Hornberger L K, Sahn D J, Kleinman C S, Copel J, Silverman N H
Division of Pediatric Cardiology, University of California, San Diego School of Medicine.
J Am Coll Cardiol. 1994 Feb;23(2):417-23. doi: 10.1016/0735-1097(94)90429-4.
The purpose of this study was to test observations that might aid prenatal prediction of the presence of coarctation of the aorta in newborn infants with and without other forms of heart disease.
Previous reports have suggested that abnormal growth of the aortic arch in utero may be identifiable as a marker for the diagnosis of coarctation.
We reviewed the prenatal echocardiograms and postnatal outcome of 20 infants (gestational age at initial study 18 to 36 weeks) with coarctation of the aorta established postnatally, to identify echocardiographic findings that would most facilitate the prenatal diagnosis of coarctation. Associated cardiac lesions included double-inlet left ventricle anatomy (n = 5), double-outlet right ventricle (n = 4), abnormal aortic valve (n = 5), unbalanced atrioventricular canal (n = 3), and membranous ventricular septal defect (n = 1). Chromosomal abnormalities included XO karyotype (n = 1), trisomy 18 (n = 1), and trisomy 21 (n = 1).
Hypoplasia determined by measurement of the distal aortic arch was the most frequently observed finding among the fetuses with coarctation. In 12 of 15 fetuses with a well visualized transverse arch at initial prenatal study, the diameter of the transverse arch was < or = 3rd percentile for gestational age as compared with that in a normal group of fetuses. Ten of 10 fetuses with adequate images of the isthmus had isthmus hypoplasia at prenatal study with a diameter < or = 3rd percentile for gestational age. On serial study in six of seven, including three fetuses with normal distal arch measurements at initial study, the distal arch became progressively more hypoplastic for gestational age. In three there was no growth of the transverse arch or isthmus on serial study, and in three there was reversal of flow from antegrade to retrograde through the distal arch.
In our study, quantitative hypoplasia of the isthmus and transverse arch was the most consistent observation and therefore the most definitive antenatal sign of postnatal coarctation. The potential for progression of distal arch hypoplasia necessitates serial study in fetuses with associated cardiac and noncardiac lesions.
本研究旨在验证一些观察结果,这些结果可能有助于对患有或不患有其他形式心脏病的新生儿主动脉缩窄的存在进行产前预测。
先前的报告表明,子宫内主动脉弓的异常生长可被识别为诊断主动脉缩窄的标志物。
我们回顾了20例出生后确诊为主动脉缩窄的婴儿(初次研究时的孕周为18至36周)的产前超声心动图和产后结局,以确定最有助于主动脉缩窄产前诊断的超声心动图表现。相关心脏病变包括双入口左心室解剖结构(n = 5)、双出口右心室(n = 4)、主动脉瓣异常(n = 5)、不平衡房室通道(n = 3)和膜周室间隔缺损(n = 1)。染色体异常包括XO核型(n = 1)、18三体(n = 1)和21三体(n = 1)。
在患有主动脉缩窄的胎儿中,通过测量主动脉弓远端确定的发育不全是最常观察到的表现。在初次产前研究中,15例可清晰显示横弓的胎儿中有12例,其横弓直径与正常胎儿组相比小于或等于孕周的第3百分位数。10例峡部图像充足的胎儿在产前研究中峡部发育不全,直径小于或等于孕周的第3百分位数。在7例中的6例进行系列研究,包括3例初次研究时主动脉弓远端测量正常的胎儿,随着孕周增加,远端弓逐渐发育不全。在3例中,系列研究显示横弓或峡部没有生长,在3例中,通过远端弓的血流从正向转为逆向。
在我们的研究中,峡部和横弓的定量发育不全是最一致的观察结果,因此是产后主动脉缩窄最明确的产前征象。对于伴有心脏和非心脏病变的胎儿,由于远端弓发育不全有进展的可能,因此需要进行系列研究。