胎儿心脏异常钙化病因及超声特征

目的 探讨胎儿心脏异常钙化的病因及超声特征。方法 回顾性分析12胎心脏异常钙化胎儿的超声及病理学资料,分析其妊娠结局、病因及超声表现。结果 12胎中,母体抗SSA/SSB抗体（+）胎儿8胎,超声表现为心房壁、房间隔、房室瓣环等处广泛性增厚、回声增强;心肌营养不良性钙化3胎,超声表现为心室壁内局限性或广泛性高回声;特发性婴儿动脉钙化1胎,超声表现为主肺动脉和主动脉系统广泛性管壁增厚、回声增强、管腔狭窄。妊娠结局：1胎营养不良性心肌钙化病例继续妊娠中,1胎母体抗SSA/SSB（+）胎儿出生,10胎终止妊娠。结论 胎儿心脏异常钙化病因与母体抗SSA/SSB抗体（+）有关,不同病因所致超声表现有所差异。     

胎儿超声心动图产前诊断二尖瓣发育异常

目的 探讨胎儿超声心动图在产前诊断二尖瓣发育异常中的价值。方法 回顾性分析79胎胎儿二尖瓣发育异常的超声心动图表现,并与随访结果比较。结果 二尖瓣闭锁47胎(47/79,59.49％),二尖瓣重度狭窄22胎(22/79,27.85％),二尖瓣反流10胎(10/79,12.66％),其中轻度反流4胎,中度反流4胎,重度反流2胎。胎儿超声心动图可清晰显示胎儿二尖瓣形态、结构以及开闭活动,CDFI可显示二尖瓣跨瓣血流情况,评价血流动力学情况。结论 胎儿超声心动图在二尖瓣发育异常的产前诊断中具有重要作用。     

脐带绕颈深度与胎儿大脑中动脉、脐动脉血流参数的相关性

目的 探讨脐带绕颈深度与大脑中动脉（MCA）及脐动脉（UA）血流参数的关系。方法 选取孕晚期脐带绕颈胎儿139胎及正常胎儿28胎。采用多普勒超声检测胎儿MCA及UA的收缩期最大速度/舒张最小速度（S/D）、阻力指数（RI）、搏动指数（PI）,并分析脐带绕颈胎儿压迹深度与MCA、UA血流参数的相关性。结果 脐带绕颈胎儿压迹深度与MCA的S/D、RI、PI呈正相关（绕颈1周r=0.32、0.32、0.35,绕颈2周r=0.71、0.69、0.53;P均<0.05）,与UA的S/D、RI、PI无相关性。脐带绕颈胎儿与正常胎儿UA血流参数差异无统计学意义（P均>0.05）,脐带绕颈1周压迹深度≥0.80 cm及脐带绕颈2周及以上胎儿MCA的S/D、RI、PI均高于正常胎儿（P均<0.05）。与正常胎儿比较,脐带绕颈2周胎儿的剖宫产率明显增高,脐带绕颈1周且压迹深度≥0.80 cm的胎儿胎心监护异常率升高,第二产程时间延长,差异均有统计学意义（P均<0.05）。结论 孕晚期脐带绕颈胎儿的MCA血流参数较UA更敏感,绕颈1周压迹深度≥0.80 cm可能引起胎儿宫内缺氧。     

超声观察中晚孕期正常胎儿脐动脉和脑、肾动脉血流动力学

目的 探索正常胎儿脐动脉(UA)、大脑中动脉(MCA)和肾动脉(RA)血流参数随孕期变化的规律;建立正常胎儿不同孕期UA、MCA和RA血流参数的参考值范围。方法 应用彩色多普勒血流显像(CDFI)检测220胎21~41孕周正常单胎胎儿UA、MCA和RA血流,测量收缩期峰值流速(PS)、搏动指数(PI)、阻力指数(RI)及收缩期峰值流速与舒张末期流速比值(S/D)。结果 正常胎儿UA、MCA和RA的PS值随着孕周增加而增加;UA和RA的PI、RI和S/D值随着孕周增加而减低;而MCA的PI、RI和S/D值随着孕周增加呈先升高后降低的抛物线状。至足月,PS参考值范围分别为:UA PS(54.96±14.57)cm/s、MCA PS(65.11±11.35)cm/s和RA PS(58.54±10.72)cm/s;UAS/D测值为2.14±0.30;RA RI测值为0.79±0.04;MCA RI测值为0.72±0.05。所有参数的变化在不同孕周组差异均有统计学意义(P均<0.05)。结论 CDFI产前检测胎儿UA、MCA和RA随着孕期变化的血流动力学参数可以同时了解胎儿胎盘循环、颅脑循环及周围循环状态。不同孕期的血流参数的参考值范围可为超声预测胎儿宫内缺氧提供理论依据。     

