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孕早期胎儿对贫血的血流动力学反应:以血红蛋白Bart病作为研究模型

Fetal Hemodynamic Response to Anemia in Early Gestation: Using Hemoglobin Bart's Disease as a Study Model.

作者信息

Luewan Suchaya, Tongprasert Fuanglada, Srisupundit Kasemsri, Traisrisilp Kuntharee, Jatavan Phudit, Tongsong Theera

机构信息

Obstetrics and Gynecology, Chiang Mai University, Chiang Mai, Thailand.

出版信息

Ultraschall Med. 2023 Apr;44(2):e83-e90. doi: 10.1055/a-1499-7045. Epub 2021 Nov 8.

DOI:10.1055/a-1499-7045
PMID:34749405
Abstract

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.

摘要

目的

以胎儿血红蛋白Bart’s病为研究模型,评估妊娠早期贫血时胎儿的血流动力学变化。

方法

对妊娠12 - 14周有胎儿血红蛋白Bart’s病风险的孕妇进行前瞻性研究。在进行诊断性侵入性操作前,通过二维超声、多普勒速度测量和心脏STIC全面评估胎儿血流动力学。比较受累和未受累胎儿的各种血流动力学参数。

结果

在56例有风险的胎儿中,17例患有血红蛋白Bart’s病,39例未受累。受累胎儿的右心室和联合心室心输出量(CO)显著更高(分别为0.993对1.358;p<0.001和1.010对1.236;p<0.001),而左心室CO虽有升高趋势但不显著(1.027对1.113;p = 0.058)。心脏尺寸、大脑中动脉收缩期峰值速度、Tei指数和等容收缩时间显著增加,而整体球形指数显著降低。有趣的是,心脏前负荷、心室壁厚度、缩短分数、等容舒张时间和胎儿心率未改变。4例胎儿有水肿改变,但所有心功能均正常。

结论

胎儿贫血导致血容量过多并增加心输出量以满足组织氧需求,导致心脏增大但无肥厚,容量负荷增加但无压力负荷,球形指数降低。心脏功能良好但工作更努力,尤其是心室收缩负荷。贫血引起的胎儿水肿似乎并非如先前认为的那样由心力衰竭所致,至少在妊娠早期是由血管通透性高导致的容量负荷引起的。

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