was not responsible for reported mortality in children with
DS in our recent study.
Our study has several limitations. Because of its
retrospective design, we used data from questionnaires
completed by paediatricians and have no on follow-up data.
Furthermore, there was a sample bias since we could not
use the data of all 820 children with DS who were
registered by the DPSU, 630 (76.8%) questionnaires were
returned and not all questionnaires relating to children with
trisomy 21 had complete data on cardiac status. On the
other hand, the fall out cases were distributed between both
the CHD and non-CHD children with DS.
Though the definition of PPHN was not specifically
defined, diagnosis was based on the clinical assessment and
an echocardiogram performed by the neonatologists and
pediatric cardiologists who answered the questionnaires. It
was impossible to draw a definitive conclusion on the exact
role of the AVSD in the seven children with an AVSD in
relation to the cause of the pulmonary hypertension; nevertheless,
there were at least 18 other children (3.7% of total) with
PPHN that was not related to a CHD, which is still a high level.
In conclusion, we have demonstrated a 43% prevalence
of CHD in neonates with DS and a significantly increased
and elevated incidence of PPHN in neonates with DS
(5.2%) compared to the general population. Early recognizing
the cardiac condition of neonates with DS seems
justified. CHDs had no relationship with neonatal factors
such as gestational age, Apgar score and birth weight of
children with DS. There are no conflicts of interests