Prenat Diagn. 2014 Dec;34(13):1301-6. doi: 10.1002/pd.4471.

Use of the myocardial performance index as a prognostic indicator of adverse fetal outcome in poorly controlled gestational diabetic pregnancies.

 

Bhorat IE, Bagratee JS, Pillay M, Reddy T.

Department of Obstetrics and Gynaecology, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, Durban, South Africa.

 

Abstract

OBJECTIVE: The aim of this study was to determine whether there are any changes in cardiac function in fetuses of poorly controlled gestational diabetics and whether these changes influence perinatal outcome.

METHODS: Twenty-nine pregnant women with severe gestational diabetes on insulin therapy in the third trimester of pregnancy were recruited and matched with 29 women with normal pregnancies (control group). Using Doppler echocardiography, the modified myocardial performance index (Mod-MPI) and E wave/A wave peak velocities (E/A) ratios were determined. Placental resistance Doppler markers were also determined in both groups. Adverse perinatal outcome was defined as perinatal death, admission to the neonatal intensive care unit, cord pH <7.15, 5-min Apgar score <7 and presence of cardiomyopathy.

RESULTS: The median Mod-MPI was increased (0.59 vs 0.38; p < 0.0001) and the E/A ratio was decreased (0.65 vs 0.76; p < 0.0001) in fetuses of diabetic mothers compared with controls. An MPI >0.52 had a sensitivity of 100% [95% confidence interval (CI) 85-100%] and specificity of 92% (95% CI 70-92%) for prediction of adverse perinatal outcome, including one stillbirth and one neonatal death. No abnormal outcomes occurred in the control group.

CONCLUSIONS: There is significant impairment of cardiac function in fetuses of poorly controlled gestational diabetics. Mod-MPI and E/A ratio have the potential to improve fetal surveillance in diabetic pregnancies.

PMID: 25088046

 

Supplements:

The pathophysiology of gestational diabetes starts with abnormal glucose tolerance in the mother causing maternal hyperglycaemia resulting in fetal hyperglycaemia and subsequently fetal hyperinsulinaemia. A prolonged period of uncontrolled maternal hyperglycaemia acts on the fetal pancreas to cause beta-cell hyperplasia and precocious pancreatic maturation. Once this is in place despite good maternal glycaemic control, the hyperplastic fetal pancreas will respond with a disproportionally high insulin response to any glucose load. It is the fetal hyperinsulinaemia that results in fetal complications in gestational diabetes resulting in augmented growth and increased metabolism, either directly through its anabolic effect on nutrient uptake and utilization or indirectly through peptides like insulin growth factor. Gestational diabetes is thus characterized by three main factors: 1) macrosomia, 2) increased metabolic rate and 3) large vascular cross sections. An important and critical finding in diabetic pregnancies is that significant acidaemia and hyperlacticemia can occur in fetuses in the absence of hypoxaemia1. Thus “unexplained” stillbirths of diabetic pregnancies could most likely be due to fetal acidaemia as a consequence of increased metabolic rate. A significant association has also been reported between fetal plasma insulin concentration and the degree of fetal acidaemia. Hyperinsulinaemia results in an increased metabolic rate which results in increased glucose oxidation and oxygen consumption. The capacity for oxidative metabolism is however reduced in fetuses due to low pyruvate dehydrogenase activity thus increasing the risk for acidosis. This leads to the conclusion that fetal monitoring models have to recognize the pathophysiology outlined above. Yet the most widely used antenatal surveillance technique in monitoring diabetic pregnancies is umbilical artery Doppler velocimetry. However umbilical artery Doppler velocimetry measures resistance to placental flow which is not the problem in gestational diabetes. The same would apply to other antenatal surveillance techniques including middle cerebral artery Doppler and ductus venosus Doppler. Standard fetal monitoring models presently used in diabetic pregnancies are inappropriate and insufficient and do not answer the question of fetal compromise in gestational diabetes (in the absence of microvascular complications). Thus the need to research other fetal monitoring models. Elements of fetal cardiac dysfunction eg impaired ventricular filling and increased interventricular septal thickness, have been described in fetuses in diabetic pregnancies but the challenge was to channel these elements of cardiac dysfunction via an appropriate and quantifiable monitoring parameter into a viable and reproducible monitoring model. Furthermore if cardiac function was indeed altered in these fetus would this be a prognostic indicator of adverse outcome. In the above study we used the myocardial performance index (MPI) to quantify fetal cardiac function. The MPI is a useful predictor of global cardiac function combining assessment of systolic and diastolic function and is known to be independent of ventricular geometry and heart rate. The MPI is defined as the sum of the isovolumetric contraction time (ICT) and isovolumetric relaxation time (IRT) divided by the ejection time (ET). E/A ratio was also used to determine diastolic function alone which is a reflection of ventricular compliance.

This importance of this study is that for the first time a link between fetal cardiac dysfunction, as measured by the MPI and E/A ratio, and adverse outcomes in poorly controlled gestational diabetes was established and creates for the first time a viable and reproducible fetal monitoring model to establish fetal wellbeing in poorly controlled gestational diabetes which hitherto standard fetal monitoring models proved ineffective in detecting fetal compromise. This is due to the fact that standard monitoring models focus on placental disease and hypoxia and are not predictive of metabolic shifts and abnormal metabolic milieus in gestational diabetes where the concept of hyperlacticaemia and acidosis in the absence of hypoxia exists. Fetal cardiac dysfunction as quantified through the MPI and E/A ratio appears to predict metabolic shifts and abnormal metabolic mileus in diabetic pregnancies and could serve as a guide to clinicians to establish timing of delivery and thus reduce perinatal morbidity and mortality.

 

References

  1. Bradley RJ, Brunedell JM, Nicolaides KH. Fetal acidosis and hyperlacticaemia diagnosed by cordocentesis in pregnancies complicated by maternal diabetes mellitus. Diabet Med 1991;8:464-468.

Pathophysiology of Gestational Diabetes

IB Fig1

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