Conclusions
To our knowledge, this is the first study investigating the effect of
neuroprotective magnesium sulfate therapy on fetal mod-MPI regarding
fetal cardiac function.
Neonatal mild myocardial injury and cardiac dysfunction of babies of
preeclamptic mothers has been shown previously [20]. Therefore,
cardiovascular risks of neonates from preeclamptic women might begin in
utero. Acknowledging this, the effects of magnesium sulfate therapy on
the fetal heart are unknown. This study showed that there was a
significant increase in mod-MPI after magnesium sulphate therapy.
Promket et al. showed that fetuses of preeclamptic women and of healthy
pregnancies did not differ in mod-MPI and that the mean mod-MPI was 0.44
± 0.11. Api et al. compared mod-MPI of severe preeclampsia, mild
preeclampsia and normotensive pregnant women fetuses and found that they
also did not differ in mod-MPI (severe preeclamptic women fetuses had a
mean mod-MPI of 0.44 ± 0.06) [17]. Our study results were similar to
these studies. When our mod-MPI results were evaluated with reference
mod-MPI measurements, it seems that reference values have a wide range.
Falkensammer et al. declared left heart mod-MPI as a constant value of
0.4 whereas Eidem et al. found it to be 0.35 [21,22]. Friedman et al
reported 0.53 [23]. In addition, Hernandez-Andrade et al. found a
slight increase in mod-MPI from 19 to 39 weeks of gestation, as 0.35 and
0.37, respectively. According to Hernandez-Andrade et al., the
5th, 50th and 95thpercentile of mod-MPI for the mean gestational age of our study group
would be 0.29-0.37-0.44, respectively [15]. The mean mod-MPI of our
study (0.41 ± 0.18) lies between the 50th and
90th percentiles.
The initial fetal mod-MPI mean in this study is compatible with the
literature. However, magnesium sulfate therapy increased the fetal
mod-MPI to above reference ranges. This might indicate an adverse effect
of magnesium sulfate therapy on fetal cardiac function.
Magnesium effects on MPI, effect of timing of therapy and how
isovolumetric contraction time is affected are unknown. Magnesium is
known as a strong vasodilatator that does not increase cardiac output
but increases stroke volume and decreases sinus rate and thus has
antiarrythmic effects. Nakaigiwa et al. showed that elongation of
isovolumetric relaxation time is directly proportional to magnesium
dose. As isovolumetric relaxation time is directly proportional to
mod-MPI, the increase might be an effect of increased isovolumetric
relaxation time. The important point is the adverse effect on mod-MPI
and therefore adversely affected cardiac function, which is added to the
adverse effects of being a newborn of a preeclamptic mother. This
finding may not be clinically important but we suggest this should be
taken into consideration.
The study results were compared with the literature, there could not be
a control group comparison since without an indication, magnesium
therapy cannot be given to uncomplicated pregnancies beyond the 32nd
gestational age. In addition, all of the pregnant women were on
antihypertensive therapy. There is no known evidence regarding the
synergetic or antagonistic effect of antihypertensive medication with
magnesium on fetal cardiac function. Future studies might investigate
magnesium effects on fetal mod-MPI only used in neuroprophylaxis.
Furthermore, the mean maternal magnesium level of pregnant women in this
study was lower than the target level range of plasma magnesium known to
prevent eclampsia. Future studies might use a loading dose of 6 gr and
continue magnesium infusion as 2 gr per hour, thus preventive maternal
magnesium levels could be reached and fetal mod-MPI could be
investigated.