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J Thorac Cardiovasc Surg 2007;134:697-701
© 2007 The American Association for Thoracic Surgery
Surgery for Acquired Cardiovascular Disease |
a Cardiac Surgery Division, Civic Hospital, Brescia, Italy
b Department of Thoracic and Cardiovascular Surgery, Villa Maria Eleonora Hospital, Palermo, Italy.
Received for publication February 2, 2007; revisions received March 19, 2007; accepted for publication April 11, 2007. * Address for reprints: Pasquale Totaro, MD, Via San Vincenzo, 38, 20123 Milan, Italy. (Email: ptotaro{at}yahoo.com).
| Abstract |
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Methods: Ninety-two patients who underwent mitral valve replacement and received Carpentier–Edwards stented bioprosthesis (Edwards Lifesciences, LLC, Irvine Calif) were enrolled. Hemodynamic performances were evaluated at discharge, and the incidence of in vivo patient–prosthesis mismatch (indexed effective orifice area
1.2 cm2/m2) was evaluated. Correlation between in vivo patient–prosthesis mismatch and predicted patient–prosthesis mismatch, based on previously published in vitro hemodynamic parameters, was also investigated.
Results: Five patients died within 30 days of the operation (5.4% mortality). Mean prosthesis size was 29.8 ± 2. Mean postoperative effective orifice area and indexed effective orifice area (2.5 ± 0.8 cm2 and 1.5 ± 0.4 cm2/m2, respectively) compared favorably with those predicted in vitro (2.2 ± 0.7 cm2 and 1.3 ± 0.5 cm2/m2, respectively). In the subgroup of patients receiving prosthesis size of 27 or smaller, the difference reached statistical significance (2.47 ± 0.83 and 1.61 ± 0.7 for postoperative and predicted effective orifice areas, respectively; P < .001). Postoperative patient–prosthesis mismatch was recorded in 8 patients (8.6%), comparing favorably with the predicted patient–prosthesis mismatch (39% for overall population and 80% for patients receiving prosthesis size
27). No significant correlation between size of prosthesis and early hemodynamic and clinical outcomes was shown.
Conclusions: In our study, stented mitral bioprostheses showed satisfactory postoperative hemodynamic performance, even in smaller prosthesis sizes (
27 mm). Risk of in vivo postoperative patient–prosthesis mismatch seems to be less relevant than preoperative risk prediction based on in vitro data. Further studies are needed to evaluate the potential clinical impact of mitral patient–prosthesis mismatch.
| Introduction |
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The term patient–prosthesis mismatch (PPM) was introduced in the late 1970s by Rahimtoola1
to describe the condition in which the effective orifice area (EOA) of the prosthetic valve inserted into the patient was not matching the area of the native valve, thus causing an abnormal residual pressure gradient across the valve with obstruction to ventricular outflow or inflow, or both. Since then, several studies have been designed and carried out to better clarify the cutoff value for PPM to occur, as well as the clinical relevance of such a complication. The majority of these studies, however, have concentrated on PPM after aortic valve replacement.2-7
It is only in the recent era that the clinical consequence of mitral PPM has been considered.8
In this study we evaluate early postoperative hemodynamic performance and early clinical outcomes in patients undergoing MVR with a stented bioprosthesis to better clarify the real risk and the early clinical relevance of mitral PPM.
| Patients and Methods |
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Two types of Carpentier–Edwards stented bioprostheses (Perimount pericardial and SAV porcine; Edwards Lifesciences, LLC, Irvine Calif) were used according to surgeon preference. Patient characteristics are summarized in Table 1. Preoperative and postoperative hemodynamic performances were recorded for all survivors and compared with the in vitro data published by the manufacturer for the implanted prosthesis. Incidence of postoperative PPM was evaluated and correlated to the predicted incidence of PPM. Finally, postoperative hemodynamic performance and clinical outcome were correlated to the size of bioprosthesis implanted.
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Surgical Technique
All procedures were performed through a standard midline sternotomy and full cardiopulmonary bypass. Antegrade cold blood cardioplegia was used as conventional myocardial protection strategy. The mitral valve was approached with a standard left atrial incision. Native posterior leaflet or subvalvular apparatus, or both, were preserved whenever possible. All prostheses were implanted with interrupted everting 2–0 Ethibond (Ethicon Inc, Somerville, NJ) non–pledget-supported sutures (except under specific conditions).
Statistical Analysis
Values are expressed as mean ± standard deviation. Noncontinuous parameters were compared by the
2 test or Fisher exact test when appropriate. Continuous variables were compared by the Student t test for paired and unpaired data when appropriate. Simple least squared linear regression was used to test the association between continuous variables.
| Results |
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| Discussion |
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PPM was first described by Rahimtoola1
in 1978 as a clinical syndrome after valve replacement with a prosthesis too small compared with the patients body surface area. This concept has become extremely popular in the past two decades, and several articles have been published addressing this issue. The vast majority of such studies2-7
have focused on PPM after aortic valve replacement, inasmuch as the prosthesis implanted in this position is generally smaller. In this respect, several aspects related to the definition,3,4
the consequences,6,7
and the prevention6,7
of PPM have been addressed. Several steps forward have been made, therefore, regarding the better understanding of aortic PPM. Conversely, regarding mitral PPM, only limited experience has been reported so far.
