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Published on: June 29, 2013
Ventricular Diastolic Function in Normal Fetuses and Fetuses with Hb Bart's Disease Assessed by Color M-Mode
Insights
Fetal anemia causes hydrops fetalis initially through hypervolemia, not diastolic dysfunction. Ventricular diastolic compromise is a late consequence of persistent hypervolemia in fetal Hb Bart's disease.
Area of Science:
- Fetal Medicine
- Cardiology
- Genetics
Background:
- Fetal anemia, such as in Hb Bart's disease, can lead to hydrops fetalis and cardiac failure.
- Understanding the mechanisms of fetal cardiac dysfunction is crucial for timely intervention.
Purpose of the Study:
- To investigate the role of ventricular diastolic dysfunction in the pathogenesis of fetal cardiac failure.
- To utilize fetal Hb Bart's disease as a model and cardio-STIC-M for diagnosis.
Main Methods:
- Acquired color cardio-STIC volume datasets from fetuses (18-22 and 28-32 weeks gestation).
- Analyzed velocity propagation (Vp) of ventricles to assess diastolic function.
- Compared Vp in normal fetuses, those with Hb Bart's disease, and those with hydrops fetalis.
Main Results:
- No significant difference in Vp between normal fetuses and those with Hb Bart's disease at 18-22 weeks.
- Significantly lower Vp in fetuses with hydrops fetalis (Hb Bart's disease) compared to normal fetuses at 28-32 weeks (p < 0.001).
- Inter-observer variability showed fair agreement (ICC = 0.531).
Conclusions:
- Hydrops fetalis in fetal anemia is primarily driven by hypervolemia, not initial ventricular diastolic dysfunction.
- Ventricular diastolic compromise develops later as a consequence of sustained hypervolemia.
- This mechanism differs from hydrops caused by primary cardiac issues.
Abstract:
Purpose: To determine whether ventricular diastolic dysfunction contributes to the pathogenesis of fetal cardiac failure due to fetal anemia using fetal Hb Bart's disease as a live model and cardio-STIC-M as a diagnostic tool. Materials and Methods: Color cardio-STIC volume datasets were acquired from fetuses at risk for Hb Bart's disease during 18 - 22 weeks of gestation and normal pregnancies and pregnancies with hydrops fetalis caused by Hb Bart's disease at 28 - 32 weeks. The volumes were analyzed off-line for velocity propagation (Vp) of the right and left ventricles to assess ventricular diastolic function using color cardio-STIC-M. Results: The Vp for the right and left ventricles was studied in fetuses at 18 - 22 weeks, including 64 normal fetuses (group 1) and 22 fetuses with Hb Bart's disease (group 2), and in fetuses at 28 - 32 weeks, including 22 normal fetuses (group 3) and 16 fetuses with Hb Bart's hydrops fetalis (group 4). The Vp of the fetuses in group 1 and group 2 was not significantly different. However, the Vp for the right and left ventricles in group 4 was significantly lower than in group 3 (19.02 vs. 9.78, p < 0.001; and 20.24 vs. 13.40, p < 0.001, respectively). The inter-observer variability had fair agreement with the intra-class correlation coefficient of 0.531 (95 % CI 0.393 - 0.646, p < 0.001). Conclusion: Hydrops fetalis secondary to fetal anemia is initially caused by hypervolemia rather than ventricular diastolic dysfunction while ventricular diastolic compromise is a late occurring consequence of persistent hypervolemia, different from the mechanism of hydropic changes caused by cardiac causes.
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