly associated with the recurrence of CHF; overall, the mean SPAP of patients with CHF was greater than that of their counterparts (47.6 ± 11.3 vs 42.8 ± 13.4 mm Hg, P = .04). In patients with recurrent CHF, there was no correlation between IEOA and SPAP (P = .6). The known detrimental impact of residual or recurrent PHTN, due to mitral valve disease, on functional outcome and survival has been reported.25-28
Mitral Valve Patient–Prosthesis Mismatch and Postoperative Pulmonary Hypertension
The unadjusted 1, 5, and 10-year cumulative incidence of postoperative PHTN was 1%, 7%, and 22%, respectively; once adjusted for smaller mitral valve size (27), the rates were higher in patients with size 25 and 27 prostheses at 1, 5, and 10 years (2% vs 1%, 18% vs 4%, 33% vs 20%, respectively, P = .005). When we looked at 1, 5, and 10-year rates of postoperative PHTN in patients with MVPPM versus NOMVPPM, there was no difference (2% vs 1%, 4% vs 8%, 31% vs 22%, respectively, P = .6). These results sharply contrasted with those reported by Li and colleagues,16 showing a postoperative PHTN prevalence rate of 68% in patients with MVPPM. This difference, along with the lack of correlation between IEOA and SPAP (rs = 0.03, P = .4), could be attributable to several factors: First, the proportion of patients in our study who received smaller sized prostheses (25 and 27) was 26% (mechanical 25%, bioprosthesis 28%) in comparison with the 52% reported. This might constitute an unusually elevated proportion by current standards.24,29,30 This would mean that 29 of the 56 patients in Li and colleagues’ study were already at a higher risk of having MVPPM and postoperative PHTN; this was confirmed by the elevated incidence of MVPPM (71%). Second, the population selected by Li and coworkers, because of the greater proportion of smaller valves, would take longer to normalize any preoperative PHTN and would therefore be subject to higher postoperative SPAP, especially in patients with MVPPM, thus possibly strengthening the correlation between IEOA and SPAP that the authors described. In contrast, our patients had an almost equal proportion of patients with PHTN irrespective of MVPPM adjustments (57% vs 55%, P = .2). Third, there is the issue of body surface area; the mean body surface area of our patients without MVPPM was 1.76 ± 0.18 m2, a number almost equivalent to Li and colleagues’ group of patients with MVPPM (1.75 ± 0.16 m2). This would lead us to conclude that a significant proportion of patients with borderline body surface area likely did not receive a valve sufficiently large enough, thus predisposing them to MVPPM. Finally, a point of concern is the fact that the rate of postoperative PHTN was observed to be increasing over time, leading us to question the exact contribution of other confounders (age, atrial fibrillation, type of prosthesis, and left ventricular function).
The IEAO was not predictive of postoperative PHTN, but its surrogate marker (valve size 27) and elevated mean mitral gradients were. This lack of correlation could be explained by the incomplete reporting of SPAP in the echocardiograms collected. In a similar analysis in children, Masuda and colleagues12 reported the absence of correlation between IGOA and catheterized pulmonary artery wedge pressure; however, good correlation was seen between maximal transprosthetic flow velocity (Vmax) and IGOA and between Vmax and catheterized pulmonary artery wedge pressure. It has been postulated that MVPPM post-MVR may predispose one to persistence of high afterload on the right ventricle, resulting in stunning and right ventricular failure leading to increased early mortality.17 This may be extrapolated to patients with MVPPM and a chronic decline of right ventricular function over time, which would ultimately lead to right ventricular failure and death.
In view of the relative inconsistency of the relationships between PHTN markers (SPAP, IEOA, Vmax, pulmonary wedge pressure, transprosthetic gradients, and pulmonary vascular resistance and compliance) reported here and in the literature, further data are required to elucidate the potential mechanistic and hemodynamic ramifications of PHTN post-MVR and its impact on clinical outcomes.
Mitral Valve Patient–Prosthesis Mismatch and Survival
The overall survival for our cohort of patients post-MVR was acceptable and approached 75% at 10 years. The 1, 5, and 10-year survivals for patients with MVPPM were significantly worse than those of their counterparts. Fernandez and coworkers18 were among the first to report on the clinical implications of MVPPM; however, in their study, the GOA, which often overestimates the valve area, was used to calculate the IGOA. They did not find any association between indexed valve area and early and late morbidity or late mortality. A second report by Yazdanbakhsh and colleagues17 on the impact of IGOA on outcomes stated that the lower tail end of IGOA ( 1.9 cm2/m2) was associated with early mortality (HR 4.3, 1.6–9.5) but had no effect on late mortality. Once again, the GOA was used in the calculations of IGOA and may have led to overestimation of IGOA and thus biased the effect of the latter on late mortality. In our study, an IEOA of 1.25 cm2/m2 or less was a predictor of poor late survival. As previously stated, we believe that the IEOA is a better prognostic indicator than the IGOA because it has been shown to be a reliable predictor of clinical outcomes.21 We must caution that, as is the case in most retrospective studies, a finding of association does not automatically imply causation. The presence of other significant clinical correlates (age, coronary artery disease, left ventricular function, preoperative CHF, and PHTN) to survival would indicate a multifactorial cause that will require further elucidation.
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Limitations |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionLimitationsConclusionsLogistic regression analysis of...References |
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We have made all efforts to use primarily only published EOAs rather than GOAs in the calculation of IEOA values. However, because of the limited availability of reports on mitral EOAs for all of the valve types and brands, we did not discriminate against EOA values obtained by the pressure half-time method; this latter is known to overestimate EOAs. When an EOA for a particular valve brand and size was not available, we had to use the GOA. These 2 conditions may have led to an underestimation of the true incidence of MVPPM in this cohort of patients.
Furthermore, Cox proportional hazards models require an assumption of independent censoring that may not always be met. In this regard, it is possible that patients lost to follow-up after a number of visits may have had subsequent outcomes that were not accounted for in the analyses. Similar to that of other observational cohorts, the results of these analyses may not be generalizable to all patients who have undergone prosthetic valve replacement at other centers.
Finally, as mentioned previously, in view of the relative inconsistency and scarce amount of information on the relationships between PHTN markers (SPAP, IEOA, Vmax, pulmonary wedge pressure, transprosthetic gradients, pulmonary vascular resistance, and compliance), further data will be required to elucidate the potential mechanistic and hemodynamic ramifications of PHTN post-MVR.
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Conclusions |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionLimitationsConclusionsLogistic regression analysis of...References |
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This study constitutes an initial report associating IEOA post-MVR and clinical outcomes (recurrent CHF, postoperative PHTN, and late survival). By using an IEOA of 1.25 cm2/m2 or less as a cutoff point to define MVPPM, we demonstrated that the incidence of MVPPM was higher than anticipated. We also determined that patients with MVPPM were 4 times more likely to experience recurrent CHF. MVPPM was also associated with postoperative PHTN (SPAP > 40 mm Hg), although smaller valve size rather than IEAO was a predictor of PTHN. Finally, MVPPM was associated with a decrease in late survival.
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Logistic regression analysis of valve parameter effects on congestive heart failure recurrence |
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| See related editorial on page 1405.
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29) sized valve (P = .005). C, Adjusted survival according to MVPPM versus NOMVPPM (P = .05). CHF, Congestive heart failure; PHTN, pulmonary hypertension; MVPPM, mitral valve patient–prosthesis mismatch.
