Altered fetal circulation in type‐1 diabetic pregnancies

Lisowski, Lukas A.; Verheijen, Paul M.; Smedt, M. M. C. de; Visser, Gerard H.A.; Meijboom, E. J.

doi:10.1002/uog.88

Cited by 27 publications

(20 citation statements)

References 29 publications

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“…Increased peak velocities in the aorta and pulmonary arteries in fetuses of diabetic mothers compared with normal values have been reported (Rizzo et al, 1992). Although fetuses of diabetic pregnancies may have an accelerated increase in maximum and mean temporal velocities across the atrioventricular valves relative to normal pregnancies (Lisowski et al, 2003), interpretation of valve flow velocity patterns and ventricular performance via echocardiography has some limitations, as these parameters are affected by heart rate, afterload, preload, and ventricular compliance. In normal pregnancies and those with pregestational diabetes, there is a progressive decrease in placental vascular resistance with gestation.…”

Section: Discussionmentioning

confidence: 99%

Fetal cardiac effects of maternal hyperglycemia during pregnancy

Corrigan

Brazil

McAuliffe

2009

Birth Defects Research

120

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Maternal diabetes mellitus is associated with increased teratogenesis, which can occur in pregestational type 1 and type 2 diabetes. Cardiac defects and with neural tube defects are the most common malformations observed in fetuses of pregestational diabetic mothers. The exact mechanism by which diabetes exerts its teratogenic effects and induces embryonic malformations is unclear. Whereas the sequelae of maternal pregestational diabetes, such as modulating insulin levels, altered fat levels, and increased reactive oxygen species, may play a role in fetal damage during diabetic pregnancy, hyperglycemia is thought to be the primary teratogen, causing particularly adverse effects on cardiovascular development. Fetal cardiac defects are associated with raised maternal glycosylated hemoglobin levels and are up to five times more likely in infants of mothers with pregestational diabetes compared with those without diabetes. The resulting anomalies are varied and include transposition of the great arteries, mitral and pulmonary atresia, double outlet of the right ventricle, tetralogy of Fallot, and fetal cardiomyopathy.A wide variety of rodent models have been used to study diabetic teratogenesis. Both genetic and chemically induced models of type 1 and 2 diabetes have been used to examine the effects of hyperglycemia on fetal development. Factors such as genetic background as well as confounding variables such as obesity appear to influence the severity of fetal abnormalities in mice. In this review, we will summarize recent data on fetal cardiac effects from human pregestational diabetic mothers, as well as the most relevant findings in rodent models of diabetic cardiac teratogenesis.

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Section: Discussionmentioning

confidence: 99%

Fetal cardiac effects of maternal hyperglycemia during pregnancy

Corrigan

Brazil

McAuliffe

2009

Birth Defects Research

120

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“…Fetuses of diabetic pregnancies have been shown to have an accelerated increase in maximum and mean temporal velocities across atrioventricular valves through gestation relative to normal pregnancies. 9 Increased left and right ventricular outputs adjusted for fetal weight have also been observed. 9 Lower right atrioventricular valve inflow E (early diastole)/A (atrial systole) velocity ratios have been demonstrated, particularly later in gestation.…”

Section: Evolution Of Fetal Myocardial Changes In Maternal Diabetesmentioning

confidence: 97%

“…9 Increased left and right ventricular outputs adjusted for fetal weight have also been observed. 9 Lower right atrioventricular valve inflow E (early diastole)/A (atrial systole) velocity ratios have been demonstrated, particularly later in gestation. 10 11 Of these parameters, only lowered E/A wave ratio has been shown to be associated with worse maternal glycaemic control, which may be indirectly due to changes in fetal heart rate, ventricular wall thickness and haematocrit.…”

Section: Evolution Of Fetal Myocardial Changes In Maternal Diabetesmentioning

confidence: 97%

Maternal diabetes and the fetal heart

Hornberger

2006

Heart

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Maternal diabetes mellitus significantly affects the fetal heart and fetal-placental circulation in both structure and function. The influence of pre-conceptional diabetes begins during embryonic development in the first trimester, with altered cardiac morphogenesis and placental development. It continues to have an influence on the fetal circulation through the second and third trimesters and into the perinatal and neonatal period.

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“…Increased metabolic demand and relative hypoxia can act as a haemodynamic stimulant and significantly increase cardiac output. 22 In addition, corticosteroids can have a direct anabolic effect on myocardium, 2 cause systemic hypertension, and increase the afterload. 13 This type of hemodynamic stimulant, hyperinsulinaemia and or iatrogenic corticosteroids, can cause neonatal cardiac hypertrophy.…”

Section: Discussionmentioning

confidence: 99%

Molecular characterisation of neonatal cardiac hypertrophy and its regression

Gopinath

Trent

2004

Cardiol Young

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Neonatal cardiac hypertrophy associated with diabetic pregnancy is transient and regresses naturally, but is associated with increased morbidity and mortality. This study was undertaken to analyse the changes in expression of 5 cardiac genes, including atrial natriuretic peptide, alpha- and beta-myosin heavy chain, and cardiac and skeletal alpha-actin genes, using a rat neonatal model, in which cardiac hypertrophy was induced via maternal diabetes. In the hypertrophied left ventricle of neonates from diabetic mothers, the levels of mRNA from all the above genes except skeletal alpha-actin were increased by between 1.8- and 12-fold compared with the controls at birth (p < 0.05). In the first 28 days, the level of mRNA for alpha-myosin heavy chain increased slightly, while that for atrial natriuretic peptide and beta-myosin heavy chain decreased continuously similar to the controls, but at a significantly faster rate. No significant difference between the two groups of neonates was observed in all 5 genes after 1 month, indicating complete regression. Expression of 5 cardiac genes in the neonatal cardiac hypertrophy was characterised in both hypertrophic and regressive phases. Hypertrophic regression provides a unique model for the testing of new drugs or genetic modifying factors in cardiac hypertrophy.

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Altered fetal circulation in type‐1 diabetic pregnancies

Abstract: ABSTRACT

Cited by 27 publications

References 29 publications

Fetal cardiac effects of maternal hyperglycemia during pregnancy

Fetal cardiac effects of maternal hyperglycemia during pregnancy

Maternal diabetes and the fetal heart

Molecular characterisation of neonatal cardiac hypertrophy and its regression

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