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J Thorac Cardiovasc Surg 2008;135:465-466
© 2008 The American Association for Thoracic Surgery
Letter to the Editor |
a Cardiac Surgery Division, Civic Hospital, Brescia, Italy
b Department of Thoracic and Cardiovascular Surgery, Villa Maria Eleonora Hospital, Palermo, Italy
We thank Pibarot and coauthors for their comments regarding our article.1
It is surely a privilege that such distinguished colleagues take an interest in our study. Nevertheless, we found some of the comments inappropriate.
First, as far as the title was concerned, it was obviously provocative and was chosen just to underline an important matter related to this issue. As Pibarot and coauthors stressed in their comment, patient–prosthesis mismatch (PPM) is a hemodynamic phenomenon and therefore should be diagnosed on the basis of hemodynamic parameters related to a specific patient. This is the key point related to PPM after mitral valve replacement. In other words, to evaluate clearly the impact of PPM on functional and clinical outcomes, we have to be sure that we are comparing patients with PPM to patients without PPM.
As we clearly stated, this was the main objective of our study, which was indeed focused on the identification of patients with real PPM and on the evaluation of accuracy of prediction and diagnosis of PPM with data not obtained in vivo postoperatively and therefore not related to a specific patient.
In their comments, Pibarot and coauthors express serious concerns about the validity of our Doppler echocardiographic data, especially those related to effective orifice area (EOA). We would stress that the methodology we used (continuity equation method) was validated for assessing mitral valve bioprosthesis by their own group2; they also confirmed the good correlation between the mean in vitro and in vivo areas for mitral prostheses. In our hands in vivo postoperative measured EOA was indeed larger than the EOA measured in vitro by the manufacturer. We stressed such interesting results in our discussion, and we also stressed that these findings were surely unexpected on the basis of what has clearly been demonstrated for aortic prostheses. We do believe, however, that our results deserve a further analysis rather than mere criticism. It is notable that, despite few data on postoperative hemodynamic performance after mitral valve replacement being available, Firstenberg and colleagues3 in 2001 reported echocardiographic data consistent with our findings. They specifically evaluated postoperative in vivo hemodynamic performances of the mitral Carpentier Edwards Perimount valve, and the postoperative in vivo EOAs they reported were consistent with our data. We do stress that they also reported a discrete variability (expressed in terms of SD), once more similar to our own findings. We are still collecting and analyzing our data for better evaluation of the reason for such variability, but we do believe that it is related to the fact that the postoperative prosthetic valve in vivo EOA depends on other physiopathologic parameters than simple prosthesis size. Different sensitivities of mitral valve hemodynamics to chronotropic conditions, which may vary extensively from one patient to another was furthermore previously noted by Pibarot and Dumesnil4 themselves in their Journal editorial of June 2007. Further studies addressing postoperative in vivo hemodynamic parameters could be more helpful in better understanding such variability, rather than criticizing our results and doubting their validity. In contrast to what they stated in their comments, we did not mention at all the "the complete absence of correlation between the EOA and the transprosthetic gradient" (which was, however, previously shown by Firstenberg and coworkers3), but rather the absence of correlation between increased prosthesis size and improved postoperative hemodynamic performance. A similar concept was also previously presented by Badano and associates5 and therefore is not a unique finding of our study.
We do not agree at all with Pibarot and coauthors' concerns about the "large proportion of the patients included in this series [who] were misclassified with respect to the presence or absence of PPM." Misclassification is definitively more frequent when the classification is based on fixed data, either from in vitro study or previously published studies, and not when the classification is based on real in vivo data that reflect the hemodynamic condition of a specific patient. The question of why some patients with the same prosthesis size had such different postoperative EOAs is surely matter for further discussion and evaluation, but postoperative in vivo EOA must anyway be considered the criterion standard for PPM identification and cannot be considered simply misleading just because different patients have different EOAs.
The final two comments of Pibarot and coauthors are all related to the clinical effect of PPM. With respect to the effect of PPM on pulmonary arterial pressure, Pibarot and coauthors simply underlined what we had already stated in our Discussion section. Furthermore, among three recent studies quoted by Pibarot and coauthors, the one from Li and colleagues6 was also a key reference in our study, and the two from Magne and coauthors7 and Lam and coworkers8 were published well after we sent our article for consideration for publication in the Journal (February 2007, as clearly reported on the first page1).
With respect to clinical impact of PPM in terms of operative and late mortalities, we also clearly stated in the Discussion section that our study could not be elucidative because only 8 patients had PPM. Clinical relevance of PPM has to be better elucidated and surely represents an important matter. We would like to stress, however, that once more the evidence must come from a complete evaluation and analysis of different experiences published in the literature. Recent experiences quoted by Pibarot and coauthors7,8 clearly identify PPM as risk factor for poor outcome. Previous experience from Lorusso and associates9 and Ruel and coworkers,10 however, did not confirm different outcome in patients receiving small prostheses. Because Lam and coworkers' definition of patients with PPM was not based on postoperative in vivo data,8 patients classified as having PPM should mainly be patients receiving small prostheses. These data are therefore in contrast and deserve further evaluation and further studies. In conclusion, in our opinion only a multicenter, prospective study that is based on in vivo postoperative evaluation of PPM could reach a better level of evidence regarding the exact definition of PPM at the mitral level, the real incidence of postoperative mitral PPM, and its clinical impact. Our study was not meant to contradict results from other researchers but simply to warn about the real potential for misclassification of patients has having PPM solely on the basis of fixed data rather than dynamic data specific to that patient. For the patient receiving a mitral prosthesis, specific postoperative in vivo evaluation should be mandatory to evaluate the real incidence of mitral PPM.
Finally, we would respectfully underline that the appropriate scientific controversy should call for a different attitude and approach to other investigators simply driven by the same enthusiasm for proven data about a scientific aspect whose explanation, unless proven, is usually not in the hands of a unique group of investigators.
References
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