Backgroud: The clinical efficacy and safety of cervical pessary versus cervical cerclage in preventing spontaneous preterm birth remain uncertain. Objectives: To systematically review the clinical efficacy of cervical pessary versus transvaginal cervical cerclage in preventing spontaneous preterm birth caused by cervical shortening. Search Strategy: The Cochrane Library, PubMed, EMbase, WanFang Data, CNKI, VIP Data and CBM Data were electronically searched. Selection Criteria: Randomized controlled trials (RCTs) and non-randomized controlled trials (non-RCTs, including cohort studies) comparing cervical pessary and transvaginal cervical cerclage in preventing spontaneous preterm birth from the inception of the database to August 2020. Main Results: A total of 9 studies (2 RCTs and 7 non-RCTs) were included, involving 1174 patients with a short cervix in the second trimester (cervical length <25mm), 693 in the cervical pessary group and 481 in the cervical cerclage group. The results of meta-analysis showed that the incidence of preterm premature rupture of the membranes (PPROM) in the cervical pessary group was significantly lower than that in the cervical cerclage group (RR=0.48, 95% CI: 0.35 to 0.67, P<0.00001), and the premature birth rate before 34 weeks in the cervical pessary group was also significantly lower than that in the cervical cerclage group (RR=0.68, 95%CI: 0.51 to 0.89, P<0.006). Conclusion: Compared with transvaginal cervical cerclage, use of a cervical pessary may decrease the risks of PPROM and premature birth before 34 weeks. Given its advantages of easy-to-use and minimal damage, cervical pessary may become a useful preventive intervention that deserves widespread clinical application.

Methods The study included 59 patients with normal fetal heart structure, blood flow, and heart rhythm (fetal abnormality-negative group) and 50 patients with abnormal fetal heart structure, blood flow, and/or heart rhythm (fetal abnormality-positive group). aCMQ was performed in both groups to obtain left and right ventricular endocardial global longitudinal strain (GLSendo), mid-myocardial global longitudinal strain (GLSmid), and epicardial global longitudinal strain (GLSepi). Parameters between the two groups were compared and correlation analyses performed. A deformation analysis was performed by two trained observers, and reproducibility was assessed. Results The fetal left ventricular and right ventricular global longitudinal strain (LV-GLS and RV-GLS, respectively) decreased in a gradient from the endocardium to the epicardium. LV-GLS and RV-GLS of all myocardial layers were lower in the fetal abnormality-positive than -negative group (all P<0.05). Correlation analysis showed that neither LV-GLS nor RV-GLS was significantly correlated with gestational age in the fetal abnormality-negative group (all P>0.05), whereas left ventricular GLSendo, GLSmid, and GLSepi were negatively correlated with gestational age in the fetal abnormality-positive group (r=−0.39 to −0.44, all P<0.05). Repeatability testing showed that the inter-observer and intra-observer intraclass correlation coefficients for LV-GLS and RV-GLS in each myocardial layer were >0.75 (all P<0.001). Conclusions As a new speckle tracking echocardiography tool, aCMQ has feasibility and repeatability in evaluating myocardial deformation of the fetal ventricle. This technique might provide helpful information on ventricular myocardial deformation in fetal hearts with abnormal structure or rhythm for clinical guidance in pregnancy.

We report what apprears to be the first case of fetal noncompaction cardiomyopathy in both ventricles accompanied by a mutation in the calmodulin gene (CALM2): A 25-year-old woman was referred to our hospital at 25+1 weeks of gestation for evaluation of fetal defects. A postnatal echocardiography showed biventricular noncompaction cardiomyopathy. After terminated the pregnancy, fetal noncompaction cardiomyopathy was comfirmed by autopsy and histopathologic examination. And the whole-exome sequencing of genomic DNA demonstrated a de novo heterozygous mutation (c.389A>G;p.D130G) in CALM2, whereas the parents were normal. In this case report, we highlight the gene mutation in noncompaction cardiomyopathy.