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Fetal Hemodynamic Response to Anemia in Early Gestation: Using Hemoglobin Bart's Disease as a Study Model
Suchaya Luewan1, Fuanglada Tongprasert1, Kasemsri Srisupundit1
1Obstetrics and Gynecology, Chiang Mai University, Chiang Mai, Thailand.
Insights
Fetal anemia in early pregnancy increases cardiac output and blood volume to meet oxygen needs. This leads to a larger heart working harder, not failing, in conditions like Hb Bart
Area of Science:
- Perinatology
- Fetal Medicine
- Cardiology
Background:
- Fetal anemia, particularly Hb Bart's disease, presents a significant challenge in early gestation.
- Understanding the hemodynamic adaptations to anemia is crucial for managing affected pregnancies.
Purpose of the Study:
- To evaluate fetal hemodynamic alterations in response to anemia during early pregnancy.
- To utilize fetal Hb Bart's disease as a model for assessing these changes.
Main Methods:
- A prospective study involving pregnancies at risk for fetal Hb Bart's disease (12-14 weeks gestation).
- Comprehensive fetal hemodynamic assessment using 2D ultrasound, Doppler velocity, and cardio-STIC.
- Comparison of hemodynamic parameters between affected and unaffected fetuses prior to diagnostic procedures.
Main Results:
- Fetuses with Hb Bart's disease exhibited significantly higher right and combined ventricular cardiac outputs.
- Increased cardiac dimensions, middle cerebral artery peak systolic velocity, and Tei index were observed in affected fetuses.
- Despite increased workload, cardiac preload, heart rate, and contractility measures remained unchanged, and hydrops fetalis was not linked to heart failure.
Conclusions:
- Fetal anemia triggers compensatory hypervolemia and increased cardiac output to maintain tissue oxygenation.
- The fetal heart adapts to anemia with increased volume load and systolic ventricular stress, rather than pressure load or failure.
- Early-gestation hydrops fetalis in anemic fetuses is likely due to volume overload and increased vascular permeability, not cardiac insufficiency.
Objective:
To assess fetal hemodynamic changes in response to anemia in early gestation, using fetal Hb Bart's disease as a study model.
Methods:
A prospective study was conducted on pregnancies at risk for fetal Hb Bart's disease at 12-14 weeks of gestation. Fetal hemodynamics were comprehensively assessed by 2D ultrasound, Doppler velocity, and cardio-STIC just prior to the invasive procedure for diagnosis. The various hemodynamic parameters of the affected and unaffected fetuses were compared.
Results:
Of 56 fetuses at risk, 17 had Hb Bart's disease and 39 were unaffected. The right and combined ventricular cardiac outputs (CO) were significantly higher in the affected fetuses (0.993 vs. 1.358; p < 0.001 and 1.010 vs. 1.236; p < 0.001, respectively), whereas the left CO tended to be higher but not significantly (1.027 vs. 1.113; p = 0.058). Cardiac dimensions, middle-cerebral artery peak systolic velocity, Tei index, and isovolemic contraction time were significantly increased, while the global sphericity index was significantly decreased. Interestingly, cardiac preload, ventricular wall thickness, shortening fraction, isovolemic relaxation time, and fetal heart rate were unchanged. Four fetuses had hydropic changes, but all cardiac functions were normal.
Conclusion:
Fetal anemia induces hypervolemia and increases cardiac output to meet the tissue oxygen requirement, resulting in an increase in size without hypertrophy, volume load without pressure load, and a decrease in the globular sphericity index. The heart works very well but works harder, especially systolic ventricular load. Hydrops fetalis due to anemia appears not to be caused by heart failure as previously believed but rather by volume load with high vascular permeability at least in early pregnancy.