超声检测水肿胎儿静脉导管血流频谱的变化

目的 分析水肿胎儿的静脉导管(DV)血流参数,观察心源性水肿及重型α-地中海贫血引起的胎儿水肿者DV血流频谱改变。 方法 选取产前超声检查发现的69胎水肿胎儿,根据病因分心源性水肿组(17胎)和重型α-地中海贫血组(52胎),分别测量DV血流频谱并进行参数分析。 结果 心源性水肿组88.24%(15/17)DV出现心室收缩期峰值速度(S)波降低、心房收缩期峰值速度(a)波缺失或反向,静脉峰值流速指数(PVIV)、DV搏动指数(DVPI)及DV阻力指数(DVRI)升高。重型a-地中海贫血组50.00%(26/52)表现为S波增高,59.62%(31/52)a波增高,69.23%(36/52)PVIV减低,80.77%(42/52)DVRI降低,86.53%(45/52)DVPI降低。两组比较,水肿胎儿DV血流频谱与相应孕周正常胎儿DV参考值的差值差异有统计学意义(P<0.01)。 结论 两组水肿胎儿DV血流频谱改变不同。DV血流参数对于鉴别胎儿水肿病因及指导临床诊疗有重要意义。     

超声速度向量成像三维数据成像技术观察心律失常胎儿心脏传导状态

目的 应用超声速度向量成像(VVI)三维数据成像技术评价胎儿不同类型心律失常中的房室传导模式.方法 收集经超声心动图检查确诊的心律失常胎儿60胎及正常胎儿40胎,行VVI,应用Siemens Syngo Workplace工作站分析三维数据成像.结果 VVI三维数据成像可清晰显示胎儿不同类型心律失常的房室传导形式.下传心房早搏提前出现的心房收缩后有心室收缩,后伴不完全代偿间期,未下传心房早搏在心房提前收缩后发生传导阻滞,其后无心室收缩;与窦性心律兴奋点比较,心房早搏位置轴发生改变.室上性心动过速伴不规律房室传导阻滞时,房室激动的速度轴降低,时间轴和位置轴无变化.心房颤动和心房扑动伴房室传导紊乱时心室律绝对不齐,房室激动的速度轴明显降低.Ⅱ度房室传导阻滞时,房室呈2∶1下传,完全性房室传导阻滞房室间运动无关联;房室激动的速度轴、时间轴和位置轴均无变化.结论 应用VVI三维数据成像可立体观察胎儿心脏传导状态.     

超声评价子痫前期患者胎儿主动脉峡部血流指数

目的 通过测量峡部血流指数（IFI）定量分析子痫前期（PE）患者胎儿主动脉峡部（AOI）血流变化特点与规律。方法 纳入38例PE患者（PE组）和孕周相匹配的38名正常单胎妊娠孕妇（对照组）。采集胎儿AOI、脐动脉（UA）、静脉导管（DV）的多普勒频谱,计算IFI,并分为Ⅰ~Ⅲ型,计算PE组胎儿AOI、UA舒张期血流及心房收缩波（DA-a）消失或反向率。结果 对照组胎儿IFI均为Ⅰ型,IFI值为1.40±0.09,AOI舒张期血流均为前向;PE组胎儿IFI Ⅰ型21胎,Ⅱ型10胎,Ⅲ型7胎,IFI值为0.81±0.80;2组IFI差异有统计学意义（t=4.439,P<0.001）。PE组胎儿AOI、UA舒张期血流和DV-a波消失或反向率分别为44.74%（17/38）、13.16%（5/38）和0,与对照组比较差异有统计学意义（χ²=25.796,P<0.001）。结论 PE患者胎儿IFI降低。检测胎儿AOI多普勒频谱可于胎儿循环缺氧早期检测其血流动力学变化。     

