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Published on: May 13, 2016
Hyperglycemia Alters the Structure and Hemodynamics of the Developing Embryonic Heart
Taylor B Lawson1, Devon E Scott-Drechsel2, Venkat Keshav Chivukula3
1Biomedical Engineering Department, Oregon Health & Science University, Portland, OR 97239, USA. tlawson@bu.edu.
Insights
Maternal diabetes causes hyperglycemia, increasing congenital heart defect risk. This study shows high glucose alters embryonic heart outflow tract development and blood flow, potentially explaining increased cardiac malformations.
Area of Science:
- Developmental Biology
- Cardiovascular Science
- Endocrinology
Background:
- Congenital heart defects (CHDs) are common birth defects, with outflow tract malformations being frequent.
- Maternal diabetes is a significant risk factor, increasing CHD incidence by 3-5 fold.
- The impact of hyperglycemia on embryonic heart hemodynamics during early development remains poorly understood.
Purpose of the Study:
- To investigate the effects of induced hyperglycemic conditions on embryonic heart development, specifically the outflow tract (OFT).
- To assess structural and hemodynamic alterations in the OFT under sustained high glucose levels.
- To elucidate potential mechanisms linking maternal diabetes to increased CHD risk.
Main Methods:
- Utilized chick embryo model to induce sustained hyperglycemia (average plasma glucose 180 mg/dL).
- Employed optical coherence tomography (OCT), confocal microscopy, and microcomputed tomography for structural analysis.
- Assessed hemodynamic changes, including blood flow velocity and reversal, within the OFT.
Main Results:
- Hyperglycemic embryos exhibited asymmetric endocardial cushions in the proximal OFT.
- Significant alterations in OFT curvature and torsion were observed.
- Reduced blood flow velocity and 30% flow reversal during the cardiac cycle were noted in hyperglycemic embryos.
Conclusions:
- Hyperglycemia during early gestation induces structural and hemodynamic abnormalities in the developing heart's OFT.
- These findings suggest a potential pathway by which maternal diabetes contributes to congenital heart defects.
- Identifies early developmental alterations that may underlie increased cardiac malformations in offspring of diabetic mothers.
Abstract:
Congenital heart defects (CHDs) represent the most common form of human birth defects; approximately one-third of heart defects involve malformations of the outflow tract (OFT). Maternal diabetes increases the risk of CHD by 3-5 fold. During heart organogenesis, little is known about the effects of hyperglycemia on hemodynamics, which are critical to normal heart development. Heart development prior to septation in the chick embryo was studied under hyperglycemic conditions. Sustained hyperglycemic conditions were induced, raising the average plasma glucose concentration from 70 mg/dL to 180 mg/dL, akin to the fasting plasma glucose of a patient with diabetes. The OFTs were assessed for structural and hemodynamic alterations using optical coherence tomography (OCT), confocal microscopy, and microcomputed tomography. In hyperglycemic embryos, the endocardial cushions of the proximal OFT were asymmetric, and the OFTs curvature and torsion were significantly altered. The blood flow velocity through the OFT of hyperglycemic embryos was significantly decreased, including flow reversal in 30% of the cardiac cycle. Thus, hyperglycemia at the onset of gestation results in asymmetric proximal endocardial cushions, abnormal OFT curvature, and altered hemodynamics in the developing heart. If present in humans, these results may identify early developmental alterations that contribute to the increased risk for cardiac malformations in babies from diabetic mothers.
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