Journal of Labor and Childbirth

Mini Review - Journal of Labor and Childbirth (2023) Volume 6, Issue 3

Cardiovascular Changes in Newborn Children of Diabetic Mother

Andrea Ricci*

Department of Gynecology, Arden University of Berlin

*Corresponding Author:
Andrea Ricci
Department of Gynecology, Arden University of Berlin
E-mail: ricci@adu.ac.gn

Received: 01-Jun-2023, Manuscript No. jlcb-23-102621; Editor assigned: 05-Jun-2023, Pre QC No. jlcb-23-102621(PQ); Reviewed: 19-Jun-2023, QC No. jlcb-23-102621; Revised: 22-Jun-2023, Manuscript No. jlcb-23-102621(R); Published: 29-Jun-2023, DOI: 10.37532/jlcb.2023.6 (2).01-04

Abstract

A systemic chronic metabolic disorder known as Diabetes Mellitus (DM) is characterized by either defective beta cells or elevated insulin resistance. It affects everyone, from infancy through late adulthood, including newborns and children. A significant risk factor for Congenital Heart Diseases (CHDs) is gestational diabetes. In addition, maternal smoking during pregnancy, low maternal education, a high body mass index at conception, undiagnosed pre-gestational diabetes, inadequate antenatal care, and improper diabetes management all increase the risk. The structure and function of the fetus’ heart and the fetus-placental circulation are significantly impacted by maternal diabetes. Myocardial hypertrophy and cardiac defects are three times more common in Diabetic Mothers’ Infants (IDMs). Foetal electrocardiography and echocardiography can be used to examine the structure and function of the heart during pregnancy. Post pregnancy heart assessment can be performed with natal and post pregnancy electrocardiography and echocardiography, recognition of early atherosclerotic changes by estimating aortic intima-media thickness, and retinal vascular changes by retinal photography. Preventing diabetes before and during pregnancy is the most important factor in reducing the effects of diabetes on the unborn child. However, additional research is still needed on other risk-reducing measures like taking prescription drugs, taking nutritional supplements, or taking probiotics. The various cardiac outcomes of gestational DM on the foetus and offspring, cardiac evaluation of foetuses and IDMs, and how to alleviate the consequences of gestational DM on the offspring are discussed in this review, as are the mechanism of foetal sequels and the risk factors that increase the prevalence of CHDs in gestational DM.

Keywords

Diabetes mellitus • Congenital heart disease • Pre gestational diabetes • Myocardial hypertrophy • Fetal electrocardiography

Introduction

A systemic chronic metabolic disorder known as Diabetes Mellitus (DM) is characterized by either defective beta cells or elevated insulin resistance. It is a micro vascular disease that strikes at any age, from infancy to old age. Diabetes during pregnancy can be a de novo condition that occurs for the first time during pregnancy and can either disappear or persist after delivery (gestational DM) or begin pregestationally, prior to the start of pregnancy. The average prevalence of diabetes in the general population is correlated with the prevalence of impaired glucose tolerance in pregnant women, which ranges from 3 to 10%. Overweight and obesity, advanced maternal age at conception (> 30 years), glucosuria on more than two occasions, previous history of gestational diabetes, family history of type-2 diabetes, polycystic ovary syndrome, polyhydramnios, male foetus, multiple pregnancy, previous big baby (> 4 kg), ethnicity (non-white ancestry), lifestyle (physical inactivity before and during pregnancy), environmental factors (such as cigarette smoking, persistent organic pollutants, and Despite the high fasting insulin levels, there is a 30% increase in basal endogenous glucose production (primarily hepatic) by the end of a normal pregnancy. However, due to the increased plasma volume in early pregnancy (dilutional hypoglycemia) and the increased glucose utilization in late pregnancy, hypoglycemia may occur. In addition, by late gestation, peripheral insulin sensitivity may have decreased by approximately 50%, resulting in an increase in insulin secretion of 2–3 times in women with normal glucose tolerance and potential disruptions to the maternal amino acid and lipid metabolism. Due to the increased stress placed on cells by excessive gestational weight gain and rising insulin resistance, gestational diabetes may result in cell dysfunction; or because autoantibodies against particular cell antigens cause damage to cells. When compared to a normal pregnancy, the rate of insulin-stimulated glucose uptake in gestational diabetes is reduced by 54% [1, 2].