胎儿超声心动图血流动力学参数与孕龄的关系

目的 探讨孕20~34周正常胎儿各孕周心脏房室瓣口、大动脉瓣口、胎儿静脉系统及重要生理通道的血流峰值速度随孕龄增长的变化规律。方法 回顾性分析2529名孕龄20~34周的正常单胎胎儿超声心动图资料,应用回归分析检测各参数与孕龄的相关性。结果 正常胎儿二尖瓣口和三尖瓣口舒张早期E峰、舒张晚期A峰和E峰/A峰,主动脉瓣口和肺动脉瓣口收缩期峰值流速,主动脉弓横弓部和动脉导管收缩期峰值流速和舒张期峰值流速,肺静脉左心房开口处收缩期S峰、舒张期D峰和心房收缩期A峰均随孕周增加略有增加;下腔静脉收缩期S峰、舒张期D峰及心房收缩期A峰无明显变化。上述胎儿血流动力学参数均与孕周存在相关关系(P均<0.05)。结论 胎儿超声心动图技术可评价心脏血流动力学状态,为胎儿超声心动图检查提供指导。     

产前超声诊断静脉导管缺失及走行异常

目的 探讨胎儿静脉导管(DV)缺失及走行异常的产前超声图像特征及其临床意义。方法 回顾性分析本院诊断为胎儿DV缺失及走行异常9胎的临床及声像图特征。结果 7胎DV缺失,脐静脉直接回流至右心房伴静脉导管缺失;2胎DV走行异常,1胎汇入冠状静脉窦,1胎汇入肝静脉。胎儿结局:5胎因合并畸形引产,1胎生后由于膈疝缺口太大及肺发育不良死亡,1胎28周早产死亡,2胎生后暂未见明显异常;8胎合并其他畸形,1胎孤立性DV走行异常;7胎合并心内畸形,3胎合并心外畸形。结论 产前超声检查可诊断DV缺失及走行异常;应结合畸形严重程度及染色体检查结果评价预后。     

产前超声检测中孕期胎儿心脏发育

目的 建立21~25孕周正常胎儿心脏解剖结构及血流动力学情况的正常参考值范围。方法 采用节段分析法对203胎中孕期(21~25周)正常妊娠单胎胎儿行超声心动图检查,测定心脏房室、肺动脉、主动脉、动脉导管内径及房室瓣血流速度、半月瓣血流速度、动脉导管血流速度及静脉导管血流速度。对各测量值与孕周行直线回归分析。结果 ①心脏各房室、大血管及动脉导管内径随孕周增加而增大;②肺动脉与升主动脉内径比值不随孕周改变;③房室瓣口血流峰值流速不随孕周改变;④三尖瓣及二尖瓣血流A峰大于E峰;⑤半月瓣口、动脉导管、静脉导管血流峰值流速随孕周增加而增大。结论 建立21~25孕周胎儿心血管各结构内径及血流动力学的正常参考值范围,可为筛查胎儿先天性心脏病提供参考。     

冠状动脉扩张是胎儿生长受限预后不良的独立危险因素

目的探讨冠状动脉扩张在胎儿生长受限(FGR)中的预后评估价值。方法收集2019年1月~2020年12月我院超声诊断并出生后证实FGR胎儿73例,超声观察冠状动脉(CA)扩张、脐动脉、大脑中动脉(MCA)、静脉导管的血流频谱特征。根据胎儿妊娠结局分为预后良好组和预后不良组,比较胎儿的一般情况及胎儿不同血流异常情况,以超声变量特征建立Logistic回归模型,并绘制受试者工作特征曲线,评价Logistic回归模型对胎儿不良预后的预测价值。结果FGR胎儿预后不良组27例,预后良好组46例,在脐动脉异常、静脉导管异常、CA扩张组比较差异有统计学意义(P < 0.05),MCA异常组未见明显统计学意义(P>0.05)。Logistic回归分析显示CA扩张、脐动脉异常、静脉导管异常组OR值分别为9.715、4.956、11.291,为胎儿不良预后的独立的危险因素。以CA扩张、脐动脉异常、静脉导管异常3组变量建立的Logistic回归模型预测FGR胎儿不良预后(回归值>0.356)的曲线下面积为0.874,敏感度为81.48%,特异性为91.30%。结论冠状动脉扩张是FGR预后不良的独立的危险因素。以CA扩张、脐动脉异常、静脉导管异常3个血流异常变量建立的Logistic回归模型能够有效预测FGR不良预后。      

