目的 研究胎儿持续性心动过缓的病因、发病机制、胎儿期临床表现及预后。方法 回顾性分析2014年1月至2019年5月在广东省妇幼保健院产前诊断就诊并在本院超声科诊断为胎儿心动过缓的病例。结果 收集胎儿心动过缓临床病例17例。其中心脏畸形合并心动过缓7例， 占41%，6例引产，1例手术治疗，现2岁无异常。窦性心动过缓未合并心脏结构异常病例4例，占24%，其中2例母体抗SmD1阳性，1例母体有甲减病史，3例出生后正常，1例引产。房室传导阻滞6例，占35%，其中母体抗ANA谱阳性例3例，占50%；2例胎儿（其中1例为单绒毛膜双羊膜囊双胎之一）出生后装起搏器，现无异常，1例未接受治疗，观察中，幼儿心率60余次/分，现4岁；2例失访。结论 合并严重的心脏畸形的心动过缓胎儿预后较差；未合并心脏畸形及其他异常的心动过缓胎儿出生后与后较好，可能与母体抗SmD1阳性相关；房室传导阻滞的胎儿出生后部分需要接受起搏器治疗，胎儿的房室传导阻滞不仅与母体自身抗体相关，与胎儿本身的易感性相关。
Objective To investigate the etiology ,pathogenesis, clinical manifestations and prognosis of fetal persistent bradycardia. Methods A retrospective analysis fetuses with persistent bradycardia identified by M-mode and pulsed Doppler echocardiography in genetic medical center between January 2014 and May 2019.Results A total of 17 fetuses were found bradycardia. 7 fetuses were found to have cardiac malformation combined with bradycardia（41%）, of whom 6 fetuses were terminated, only one fetal have birth, now 2 years old without abnormalities. Sinus bradycardia without cardiac structural abnormalities was noted in 4 fetuses（24%）,Among them, 2 fetuses whose mother showed anti-SmD1, 1 fetal of whose mother had a history of hypothyroidism, 3 cases were normal after birth, and 1 case was terminated.. 6 cases was atrioventricular block(35%), of which 3 cases were positive for maternal anti-ANA spectrum(50%); 2 fetuses (one of which was monochorionic double amniotic sac twins) after birth pacing. There was no abnormality in the case, and 1 case was not treated. During the observation, the heart rate of the child was more than 60 times/min, now 4 years old; 2 cases were lost to follow-up. Conclusions The prognosis of patients with severe cardiac malformation with bradycardia is poor. The fetuses without cardiac malformation and other abnormal bradycardia are better after birth and may be related to maternal anti-SmD1 positive; fetus with atrioventricular block Part of the body needs to be treated with pacemaker after birth. The fetal atrioventricular block is not only related to the maternal autoantibodies, but also to the susceptibility of the fetus itself.
