4 DISCUSSION
The present study showed significant effect of PPM on long-term mortality and death from heart failure in patients undergoing bioprosthetic MVR for MR. Previous studies have also reported negative impact of PPM on long-term outcomes after MVR.4-11 Lam et al. reported that PPM in the mitral position was associated with recurrence of heart failure and late mortality.6 In their cohort, postoperative PPM occurred more frequently in bioprosthetic MVR than in mechanical MVR (57% vs. 23%, p< .001).6 However, their study included both MS and MR, which may have different impact from PPM. A study by LEE et al. have shown that PPM after MVR in patients with rheumatic MS had no influence on late clinical outcomes.13
Aziz et al. reported negative effect of PPM on long-term outcomes in patients receiving a bioprosthetic mitral valve.10However, along with other previously reported studies, reference EOA was used to define PPM. 6,8,10,11 There are three different techniques for calculating EOA: the use of reference EOA, continuity equation, and the PHT method.14 Reference EOA is a reference value provided by the manufacturer. This may not necessarily represent the actual EOA considering the different hemodynamics for each patient. The continuity equation method requires complex measurements on echocardiography, in which the measured values could vary among the examiners and may not be reproducible. Although measurements are influenced by chronotropic conditions and atrioventricular compliance,15 PHT method is the simplest and most reproducible method to calculate EOA.16,17
Magne et al. reported that moderate or severe PPM patients received prosthesis smaller than 27mm.7 However, our study suggested that the size of the mitral prosthesis was not necessarily associated with incidence of PPM. In the present study, 13 of the PPM patients (38.2%) received prosthesis larger than 29mm. This may be explained by our postoperative echocardiography data which showed significantly larger LA and LV diastolic diameters in the PPM group compared to the non-PPM group. Given that LV contractility was the same between the two groups, increase in LV dimension may have led to increase in the transmitral blood volume resulting in prolonged PHT, thus showing PPM in the same size mitral prosthesis.18
PPM in the mitral position has been suggested to cause abnormally high residual transvalvular pressure gradients. This may lead to increase LA and pulmonary arterial pressures, subsequently resulting in heart failure.7 Further, mitral PPM has been reported to be an independent risk factor for persistence of pulmonary hypertension after MVR.15 Although our study showed no significant differences in pulmonary arterial pressures (PPM: 27 ± 9 mmHg, non-PPM: 26 ± 10 mmHg, p = .69), transvalvular peak pressure gradients (PPM: 17.2 ± 8.5 mmHg, non-PPM: 14.8 ± 6.7 mmHg, p = .11) and mean pressure gradients (PPM: 6.3 ± 3.4 mmHg, non-PPM: 5.5 ± 2.9 mmHg,p = .18) between the two groups, this may be due to the timing of the echocardiography. Postoperative echocardiography in the present study was performed approximately a week after the operation in which the patients were mostly at rest in the hospital. Previous study has shown that the mean transvalvular pressure gradient increased from 5 ± 2 to 8 ± 3 mmHg after exercise in patients with a prosthetic mitral valve. Further, the pulmonary artery systolic pressure increased with exercise from 28 ± 8 to 39 ± 15 mmHg.19 Physical activity in most patients usually increases after discharge, thus the effect of insufficient EOAI on transvalvular pressure gradient and pulmonary artery systolic pressure may be influenced more at long term after surgery. Given that PPM was the predictor of heart failure and overall late death in our study, it may be important to follow-up PPM patients closely, to monitor the changes in the LA and pulmonary artery systolic pressure.