Middle cerebral artery peak systolic and ductus venosus velocity waveforms in the hydropic fetus.

OBJECTIVE: The purpose of this study was to assess whether Doppler assessment of the middle cerebral artery (MCA) peak systolic velocity (PSV) and ductus venosus (DV) velocity waveforms during sonography of hydropic fetuses may specify the cause of fetal hydrops. METHODS: A level II sonographic examination was performed in 16 hydropic fetuses, and the MCA PSV and DV velocity waveforms were assessed. The MCA PSV values divided hydropic fetuses into anemic (group 1) and nonanemic (group 2) fetuses. In group 2 fetuses, the DV was defined as normal or abnormal. Sonographic examination and Doppler assessment of these vessels specified the cause of hydrops and indicated the use of specific investigations for diagnosing the etiology of fetal hydrops. RESULTS: Seven of 16 fetuses had MCA PSV values greater than 1.50 multiples of the median (group 1). Nine of 16 fetuses had normal MCA PSV values (group 2); among them, 7 of 9 had either absent or reversed flow in the DV, and 2 had a normal DV. In group 1, the cause of fetal anemia was investigated by maternal serum tests, and 5 cordocentesis procedures were performed. In group 2, 7 of 9 fetuses had reversed flow in the DV, which suggested a cardiac abnormality confirmed by echocardiography. Five cordocentesis procedures were performed for fetal karyotype, and in 2 fetuses, the cause of hydrops was idiopathic. CONCLUSIONS: Our data suggest that assessment of the MCA PSV and DV velocity waveforms in the hydropic fetus may further our knowledge of the etiology of hydrops and may indicate which investigations among the many available should be used for diagnosing the cause of fetal hydrops.     

胎儿静脉导管闭锁产前超声表现

目的 观察静脉导管(DV)闭锁胎儿产前超声表现。方法 回顾性分析20胎DV闭锁胎儿产前超声表现，记录妊娠结局。结果 20胎DV位置及走行均正常，其中16胎(16/20,80.00%)DV管壁呈等回声，3胎(3/20,15.00%)管壁呈条索状强回声，1胎(1/20,5.00%)DV管壁回声增强，其内为低回声，呈“双轨”征；CDFI均未见DV内存在血流信号。3胎(3/20,15.00%)合并其他结构畸形，包括2胎永存右脐静脉(其中1胎染色体异常)和1胎肺动脉交叉。19胎(19/20,95.00%)出生后证实为DV闭锁，出生后新生儿Apgar评分、体质量及随访均未见异常；1胎(1/20,5.00%)死于宫内，经尸检确定DV闭锁。结论 胎儿DV闭锁产前超声可见管壁呈等回声、条索状强回声或“双轨”征，腔内无血流信号。     

Effect of antenatal glucocorticoid therapy on arterial and venous blood flow velocity waveforms in severely growth-restricted fetuses.

OBJECTIVE: To study the effects of antenatal glucocorticoid (betamethasone) therapy on blood flow velocity waveform patterns in the umbilical artery (UA), middle cerebral artery (MCA) and ductus venosus (DV) in severely intrauterine growth-restricted (IUGR) fetuses. METHODS: Fifty-five severely IUGR fetuses at 24-34 weeks of gestation were included in the study. The effect of antenatal glucocorticoid administration on Doppler findings in the UA, MCA and DV was studied using two statistical approaches, namely paired sample analysis and multilevel analysis. RESULTS: There were no effects of betamethasone on the pulsatility index (PI) of the vessels studied. The only changes noticed during the 14 days of observation were a gradual decrease of PI in the MCA, an increase in the UA-PI/MCA-PI ratio and an increase in the DV-PI. These changes with time may be explained by a progressive and gradual deterioration of the fetal condition. CONCLUSION: Antenatal glucocorticoids (betamethasone) do not affect fetal Doppler waveform patterns of the UA, MCA and DV in severely IUGR fetuses.     

