We aimed in our study to assess the effect of maternal pre-gestational and gestational diabetes on fetal cardiac morphology and function for which complete fetal echocardiogram was performed in every case to rule out any structural defects. Measurement of ventricular myocardial free walls and interventricular septal thickness was done as a tool for evaluation of cardiac hypertrophic cardiomyopathy that occurs in fetuses and neonates of diabetic mothers. Doppler-derived modified myocardial performance index (Mod-MPI) was used to assess global overall systolic and diastolic function to display whether impairment of fetal cardiac function occurred or not.
The study included 40 diabetic pregnant women and 60 control cases. Both groups were within a comparable gestational age (between 28 and 40 weeks gestation).
The mean septal thickness in the diabetics group was 0.7163 ± 0.17 cm (Figs. 6 and 7) and 0.4989 ± 0.08 cm (Fig. 5) in the normal group.
A significant difference was found regarding the septal thickness between diabetic group and normal group (P < 0.05). These results are in concordance with results of previous studies.
Joana et al. (2018) [13] demonstrated that fetuses of diabetic mothers had a significantly thicker interventricular septum compared with control subjects (median, 4.25 mm [interquartile range (IQR), 3.87–4.50 mm] vs 3.67 mm [IQR, 3.40–3.93 mm), P < .001)
Garcia-Flores et al. (2011) [6] reported that the septal thickness was increased in fetuses of diabetic mothers compared with the control group with statistical significant difference (P < 0.001) despite being comparative study between cases of controlled gestational diabetes (cases of increased HbA1c values above 6.5% were excluded) and normal ones. It was found that 66.6% (16/24) of the diabetic pregnancies were above the 95th percentile for the IVS thickness in the control group, which was estimated at 3.51 mm; however, measurements of IVS thickness in both groups were in normal ranges in this study.
Prefumo et al. (2005) [8] reported cases of marked fetal myocardial hypertrophy associated with signs of myocardial insufficiency in fetuses of diabetic mothers.
Balli et al. (2014) [14] showed that the mean septal thickness at 36 weeks gestation was 0.452 ± 0.49 cm in group of maternal diabetes compared to 0.38 ± 1.77 cm in the control group with a significant statistical difference (P < 0.001). In this study, despite being statistically different, no pathological IVS hypertrophy was found. However, evidence of diastolic dysfunction in the study group was found by application of different parameters for assessing diastolic dysfunction.
This study has shown that maternal diabetes was associated with a significantly increased thickness of all cardiac walls (Figs. 6 and 7) compared with normal pregnancies (Fig. 5), confirming in part the results of previous studies done by Jaeggi et al. 2001 [15]. Penney et al. (2003) [16] focused on cases with pre-existing diabetes, but Zielinsky, 2009 [17] applied his study on population with gestational diabetes mellitus. Both of them reported significant difference in myocardial-free walls and interventricular septal thickness between both studies and control groups.
In a series of neonates and infants, the cardiomyopathy (CM) was noticed in about 2–7%, but probably during the fetal life the prevalence is higher reaching 6–11%. The high intrauterine loss, occurring in almost one third of affected fetuses, most likely explains these differences [18].
Still, authors can find some cases with septal hypertrophy, which are not symptomatic postnatally. Although most symptoms of cardiomyopathy may spontaneously regress within few weeks, sometimes, overt congestive heart failure develops, tachycardia, tachypnea, gallop rhythm, and hepatomegaly [19].
In our study, the mean septal and myocardial free wall thickness was statistically significant compared to the control group with above 95th percentile mean value of tie index denoting evidence of hypertrophic cardiomyopathy with impairment of left ventricular function.
It was not possible in this study, to expect, whether theses fetuses would be symptomatic or not by the ultrasound and Doppler criteria. Postnatal evaluation by a specialized neonatologist and a cardiologist is recommended.
Some studies suggest that gestational diabetes can be a risk factor for congenital heart defects, but there are still controversies about the extent of such association [20].
In our study, the incidence of congenital heart defects among study cases represents 5% of the total number of cases with diabetes. Previous studies showed an 8.5% incidence of cardiac malformations in fetuses of diabetic pregnancies [21]. Our study was restricted to the limited patients’ number involved in our study; however, if a large number of diabetic patients could be included, incidence might become different.
In our study, we also aimed to assess the effect of maternal diabetes on fetal myocardial function using the Modified myocardial performance index (MPI).
MPI is a global indicator of cardiac function. Increased in MPI indicates globally impaired ventricular function in maternal diabetes during the intermediate and late pregnancy periods [22]. Hernandez-Andrade et al.(2012) [9] defined age-adjusted reference values for the left ventricular Mod-MPI in normal fetuses at 19–39 weeks gestation and calculated the 5th, 50th, and 95th percentiles for the Mod-MPI as well as its components (ICT, ET, and IRT). It was found that in normal fetuses, the Mod-MPI did not exceed 0.43 at any gestation (at a fetal heart rate of 140 bpm: median 0.45 range 0.36–0.54). Another more recent study revealed the normal value of MPI is about 0.51 ± 0.12 [23]. These values are in close agreement with our results for the control group, but are much lower than those in the study group indicating reduced left ventricular wall compliance in fetuses of diabetic mothers with subsequent impairment of fetal overall cardiac function.
Our study showed a statistically significant (P < 0.001) higher overall Mod-MPI in the study group as a whole (median 0.61, range 0.39–0.83) compared to the control group (median 0.47, range 0.32–0.62).