4 Discussion
Recently, the results of the ASO for TBV have been excellent, with low
hospital mortality rates as reported by Vergnat et al. (16)
(5.8%), Soszyn et al. (6) (5.3%), and Sinzobahamvya et
al. (7) (2.9%), among others. The risk factors for overall mortality
are related to the coronary patterns, a higher weight at the time of the
operation, preoperative PA banding, aortic arch anomaly and
postoperative subneopulmonary obstruction (1, 6, 16, 17). Results from
our study, which were achieved in LMIC show that, intraoperative
ventricular septal defect enlargement [HR = 7.23, P <
0.001], secondary aortic cross clamping (HR 28.38, P< 0.001), post-operative pneumonia (HR 5.64, P =
0.023), and post-operative sepsis (HR 5.28, P = 0.017) were
factors associated to overall mortality. These results reflect the
reality of the learning curve faced by a congenital heart program in a
LMIC as they develop their management of complex lesions, including
dealing with missed diagnosis, late presentation and nosocomial
infection.
According to many previous reports, TBV is a risk factor for
RVOTO-related reoperation after the ASO compared to simple transposition
of the great arteries (TGA) or even complex TGA (7, 8, 18, 19).
Realizing this problem, we attempted to avoid RVOTO as much as possible
by systematically checking the RVOT and totally resecting or dividing
SPTs inferiorly up to the apex of the right ventricle (14).
Interestingly, in 3 patients who required reoperation for RVOTO in our
study, 2 of them did not undergo the RVOT procedure to resect SPTs
during the ASO, as their procedures were performed in the early period
of the study. The remaining patient who developed RVOTO was a TBV
patient with type B aortic arch interruption, and her symptoms occurred
6 months after the ASO despite the attempt to resect the SPTs in the
first operation. During the reoperation, the level of the RVOTO was far
from the neo-PV, and we performed resection of the SPTs through the
neo-PV and the tricuspid valve. We also noted that the right ventricle
end diastolic volume may increase after SPT resection as the free wall
of the right ventricle is now free from the ventricular septum.
Risk for RVOTO has been reported to occur in up to 53% of patients
after ASO with TBV and remains a major cause of late morbidity (7) .
Even when a preventative strategy is applied, reintervention due to
RVOTO remains as high (20-35%). Only the experience from the Royal
Melbourne Children’s Hospital reported an RVOT reintervention rate of
less than 10%, specifically 2.2% (6). So, our rate of RVOT
reintervention of only 6%, with a larger cohort is noteworthy, and the
estimated freedom for RVOTO reoperation was 91.9% (SD=4.8) (95% CI,
0.7524 to 0.9749) at 9 years follow-up. A smaller native aortic valve
annulus has been identified as a risk factor for RVOT reintervention
(8). In contrast, we demonstrated growth of the neo-PV annulus as shown
in the Fig. 4. We attribute this RVOT growth and the low incidence of
RVOTO reintervention to our policy of aggressive division and/or
resection of SPT.
Another common reason for reoperation after the ASO is supravalvular
neo-PA stenosis (1-3, 17). However, in our series, we did not have any
patients who developed neo-PA stenosis requiring either reoperation or
reintervention. This complication was also rare in our ASO cohort (1/445
ASO patients). Attempts were made to size the autologous pericardial
patch to be equal the height of the neo-PA, while the width of the
neo-PA was equal to the diameter of the pulmonary bifurcation. We
believe that a large patch does not guarantee the normal growth of the
PA in the long term; instead, a size difference between the neopulmonary
and pulmonary bifurcation may create turbulent flow at the anastomotic
site and easily lead to stenosis. This approach has helped us avoid
torsion of the neo-PA bifurcation and has allowed for normal growth of
the neo-PA.