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Fetal hemodynamic changes and mitochondrial dysfunction in myocardium and brain tissues in response to anemia: a
Suchaya Luewan1, Nattayaporn Apaijai2,3,4, Nipon Chattipakorn2,3,4
1Department of Obstetrics and Gynecology, Division of Maternal Fetal Medicine, Chiang Mai University, Chiang Mai, Thailand.
Insights
Fetal anemia causes heart and brain cells to dysfunction despite increased cardiac output. This compensatory mechanism cannot fully prevent subtle damage to these vital organs.
Area of Science:
- Perinatal Medicine
- Fetal Cardiology
- Mitochondrial Biology
Background:
- Fetal anemia, particularly in conditions like Hb Bart's disease, presents a challenge in understanding its impact on developing organs.
- Compensatory mechanisms in anemic fetuses aim to maintain oxygen supply to vital organs, but their long-term effects are not fully understood.
Purpose of the Study:
- To compare prenatal cardiovascular adaptations and post-abortal cellular damage in the myocardium and brain of anemic fetuses versus non-anemic fetuses.
- To investigate the effects of fetal anemia on oxidative stress and mitochondrial function in key fetal organs.
Main Methods:
- Recruitment of anemic (Hb Bart's disease) and non-anemic fetuses (16-22 weeks gestation) for fetal echocardiography.
- Confirmation of diagnosis and assessment of fetal circulation using cord blood analysis.
- Analysis of fetal cardiac and brain tissues for oxidative stress markers and mitochondrial function.
Main Results:
- Anemic fetuses exhibited increased cardiac dimensions, function, cardiac output, and brain circulation without impaired contractility.
- Significant mitochondrial dysfunction, evidenced by increased membrane potential changes and ROS production, was observed in the brain and myocardium of anemic fetuses.
- Cellular damage was detected in vital organs despite apparent clinical compensation.
Conclusions:
- Fetal anemia triggers cardiac remodeling and increased output to enhance tissue perfusion, particularly cerebral blood flow.
- Despite compensatory circulatory changes, anemic fetuses show significant mitochondrial dysfunction in the heart and brain, indicating cellular damage from hypoxic stress.
- The compensatory increase in circulation is insufficient to completely prevent subtle damage to the fetal myocardium and brain.
Objective:
Whether or not the effects of anemia in the early phase, while the fetuses attempts to increase cardiac output to meet oxygen requirement in peripheral organs, is detrimental to the fetal developing vital organs is little-known. The objective of this is to compare prenatal cardiovascular changes and post-abortal cellular damages in the myocardium as a pumping organ and the brain as a perfused organ between anemic fetuses (using fetal Hb Bart's disease as a study model) in pre-hydropic phase and non-anemic fetuses.
Methods:
Fetuses affected by Hb Bart's disease and non-anemic fetuses at 16-22 weeks were recruited to undergo comprehensive fetal echocardiography. Cord blood analysis was used to confirm the definite diagnosis of fetal Hb Bart's disease and normal fetuses. Fetal cardiac and brain tissues were collected shortly after pregnancy termination for the determination of oxidative stress and mitochondrial function, including mitochondrial ROS production and mitochondrial membrane changes.
Results:
A total of 18 fetuses affected by Hb Bart's disease and 13 non-anemic fetuses were recruited. The clinical characteristics of both groups were comparable. The affected fetuses showed a significant increase in cardiac dimensions, cardiac function, cardiac output and brain circulation without deteriorating cardiac contractility and preload. However, in the affected fetuses, mitochondrial dysfunction was clearly demonstrated in brain tissues and in the myocardium, as indicated by a significant increase in the membrane potential change (p-value < 0.001), and a significant increase in ROS production in brain tissues, with a trend to increase in myocardium. The findings indicated cellular damage in spite of good clinical compensation.
Conclusion:
The new insight is that, in response to fetal anemia, fetal heart increases in size (dilatation) and function to increase cardiac output and blood flow velocity to provide adequate tissue perfusion, especially brain circulation. However, the myocardium and brain showed a significant increase in mitochondrial dysfunction, suggesting cellular damage secondary to anemic hypoxia. The compensatory increase in circulation could not completely prevent subtle brain and heart damage.
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