Discussion

Risk factor associated with cardiac diseases in diabetes mellitus

A significant risk factor for developing Congenital Heart Diseases (CHD) is gestational diabetes itself. Additionally, the infants of Diabetic Mothers (IDMs) may be at increased risk for CHD due to other factors. Another factor that raises the risk of CHD is low maternal education (less than high school). Significant risk factors for CHD in gestational diabetes include a high Body Mass Index (BMI) at conception and possibly undiagnosed pre-gestational diabetes. Compared to gestational diabetes, infants born to mothers with pregestational diabetes face higher mortality and morbidity rates a fourfold increase in the offspring risk of CHDs in mothers with pre-gestational diabetes [3, 4]. There was only a weak link between gestational diabetes and increased risk. Critical confounding factors, such as inadequate antenatal care and inadequate diabetes management, also increase the risk. Particularly in the first trimester of pregnancy, there was a strong correlation between the foetal abnormalities and elevated glycated hemoglobin levels. They also discovered that foetal heart disease was more likely to occur in pregnancies with poor glycaemic control in the first trimester. According to studies, women who have good glycaemic control and close monitoring at conception and early in pregnancy have a significantly lower risk of having a child with CHD than women who have poor control. Smoking by a pregnant woman may increase the risk of CHDs on its own. In addition, pregestational diabetes and maternal tobacco use have a stronger impact on preterm birth and the risk of Congenital Heart Defects (CHDs). On the other hand, studies demonstrated a link between a decreased risk of CHDs and early antenatal administration of antioxidants, such as lipoic acid, vitamin C, and N-acetylcysteine, in diabetic mice [5].

Effect of maternal diabetes on foetal heart

As it affects the heart, the great vessels, and the neural tube, Diabetes Mellitus (DM) is associated with diabetic embryopathy in the developing fetus during the first trimester and before conception. Diabetic fetopathy remains a prevalent clinical issue linked to high neonatal mortality and morbidity. In both gestational and pre-existing DM, the foetal heart is more susceptible to developing congenital malformations. Myocardial hypertrophy and cardiac defects are three times more common in DM-positive mothers’ children. A wide range of cardiac anomalies, from minor septal defects to major complex heart diseases, are caused by maternal diabetes, which has a significant impact on the foetal heart’s structure and function as well as the foetal placental circulation. It also alters the vascularization of the placenta [6].

Placental circulation is primarily affected by gestational diabetes. Six out of seven women with varying degrees of diabetes experience vascular dysfunction as a result of altered placental development. Villous immaturity, villous fibrinoid necrosis, infarcts, intervillous thrombosis, increased syncytial knotting, chorangiosis, and increased angiogenesis are typical placental changes in gestational diabetes. Uteroplacental circulation and maternal vascular malperfusion are the results of these placental changes. The degree to which hyperglycemia occurs early in pregnancy determines the types of dysfunction and their effects. Maternal hyperglycemia raises the thrombogenic status, which is in addition to the states of hypercoagulability that are brought on by the pregnancy. It causes vascular stasis and ischemia, which results in thrombosis in the foetal vascular tree, which restricts foetal growth and increases perinatal morbidity and mortality when combined with hyper coiling of the cord. In addition, focal intimal thickening and glycogen accumulations in the intima and media cells were pathological changes in the umbilical vessels that were consistent with early atherosclerosis. In cases of gestational diabetes, a more adverse fetal outcome is associated with a thinner umbilical cord and a single umbilical artery. Foetal hypoxia contributes to polycythaemia, increased erythropoiesis, and the production of catecholamines, both of which lead to hypertension and cardiac hypertrophy; and may be a factor in the 20%–30% stillbirth rate in diabetic pregnancies that are not managed properly. In pregnancies with complicated gestational diabetes, an altered response of the fetal autonomic nervous system to the metabolic stress raises the mean heart rate of the fetus. It reduces the variability of the heart rate [7].