胎儿静脉导管异位引流至冠状静脉窦产前超声表现:3例报告及文献复习

目的 结合文献及3例临床所见,观察胎儿静脉导管（DV）异位引流至冠状静脉窦（CS）产前超声表现。方法 回顾性分析3胎DV异位引流至CS胎儿,结合文献复习观察其产前超声特征。结果 产前超声于3胎四腔心后切面均见CS扩张,内径分别为3.6、8.2及4.8 mm;DV异位引流至扩张的CS。于1胎（序号1）见4支肺静脉汇入左心房（LA）,DV经房间隔后方于左心房顶绕行至扩张的CS;1胎（序号2）三血管气管切面肺动脉主干左侧见永存左上腔静脉（PLSVC）,旋转探头追踪观察发现DV与CS相连;1胎（序号3）4支肺静脉均回流入LA,三血管气管切面见主动脉弓位于气管右侧、左锁骨下动脉起自降主动脉起始部。结论 产前超声观察胎儿DV异位引流至CS四腔心后切面可见CS扩张,并可合并其他血管畸形。     

胎儿Ⅲ＆#176;房室传导阻滞产前超声心动图分析

目的：总结Ⅲ°房室传导阻滞（CAVB）胎儿超声心动图特征。方法应用二维超声、M型超声及多普勒技术对10例Ⅲ°房室传导阻滞胎儿进行超声心动图检查,观察胎儿心房与心室节律及其对应关系,同时观察二尖瓣、左心室流入道及流出道、静脉导管血流频谱,并对胎儿心脏大小、心功能、房室瓣反流及心包积液等心脏结构进行观察,对Ⅲ°房室传导阻滞胎儿超声心动图特征进行总结分析。结果二维超声心动图检查提示10例Ⅲ°房室传导阻滞胎儿中2例存在心内外畸形,8例无明显心内外畸形。Ⅲ°房室传导阻滞胎儿M型超声心动图特征为房室节律分离,心房节律保持在正常范围而心室节律缓慢,多普勒超声心动图特征为二尖瓣频谱提示E峰频率缓慢,A峰频率明显快于E峰频率,E、A峰无固定对应关系。胎儿超声心动图检查提示,孕妇就诊时10例胎儿中6例心脏扩大,5例心功能不全,6例房室瓣反流,7例心包积液。超声心动图检查后10例孕妇均选择引产。结论Ⅲ°房室传导阻滞是对胎儿心功能有重要影响的缓慢型心律失常,预后不佳。M型超声结合多普勒技术可对Ⅲ°房室传导阻滞胎儿进行诊断及鉴别,对临床干预治疗及判断胎儿预后有重要意义。     

Cardiovascular hemodynamics and umbilical artery N-terminal peptide of proB-type natriuretic peptide in human fetuses with growth restriction.

