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J Thorac Cardiovasc Surg 2008;135:464-465
© 2008 The American Association for Thoracic Surgery
Letter to the Editor |
Laval Hospital Research Center, Québec Heart Institute, Faculty of Medicine, Laval University, Québec City, Québec, Canada
To the Editor:
We read with interest the article of Totaro and Argano.1
We have, however, several concerns with regard to the validity of the results and conclusions presented in this article. First, the title of the article, "Patient–Prosthesis Mismatch after Mitral Valve Replacement: Myth or Reality?" is inappropriate. Mitral prosthesis–patient mismatch (PPM) is equivalent to a residual mitral stenosis, related to the fact that most prosthetic valves have a hemodynamic performance, and thus a valve effective orifice area (EOA), that is inferior to that of the normal native valve. Thus concluding that PPM is a myth would be equivalent to saying that mitral stenosis (or aortic stenosis for aortic PPM) does not exist, and that this is a benign phenomenon, which is of course not the case. In this regard, several studies have demonstrated that PPM is a frequent hemodynamic phenomenon after mitral or aortic valve replacement.2-5 The important question is rather to determine the impact of PPM on the hemodynamic, functional, and clinical outcomes, and at which degree of severity and in which categories of patients this impact of PPM becomes statistically significant and clinically relevant. Unfortunately, the data provided by Totaro and Argano1 do not permit an answer to these important questions.
There are serious concerns about the validity of the Doppler echocardiographic data, and especially of those of the valve EOA. This is a crucial aspect, because the identification and quantification of PPM are based on these data. First, it is intriguing to see that the EOAs measured in vivo by Doppler echocardiography, especially for the 25- and 27-mm valves, were larger than the EOAs measured in vitro by the manufacturer. A recent study has indeed demonstrated that, as opposed to the observation in this study, the in vitro EOAs provided by the manufacturer grossly overestimate the in vivo EOAs and are thus not valid for prediction of PPM.6 Totaro and Argano also used the label prosthesis size as a surrogate for PPM, whereas previous studies have shown that this parameter is not valid for identification of PPM and prediction of its hemodynamic and clinical consequences.3,6,7
Moreover, the huge variability in the EOA measurements for a given prosthesis size (from 1.0 to 4.9 cm2 for the 29-mm prostheses!), the complete absence of correlation between the EOA and the transprosthetic gradient, and the recording of high transprosthetic gradients (>15 mm Hg) in several patients despite the calculation of large EOAs and indexed EOAs (see Figure 3 of the article1) further support the concerns regarding the validity of the EOA measurements and thus the identification of PPM. The presence of gradients greater than 15 mm Hg in the mitral position definitely cannot be considered as "favorable hemodynamics," as concluded by Totaro and Argano.1 In fine, these observations suggest that a large proportion of the patients included in this series were misclassified with respect to the presence or absence of PPM.
Totaro and Argano only measured the valve hemodynamics and systolic pulmonary arterial pressure at predischarge examination or at 30 days. It is well known that the measurements of valve EOA, transvalvular gradients, and pulmonary pressure in the early postoperative period are often unreliable because of the poor acoustic window, hyperdynamic state, or flow acceleration in the left ventricular outflow tract. Moreover, the adverse effect of PPM on pulmonary arterial pressure may in large part occur in the long term. Thus the early postoperative pulmonary arterial pressure is obviously not an appropriate and reliable end point for adequate assessment of the effects of PPM. As opposed to the results of this study, three recent previous studies have reported that PPM is associated with a higher incidence of persistent pulmonary hypertension after mitral valve replacement.2-4
The number of patients is far too small and the follow-up too short to draw any meaningful conclusion with regard to the impact of PPM on operative and late mortalities, on the persistence of pulmonary hypertension, or on any other clinical outcomes. Importantly, there is a major discrepancy between the data reported in this small series of patients with very short follow-up and the data reported by two independent groups of investigators in much larger series of patients (>800) with more than 10 years of follow-up.3,4 These larger studies concluded that mitral PPM, and especially severe PPM, is an independent predictor of the persistence of pulmonary hypertension, the occurrence of congestive heart failure, and late mortality.
In light of the important limitations of this study and of the results of previous studies,2-4 the results and conclusions of the article of Totaro and Argano1 cannot be accepted at face value. We believe that among several prosthesis models that are equivalent in terms of durability and thromboresistance the surgeon should logically select the one with the largest possible EOA in a given annulus size to minimize the risk of PPM and associated complications after mitral valve replacement.
References
This article has been cited by other articles:
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  D. Tanne, L. Kadem, R. Rieu, and P. Pibarot Hemodynamic impact of mitral prosthesis-patient mismatch on pulmonary hypertension: an in silico study J Appl Physiol, December 1, 2008; 105(6): 1916 - 1926. [Abstract] [Full Text] [PDF]
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