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.