From the Department of Obstetrics and Gynecology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Obstet Gynecol. 2011 Jan;117(1):84-91. doi: 10.1097/AOG.0b013e3181fc3887.
To estimate fetal ventricular shortening fraction, representing cardiac contractility, derived from cardiospatiotemporal image correlation with M-mode display "STIC-M" in fetuses with hydrops fetalis secondary to high-output (fetal anemia) and low-output causes (congenital heart defects).
A cross-sectional study was conducted in normal fetuses (group 1), fetuses with hemoglobin Bart's disease with (group 2) and without (group 3) hydrops fetalis, and those with hydrops fetalis resulting from cardiac defects (group 4). Volume data sets of cardiospatiotemporal image correlations were acquired for each group for subsequent offline analysis with cardiospatiotemporal image correlation with M-mode display. Group 1 data were used to construct reference ranges of left and right ventricular shortening fraction for assessment of fetuses in the remaining groups.
A total of 606 measurements, 15-35 per week, were performed in normal fetuses to construct reference ranges as well as Z-scores of left and right ventricular shortening fraction. Both parameters were decreased with increasing gestation with weak correlation (r2=0.141, P<.001 and r2=0.055, P<.001, respectively). Shortening fraction did not significantly change among 111 fetuses with hemoglobin Bart's disease with and without hydrops. However, left and right ventricular shortening fraction were significantly decreased (mean Z-scores 5 standard deviations and 8 standard deviations below the mean, respectively) in 21 hydropic fetuses as a result of congenital heart defects (P<.001).
Fetuses with hydrops fetalis secondary to cardiac defects and anemia have a different pattern of shortening fraction. Hydrops fetalis resulting from cardiac defect is primarily caused by cardiac decompensation; whereas in fetal anemia, it is probably caused by hypervolemia with cardiac decompensation occurring when the cardiac compensatory mechanism is exhausted.
II.
利用心脏时空关联成像与 M 型显示“STIC-M”技术，评估因高输出量（胎儿贫血）和低输出量（先天性心脏缺陷）引起的心包积液胎儿的心室缩短分数，以反映心脏收缩功能。
本研究为横断面研究，纳入正常胎儿（第 1 组）、血红蛋白 Bart 病伴心包积液胎儿（第 2 组）、血红蛋白 Bart 病不伴心包积液胎儿（第 3 组）和因心脏缺陷引起的心包积液胎儿（第 4 组）。对每组胎儿进行心脏时空关联成像容积数据集采集，随后离线进行心脏时空关联成像与 M 型显示分析。第 1 组数据用于构建左、右心室缩短分数的参考范围，以评估其余各组胎儿。
在正常胎儿中，共进行了 606 次测量（每周 15-35 次），以构建左、右心室缩短分数的参考范围和 Z 评分。随着胎龄的增加，这两个参数均逐渐降低，且相关性较弱（r2=0.141，P<.001 和 r2=0.055，P<.001）。血红蛋白 Bart 病伴或不伴心包积液的 111 例胎儿的缩短分数无明显变化。然而，21 例因先天性心脏缺陷引起的心包积液胎儿的左、右心室缩短分数明显降低（平均 Z 评分分别低于均值 5 个标准差和 8 个标准差，P<.001）。
由心脏缺陷和贫血引起的心包积液胎儿的缩短分数模式不同。由心脏缺陷引起的心包积液主要由心脏失代偿引起；而在胎儿贫血中，可能是由于血容量过多引起，当心脏代偿机制耗尽时，就会出现心脏失代偿。
II 级。