OBJECTIVE: To test our hypothesis that human fetal N-terminal peptide of proB-type natriuretic peptide (NT-proBNP) secretion is increased in proportion to the severity of fetal cardiovascular compromise in intrauterine growth restriction. METHODS: This prospective cross-sectional study consisted of 42 growth-restricted fetuses who underwent Doppler ultrasonographic examination of cardiovascular hemodynamics within 7 days before delivery. Group 1 fetuses (n = 13) had normal umbilical artery (UA) velocimetry. Group 2 fetuses (n = 15) had abnormal UA and normal ductus venosus (DV) velocimetry. In Group 3 fetuses (n = 14), both UA and DV velocimetries were abnormal. At delivery, an UA blood sample was obtained for assessment of NT-proBNP. Normal values for UA NT-proBNP were determined in 49 neonates (control group) with uncomplicated pregnancy and delivery. RESULTS: Group 3 fetuses demonstrated greater (P < 0.05) UA and descending aorta pulsatility indices (PIs) and greater DV, left hepatic vein (LHV) and inferior vena cava PIs for veins (PIVs) than fetuses in Groups 1 and 2. Weight-indexed cardiac outputs and ventricular ejection forces were similar among the groups. Group 3 fetuses had higher (P < 0.05) UA NT-proBNP concentration than fetuses in Groups 1 and 2. In the control group, the 95(th) percentile value of UA NT-proBNP was 518 pmol/L. In Group 3, 13/14 neonates demonstrated abnormal UA NT-proBNP levels. The corresponding incidences were 4/13 and 7/15 in Groups 1 and 2. Significant positive correlations were found between UA, DV and LHV PIVs and UA NT-proBNP concentrations. CONCLUSION: In human fetal growth restriction, increased cardiac afterload and pulsatility in DV blood velocity waveform pattern are associated with elevated UA NT-proBNP concentrations.     

The short-term effect of nifedipine tocolysis on placental, fetal cerebral and atrioventricular Doppler waveforms.

OBJECTIVE: To evaluate the effect of nifedipine on placental and fetal middle cerebral and atrioventricular Doppler waveforms. METHODS: Doppler waveforms of uterine (UtA), umbilical (UA) and middle cerebral (MCA) arteries and both atrioventricular valves were measured from 21 pregnant women/fetuses prior to and during nifedipine therapy for preterm labor. Maternal and fetal heart rates (FHR), maternal systolic and diastolic blood pressure, the Doppler pulsatility index and systolic/diastolic ratio of the UtA, UA and MCA were measured. The total time velocity integrals (TVI) of tricuspid and mitral valves and their E-wave/A-wave (E/A) TVI ratios were measured. Wilcoxon signed pairs test was used to compare the differences in Doppler parameters before and at 3 h after nifedipine loading up to a maximum dose of 40 mg. RESULTS: Fetal arterial and UtA Doppler parameters were not different before and after nifedipine therapy. Blood flow across the atrioventricular valves and the TVI were equally unaffected by nifedipine. The TVI x FHR product was also unchanged following nifedipine therapy. CONCLUSIONS: In women with otherwise uncomplicated pregnancies, nifedipine loading and tocolysis are generally well tolerated by the mother. Placental and fetal cerebral arterial blood flow, fetal systolic and diastolic cardiac function and downstream distribution of fetal cardiac output are unaffected by nifedipine loading. These results apply to women with unchanged vital parameters. Further studies are necessary to show long-term effects of nifedipine therapy and may help to refine choice of tocolytic agents.     

Fetal hemodynamics evaluated by Doppler velocimetry in the second half of pregnancy

The objective of our study was to assess fetal hemodynamics by Doppler velocimetry during the second half of pregnancy. We carried out a longitudinal study on 33 normal fetuses between the 22nd and 38th weeks of gestation. Doppler velocimetry was performed in the aorta, suprarenal (SRA) and infrarenal (IRA) segments, middle cerebral artery (MCA) and umbilical artery (UA), on the basis of fetal peak systolic velocity (SV), end-diastolic velocity (DV) and resistance index (RI). We used a sample volume of 1 mm, a wall filter of 50 to 100 Hz, a 5 degrees to 19 degrees insonation angle in the MCA and UA, and below 60 degrees in the SRA and IRA. Between the 22nd and 38th weeks of gestation, SV and DV increased in all fetal arteries (p<0.05), but SV decreased in the UA from 52.5 to 46.2 cm/s between the 34th and 38th gestational weeks (p<0.05). The RI was unchanged in the SRA and throughout most of the gestational weeks in the IRA (p>0.05), but decreased from 0.69 to 0.56 in the UA (p<0.05). In the MCA, it decreased from 0.85 to 0.75 between the 26th and 38th gestational weeks (p<0.05). In conclusion, the volume of blood flow in the fetal organs necessary for their development is related to increased SV and DV and to decreased RI. The Doppler velocimetry measurements for normal fetuses could be compared with those for fetuses in high-risk pregnancies.