Fetal cardiovascular hemodynamics in type 1 diabetic pregnancies at near‐term gestation

Abstract

Introduction Poor glycemic control in maternal type 1 diabetes mellitus during pregnancy can affect fetal cardiac and placental function. However, studies concerning fetal central hemodynamics have revealed conflicting results. We hypothesized that in pregnancies complicated by maternal type 1 diabetes, fetal cardiovascular and placental hemodynamics are comparable to the control fetuses at near‐term gestation. In addition, we investigated the relation between newborn serum biomarkers of cardiac function and fetal cardiovascular and placental hemodynamics. Furthermore, we studied whether maternal diabetes is associated with placental inflammation. Material and methods In this prospective case‐control study, fetal central and peripheral hemodynamics were assessed by ultrasonography in 33 women with type 1 diabetes and in 67 controls with singleton pregnancies between 34+2 and 40+2 gestational weeks. Newborn umbilical cord serum was collected to analyze cardiac natriuretic peptides (atrial and B‐type natriuretic peptides) and troponin T concentrations. Placental tissue samples were obtained for cytokine analyses. Results Fetal ventricular wall thicknesses were greater and weight‐adjusted stroke volumes and cardiac outputs were lower in the type 1 diabetes group than in the control group. Pulsatility in the aortic isthmus and inferior vena cava blood flow velocity waveforms was greater in the type 1 diabetes group fetuses than in the controls. A positive correlation was found between branch pulmonary artery and aortic isthmus pulsatility index values. Umbilical artery pulsatility indices were comparable between the groups. Umbilical cord serum natriuretic peptide and troponin T concentrations were elevated in the type 1 diabetes fetuses. These cardiac biomarkers correlated significantly with cardiovascular hemodynamics. Placental cytokine levels were not different between the groups. Conclusions In maternal type 1 diabetes pregnancies, fetal cardiovascular hemodynamics is impaired. Maternal type 1 diabetes does not seem to alter placental vascular impedance or induce placental inflammation.

Progress of Pathogenesis in Pediatric Multifocal Atrial Tachycardia

“…Gestational diabetes mellitus (GDM) is the most common metabolic disease during pregnancy, with an overall prevalence of 6%−13% ( 10 , 11 ). In patients with gestational diabetes, maternal metabolic abnormalities lead to impaired fetal cardiovascular hemodynamics through a variety of mechanisms, including decreased cardiac output and increased aortic isthmus' flow velocity and pulsation ( 12 ). Furthermore, abnormal blood glucose variability in mothers with diabetes contributes to the development of cardiac diastolic dysfunction, even when obvious cardiac hypertrophy is not observed.…”

Bioinformatics study and experimental validation of METTL3 regulation of immune-related genes affecting placental vascular development

“…In addition, clinical studies have found that THBS1 is upregulated in placental trophoblast cells of preeclampsia pregnant women, and subsequent animal experiments have shown that overexpression of THBS1 inhibits the cAMP signaling pathway and affects syncytialization of trophoblast cells, thereby inducing preeclampsia (31,32). Lehtoranta et al found that decreased expression of PDGFRB caused abnormal placental hemodynamics leading to gestational diabetes (33). Based on the GEPIA database, JAG1 and VEGFA exhibited a positive correlation (34), and overexpressing JAG1 promoted the proliferation of endothelial cells (35,36).…”