The Effect of Pulmonary Valve Replacement (PVR) Surgery on Hemodynamics of Patients Who Underwent Repair of Tetralogy of Fallot (TOF)

Introduction: Pulmonary insufficiency (PI) frequently develops in patients who underwent repair of tetralogy of fallot (TOF). The aim of present study was to assess the effect of pulmonary valve replacement (PVR) on hemodynamics of patients who underwent repair of TOF. Methods: This retrospective cohort carried out between July 2010 and October 2012 among consecutive PVRs of 19 patients who underwent TOF surgery. The PVRs was performed using bioprosthetic (n=17) and mechanical (n=2) valves. Our data was collected during follow up visits within 6 to 12 month after PVR. Results: Our results show that PVR significantly decreased right ventricular end-diastolic volume (180.89±13.78 vs. 107.21±12.02 ml/m2, P < .01), right ventricular end-systolic volume (105.42±15.98 vs. 58.15±11.67 ml/m2, P < .01), RV mass (47.78±6.20 vs. 30.68±8.95 g/m2, P < .01), and PI (48.21±1.43% vs. 12.68±5.60%, P < .01). Moreover, left ventricular end-diastolic volume significantly increased (78.05±17.21 vs. 90.78±14.82 ml/m2, P < .01) after PVR. The other hemodynamics indexes did not change, significantly. Conclusion: Despite the controversies about efficacy of PVR after repair of TOF, the remarkable improvement of hemodynamic is a supportive rationale for performing PVR surgery in TOF patients.


Conclusion:
Despite the controversies about efficacy of PVR after repair of TOF, the remarkable improvement of hemodynamic is a supportive rationale for performing PVR surgery in TOF patients.
Both of mechanical or bioprosthetic valves were inserted into orthotopic position. All data of these PVRs was collected from review of medical records of surgeon and hospital database. Moreover, results of CMRI studies were collected during follow up clinical visits at the time between 6th and 12th month after PVR.

Statistical Methods
Data were analyzed using SPSS software (version 16, SPSS Inc, Chicago, IL, USA). Categorical data described as frequency (percent) and continuous data presented as mean ± standard deviation. The student t test was used to find any significant difference between hemodynamic parameters before and after surgery. The P value less than 0.05 was considered as significant level for all tests.

Result
The perioperative and late outcomes of patients after PVR surgery was summarized in Table 1. As the Table 1 shows, TOF with pulmonary stenosis (PS) is the most common (63.2%) diagnosis of our patients, and the rest of them (26.3%) had TOF with pulmonary atresia (PA), and TOF with PA and PS (10.5%). The sternum of five patients (26.3%) remains open as a strategy, because of cardiac failure, edema, and prolonged CPB. Total ICU stay of patients was 2.96±036 and their hospital stay was 15.00±1.36 day. Additionally, the only one death after PVR (with mechanical valve), was related to right ventricular failure which caused by thrombosis of prosthetic valve. As the Table 2 shows, right ventricular volumes significantly decreased after PVR surgery. The Right ventricular end-diastolic volume (RVEDV) shows significant decrease in follow-up measurements (180.89±13.78 vs. 107.21±12.02, P <.01). Also, the Right ventricular end-systolic volume (RVESV) significantly decreased after surgery (105.42±15.98 vs. 58.15±11.67, P<.01). Correspondingly, the CMRI results show the substantially shrinkage of right ventricular (RV) mass after PVR (47.78±6.20 vs. 30.68±8.95, P<.01). Moreover, right ventricular ejection fraction (RVEF) improved after valve replacement, but this improvement was not statistically significant (41.45±5.45 vs. 43.30±9.67, P=.11). As depicted in Figure 1

Discussion
Chronic forces against the cardiomyocytes is a trigger for muscular hypertrophy and cardiac wall thickening. 4 Therefore, correction of PI can result in shrinkage of RV mass by decrease of RV load. In accordance with previous studies, our results indicate a significant decrease in RVEDV and RVESV after PVR. 5,6 These results confirm the hypothesis that RV mass can significantly decreased by PVR. In other words, PVR can gradually result in RV remodeling by removal of overloaded pressure on RV myocytes. Surprisingly, despite the shrinkage of expanded RV wall and improvement of RV hemodynamic, RVEF failed to show a significant improvement. Bove and colleagues 5 founded a significant shrinkage of dilated RV (RVD) and improvement in exercise tolerance after PVR surgery but they reported only a trivial increase in RVEF. In contrary, the report of Vliegen et al 7 indicated that RVD and RVEF can improve after the surgery. Evidences suggest that the probability of RV regression considerably decreases in presence of preoperative RVEDV>160-170 ml/m 2 or RVESV>80-90 ml/m 2 . 6 Therefore, we concluded that the efficacy of PVR is limited to the RV volumes lower than this limit. Despite the fact that PVR can effectively reduce RV size, its effects on RV function may be limited because of the increased scar and fibrotic tissue in the RV wall. Silberman et al 4 studied the behavior of ventricles after implantation of stentless valves, by assessment of gradients and effective orifice area (EOA) index in patients who underwent aortic valve surgery. They concluded that rapid improvement of ventricular function is highly depended on valve performance rather than ventricular regression. High gradient across the functioning prosthetic valve can suspend recovery of RV function. Therefore, another probability is that improvement of RV function is a long-term process that may need more time to develop. The current evidences suggest that early restoration of pulmonary valve function can fully normalize the RV hemodynamic, but the exact time of PVR remains unknown. 8,9 LV dysfunction frequently is a common finding in symptomatic patients with TOF and implies that the presence of the severe RV disease may be a cause for LV dysfunction. Therefore, management of congenital RV anomalies may improve the LV function and clinical symptoms. 10 Likewise, our results show that the PVR surgery could effect on LV volumes as well as RV volumes. It was postulated that interaction between LV and RV chambers is mainly related to mutual myocardial fibers between LV and RV. Additionally, incline of the nestled interventric-ular septum into the LV cavity can decrease left ventricular refilling during diastole phase. Hence, LV hypertrophy (LVH) could result as an important compensatory mechanism for unfilled LV to increase cardiac output. 6,11 Our study supports this experience and show that parameters of LVEDV (significantly), LVESV, and LVEF (non-significantly) increased after PVR. This study has several limitations. There is a noticeable difficulty in homogeneous surgical recruitment of patients because patients may be referred for surgery at different stages of PI or RVOT dysfunction. Moreover, small size of our study population counts as another major limitation of this study.

Conclusion
In conclusion, our study indicates that PVR surgery can successfully normalize the impaired hemodynamic of patients who previously underwent repair of TOF. Although there is a controversy about effect of PVR in TOF patients among experts, the remarkable improvement of hemodynamic after PVR is a supportive rationale of performance of this surgery before RV hemodynamic reaches to RVEDV>160-170 ml/m 2 or RVESV>80-90 ml/m 2 . Unexpectedly, despite the fact that PVR significantly improves RV size and volume, RV function remained impaired after PVR. We concluded that early PVR surgery can initiate RV remodeling and improvement of RV function. Hence, in order to prevention of development irreversible alterations in cardiac walls, the PVR surgery should be consider in TOF patients with the upper threshold levels as soon as possible.