In our study, we aimed to evaluate the potential risk for increased incidence of PPM using stented bioprostheses, comparing early postoperative hemodynamic performance with the in vitro predicted hemodynamic performance. We used a definition of PPM based on calculated in vivo postoperative MEOAI, which remains, despite a certain degree of variability resulting from associate factors,12
the most valuable parameter to evaluate PPM. To reduce prosthesis-related bias, we restricted the study to patients receiving only Edwards Lifesciences bioprostheses (pericardial or porcine) used for many years and with a well-documented durability and reliability.13-15
The first important finding in our study was the lack of correlation between increased prosthesis size and improved postoperative hemodynamic performance. We confirmed, therefore, findings from Firstenberg and associates,16
who showed a trend but not a significant correlation between increased prosthesis size and postoperative EOA after MVR with a Carpentier–Edwards Perimount bioprosthesis. Badano and coauthors17
also showed no correlation between increased size of prosthesis and improved hemodynamic performance, but they evaluated only postoperative pressure gradients in patients after MVR with a mechanical prosthesis. Our experience is based on both pericardial and porcine bioprostheses (from the same company); however, we did not show any difference related to the type of prosthesis, despite previous studies that suggested improved flow geometry in pericardial compared with porcine valves.18,19
An important finding of our study is the correlation between in vivo and in vitro evaluation of hemodynamic performance of mitral bioprostheses. Despite the good linear correlation that has been shown between in vivo and in vitro EOA for each prosthesis,7,9
the latest is usually superior. In our experience, postoperative in vivo EOA was, conversely, comparable with the predicted in vitro value. Furthermore, considering only patients receiving the smaller bioprostheses (25 and 27), in vivo hemodynamic performances were significantly superior to those predicted in vitro. This finding is interesting, especially considering the opposite observation reported for aortic bioprostheses, and deserves further evaluation. We could only suppose that the postimplantation behavior of a prosthesis in the mitral position can be influenced by different physiologic aspects, significantly more than in the aortic position.
Favorable hemodynamic performance reflects the incidence of postoperative PPM in our series, significantly lower than the predicted risk based on in vitro measurement. Our results, therefore, failed to confirm recent experience from Li and coauthors,8
who reported a high incidence of PPM after MVR (71%). At least three main characteristics differentiate the series from that of Li and colleagues, however: (1) the low percentage of patients receiving a bioprosthesis (only 16%), (2) the high percentage of patient receiving a small-sized prosthesis (52%), and (3) the time of the echocardiographic data collection (median follow-up time of 43 months). These specific conditions could in part explain the differences reported in our experience. On the other hand, Chan and associates (personal communication, 2006) reported a 13.8% incidence of PPM (based on in vitro data) in 884 patients undergoing MVR mainly with mechanical prostheses (75%). In our study, furthermore, the incidence of PPM was not correlated to the size of bioprosthesis. On the basis of our experience, therefore, we would not support extreme efforts to implant a prosthesis bigger than size 25 in the patient with a small or calcified annulus. In this case, the increased surgical risk seems unjustified by a real reduction of PPM incidence. It seems clear, however, that a homogenous method of hemodynamic performance evaluation is the first step toward a better understanding of the real risk of mitral PPM. In our minds, postoperative evaluation of EOAI is mandatory for definition of PPM. As far as the clinical relevance of PPM was concerned, in our series only 8 patients had PPM, with no implications on clinical outcome. Despite our experience being limited to 30 days follow-up, previous experiences20,21
already failed to show clinical relevance of implantation of a "small" prosthesis, at least in terms of recurrence of heart failure at 5 years follow-up. Also, no effect on early or late mortality of prosthesis-related factors after MVR was shown by Fernandez and coauthors.22
On the other hand, Yazdanbakhsh and coauthors,23
using geometric valve area and a cutoff for PPM definition equal to the 10th percentile, showed significant impact of PPM on early death but not on late follow-up. In their experience, however, the cutoff, based on a very low percentile, could have selected patients with "extreme" mismatch. Concerning clinical aspects of mitral PPM, Li and coauthors8
recently showed a significant difference in persistence of pulmonary hypertension (at a mean follow-up of 43 months) in patients with mitral PPM when compared with those not having PPM. Even though we failed to confirm this finding (in our series residual pulmonary hypertension was not correlated to size of prosthesis or postoperative PPM), we have to consider that our experience is limited to 1-month follow-up and, as a previous study clearly demonstrated,23
pulmonary artery hypertension does not always regress immediately after surgery. Furthermore, as previously discussed, the group from Li and coauthors8
included 71% of patients having PPM. The correlation between size of prosthesis implanted, postoperative PPM, and persistence of pulmonary hypertension therefore deserves further evaluation as well as the potential correlation between persistence of pulmonary hypertension and long-term clinical outcome.
| Conclusions |
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| References |
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