An increased muscularization of the small pulmonary arteries may be the cause of primary pulmonary hypertension. Additionally, polycythaemia, which frequently affects these newborns, is associated with and exacerbates it. Even those with reasonable gestational glycaemic control may have impaired transitional haemodynamics due to the persistence of foetal shunts and decreased RV output in IDMs. Due to the persistent foetal circulation or the temporary increase in interstitial pulmonary fluids, which results in the transient tachypnoea of the newborn (due to the increased incidence of Caesarean section), cardiomegaly may occur in IDMs without hypertrophic cardiomyopathy. Cardiomegaly and abnormal electrocardiograms could result from neonatal hypoglycemia, which is more common in IDMs. Additionally, approximately 8% of IDMs have bradycardia, according to studies. Because eta-blockers like propranolol are used to treat symptomatic hypertrophic cardiomyopathy, the neonates should also be watched for bradycardia [8].

Gestational diabetes isn’t just bad for the baby or the newborn, but it can also affect the kids until they are adults. Because of altered gene expression, early exposure to hyperglycemia may alter important developmental pathways and program future disease risk. Atherosclerosis and cardiovascular risks are thought to start in utero and get worse after birth, according to current research. As per a few examinations, maternal gestational diabetes, particularly with a confounded pregnancy, prompts the improvement of many perceived cardiovascular gamble factors in their descendants with an unfavorable gamble profile that continues into early adulthood [9].

Mitigation the effect of diabetes on offspring

The most ideal way to enhance the impact of gestational diabetes on the posterity is to forestall the advancement of diabetes itself. We must strictly control the disease during pregnancy if possible, with the goal of maintaining adequate glycaemic control and avoiding harm to the unborn child. Obesity prevention before pregnancy, weight management, increased physical activity, and healthy eating are all ways to prevent gestational diabetes. Myo-inositol, a derivative of secondary messengers involved in a number of signaling pathways, including the insulin pathway, may play a role in the prevention of gestational diabetes, but further research is needed. Probiotics may help regulate glucose metabolism outside of pregnancy, but their effectiveness in preventing gestational diabetes is questionable. Probiotics as a means of preventing gestational diabetes mellitus (DM) do not appear to be supported by solid evidence. It appears that doing more physical activity before and during early pregnancy helps prevent gestational diabetes. Women who are most active before pregnancy are less likely to develop insulin resistance in later pregnancy and have lower rates of gestational diabetes, according to observational studies in large population-based cohorts. By strictly adhering to the guidelines and recommendations of the International Association of Diabetes and Pregnancy Study Groups (IADPSG) on the diagnosis and classification of hyperglycaemia in pregnancy, optimizing screening for gestational diabetes in pregnant women will significantly increase the number of women who are diagnosed with and treated for gestational diabetes. Pregnancy complications, particularly cardiovascular complications that are closely linked to strict glycaemic control can be reduced by diagnosing and treating gestational diabetes. The foundation of treatment is nutrition management. Metformin, insulin, and glyburide can be used to boost the nutritional treatment. There are persistent concerns regarding the use of metformin during early pregnancy due to its anti-cell growth and pro-apoptotic effects. Metformin, on the other hand, may be chosen in some instances due to its cost and ease of use [10].

Conclusion

CHDs are significantly influenced by gestational diabetes. Low maternal education, a high body mass index at conception, undiagnosed pregestational diabetes, inadequate antenatal care, improper diabetes management, and maternal smoking during pregnancy all raise the risk. The structure and function of the fetus’ heart and the fetus-placental circulation are significantly impacted by maternal diabetes. In IDMs, the prevalence of CHDs and myocardial hypertrophy is three times higher. Foetal electrocardiography and echocardiography are two methods that can be used to examine the structure and function of the developing heart. Electrocardiography, postnatal echocardiography, measuring aortic IMT, and retinal photography are all methods of postnatal cardiac evaluation. Preventing pregnancies and gestational diabetes is the primary factor in reducing the effects of gestational diabetes on the offspring. However, additional research is required on other approaches to minimizing these effects, such as nutritional interventions, medications, or probiotics.

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