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.