Impact of prosthesis–patient mismatch on tricuspid valve regurgitation and pulmonary hypertension following mitral valve replacement

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Abstract

Background

Mitral PPM can be equated to residual mitral stenosis, which may halt the expected postoperative improvement of PH and concomitant functional tricuspid regurgitation (fTR).

Aim of the present study is to evaluate the impact of mitral prosthesis–patient mismatch (PPM) on late tricuspid valve regurgitation and pulmonary hypertension (PH).

Methods

A total of 210 patients undergoing isolated mitral valve replacement (MVR) were investigated. Mitral valve effective orifice area was determined by the continuity equation and indexed for body surface area (EOAi) and PPM was defined as EOAi  1.2 cm2/m2. Pulmonary hypertension (PH) was defined as systolic pulmonary artery pressure (sPAP) > 40 mmHg. Clinical and echocardiographic follow-up (median 27 months) was 100% completed. A total of 88/210 (42%) patients developed mitral PPM.

Results

There were no significative differences in baseline and operative characteristics between patients with and without PPM. At follow-up, the prevalence of fTR  2 + (57%vs.22%; p = 0.0001), and PH (62%vs.24%;p < 0.0001) were significantly higher in patients with PPM. On multivariable regression analysis, EOAi (p < 0.0001) and preoperative left ventricular (LV) end-diastolic diameter (p < 0.0001) were found to be independently associated with fTR decrease after MVR. In addition, EOAi (p < 0.0001) and LV ejection fraction (p < 0.0001) were independently associated with PH decrease after MVR. No significant differences in mortality rates were found between patients having or not PPM.

Conclusions

This study shows that mitral PPM is associated with the persistence of fTR and PH following MVR. These findings support the realization of tricuspid valve annuloplasty when PPM is anticipated at the time of operation.

Introduction

Previous studies reported that prosthesis–patient mismatch (PPM) is associated with worse hemodynamics, less regression of left ventricular hypertrophy, more cardiac events, and higher mortality rates after aortic valve replacement [1], [2], [3], [4]. However, PPM following mitral valve replacement (MVR) has been less investigated. Previous studies reported that mitral PPM is not uncommon, ranging between 30 and 85% when in vivo evaluation of effective orifice area (EOA) is performed [5], [6], [7]. Two studies reported that mitral PPM is independently associated with increased mortality [5], [6], whereas another one found no significant impact on survival [7]. Mitral PPM can be equated to residual mitral stenosis resulting in increased trans-mitral gradients, increased left atrial pressure, and pulmonary hypertension (PH). These factors may lead to right ventricular dilatation/dysfunction and to atrial fibrillation, which may, in turn, lead to tricuspid annulus dilatation and functional tricuspid regurgitation (fTR).

Indeed, tricuspid regurgitation is not uncommon in the settings of mitral valve disease. At least moderate fTR is present in more than one-third of patients presenting with mitral stenosis and in 15% of patients with mitral regurgitation [8]. Such patients are more likely to have NYHA functional class III or IV [9], and the persistence of fTR after MVR predicts poor outcome [10].

After earlier reports supporting conservative treatment of fTR [11], it was subsequently demonstrated that fTR might not resolve after isolated MVR [12], [13]. Several factors (age, pulmonary hypertension, atrial fibrillation, and tricuspid annular diameter) may hinder the postoperative improvement of fTR [14], [15]. Hence, current guidelines [16], [17] recommend tricuspid valve repair in patients undergoing mitral valve surgery in the presence of severe tricuspid regurgitation (class I), and in the presence of moderate TR or of dilated tricuspid annulus (class IIa/b).

The objective of this study was to investigate the impact of mitral PPM on fTR and pulmonary arterial hypertension following MVR.

Section snippets

Methods

This study was reviewed and approved by the Institutional Review Board of the University of Rome, and a waiver of consent was granted.

The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology.

Perioperative analysis

A total of 210 patients undergoing isolated MVR were investigated and 101/210 (48%) of those had fTR = 2 + not addressed at surgery. Overall, 88/210 (42%) patients developed mitral PPM but none had prosthetic valve dysfunction. As expected, prosthesis–patient mismatch resulted in significant differences in both mean EOAi (0.93 ± 0.08 vs. 1.28 ± 0.07 cm2/m2 for patients with or without PPM, respectively; p < 0.0001), and mean mitral trans-prosthetic gradients (4.7 ± 1.1 vs. 3.2 ± 2.5 mmHg for patients with or

Main findings

The main finding of this study was that mitral PPM is associated with lesser regression of both fTR and PH following isolated MVR. These associations were independent of other preoperative and operative variables. In addition, patients with PPM also exhibited less improvement in NYHA functional class, thus further emphasising the clinical relevance of these results. There were no significant differences with regards to mortality between PPM and no-PPM groups, but it has to be pointed out that

Conclusion

The results of the present study suggest that mitral PPM may hinder the regression of both fTR and PH in patients undergoing isolated MVR. This negative effect was also associated with worse functional capacity. These findings provide a strong impetus for the application of preventive strategies at the time of operation to avoid PPM or reduce it severity and for the realization of tricuspid valve annuloplasty when PPM is anticipated at the time of operation.

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      This may be explained by the fact that once LV function and hemodynamics have stabilized following the early post-AVR period, the impact of a moderate PPM on subsequent outcome is less important. The increased risk of late mortality associated with severe PPM may be related to: 1) the persistence of LV hypertrophy and impaired coronary flow reserve and/or the persistence/recurrence of heart failure due to the residual LV afterload related to PPM (34,35); 2) the persistence of concomitant untreated mitral and tricuspid regurgitation (36,37); and 3) the accelerated structural degeneration of bioprosthetic valves (38,39). In contrast to what was observed for perioperative mortality, the impact of PPM on overall mortality was similar in younger versus older patients.

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      They demonstrated that 71% of 56 patients had mitral PPM, and there was a significant correlation between pulmonary artery pressure and EOAI. In another study [23], Angeloni and colleagues showed that prevalence of functional tricuspid regurgitation greater than grade 2 and pulmonary hypertension (systolic pulmonary artery pressure greater than 40 mm Hg) were significantly higher in patients with PPM compared with patients not having PPM (57% versus 22%, and 62% versus 24%, respectively). However, we could not evaluate those results because not all patients underwent follow-up echocardiography, and it was irregularly performed at the discretion of the operating surgeon or the referring physician.

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    Dr. Pibarot received research grants from Edwards Lifesciences LLC (Irvine, CA) and Medtronic Inc. (Minneapolis, MN). Other authors have nothing to disclose.

    1

    This author takes responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation.

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