Diabetes is a relatively common condition in pregnancy, affecting up to 0.5% of the pregnant population . Neonates of diabetic mothers are at increased risk of morbidity and mortality [2, 3]. A well-recognized complication of diabetic pregnancy is the condition of hypertrophic cardiomyopathy. It was mentioned by vural et al. 1995  that, while symptomatic hypertrophic cardiomyopathy occurs in 12.1% of infants of diabetic mothers, it is found in 40% when routinely searched for with an echocardiographic scan [5–7]. The primary aim of this study was to assess cardiac damage in infants of diabetic mothers, as assessed by cTnI levels and to determine whether there is a relationship between this cardiac marker and echocardiographic findings.
Troponin is an inhibitory protein complex found in all striated muscles, and the cardiac-specific isoform troponin I (cTnI) is a sensitive and specific marker of myocardial ischemia . Our study showed that the cTnI concentration is unaffected by gestation, birth weight, sex, or mode of delivery, this is inconsistent with other publications . In the current study, infants of diabetic mothers have increased plasma troponin I concentrations on the second day of life. Delivery and cardiovascular maladaptation to extra-uterine life can cause further compromise of oxygenation which lead to further myocardial compromise and troponin release . Accordingly, elevations of troponin I was not detected immediately after birth.
Cardiac troponin I level was significantly higher in neoxnates who have respiratory distress and cyanosis compared to the controls. These findings may be explained in several ways. Firstly, myocardial injury with cardiac dysfunction may result in impaired gas exchange. Alternatively, respiratory and cardiac compromise may have a common cause as diabetes in the pregnant mother is strongly associated with neonatal cardiomyopathy [11–13]. Troponin release occurs in response to ischemia, and it is possible that diabetes-induced placental micro vascular disease and abnormal placentation may lead to chronic intrauterine hypoxia, which could affect fetal myocardial function, making infants of diabetic mothers more susceptible to an acute hypoxic insult [14–16].
The thickness of the interventricular septum was significantly more common in infants born to diabetic mothers. Hypertrophic cardiomyopathy was found in 80% of IDMs which is often transient with no lasting consequences for the majority of neonates [16–19]. In this study, an important number of infants presented with cardiorespiratory manifestations (67.5% with respiratory distress and 60 % with cyanosis). These factors reflect the problem of the higher incidence of cardiomyopathy in this study. Russell et al. 2008  had reported previously that stillborn infants of diabetic mothers have heavier hearts than stillborn infants of non diabetic mothers after correction for fetal size, suggesting that cardiomyopathy may have a role in “unexplained” fetal death in diabetic pregnancy [19, 20]. The etiology of this cardiomyopathy is poorly understood with proposed mechanisms including fetal hyperglycemia, hyperinsulinemia, and chronic hypoxia [20, 21]. It has been suggested that cardiomyopathy occurs in response to functional changes evident in the first trimester in fetuses of pregestational type 1 diabetic mothers . Early pregnancy hyperglycemia may also have an effect on the developing placenta and impaired placental functioning may result in chronic intrauterine hypoxia causing ischemic damage to the fetal myocardium and thus troponin release .
An increase in cTnI serum levels in infants with HCMP pointed to subclinical myocyte injury. The mechanisms of myocyte injury in HCMP are not fully understood. It may be caused by relative myocardial ischemia resulting from an imbalance between inappropriate hypertrophy of the myocardium and insufficient oxygen supply [20, 22]. Left ventricular contractility as assessed by the ejection fraction and percentage shortening of the internal thickness was higher in infants of diabetic mothers compared with the controls. This finding could reflect myocardial compromise or an increase in the ventricular workload . These data suggest that maternal diabetes is associated with significant effects on neonatal cardiac function with correlation between interventricular septal diameter and troponin I release in diabetic pregnancy. Poor glycemic control in early pregnancy changes fetal cardiac gene activation and predisposes the fetus to myocardial hypertrophy [24, 25].
The findings in this work suggest that cTnI is a biochemical marker as sensitive as echocardiographic measurements in the detection of cardiac dysfunction and should be done to any infant born to a diabetic mother suffering from respiratory distress.