OBJECTIVETo evaluate the detection and accuracy of fetal echocardiography for congenital heart defects among high-risk populations.

METHODSA prospective observational study of prenatal diagnosis of congenital heart disease was conducted in two tertiary obstetrics and gynecology hospitals between January 2003 and December 2004. Consecutive fetuses at risk of congenital heart disease underwent detailed fetal echocardiography during the study period. B-mode and colour/pulsed Doppler flow imaging were used in all cases. Follow-up was sought for all pregnancies. Indications for referral, maternal and gestational age at diagnosis, as well as prenatal and postnatal diagnosis were recorded prospectively. By comparing prenatal and postnatal diagnoses, sensitivity, specificity, and predictive values were estimated.

RESULTSA series of 2063 high-risk fetuses underwent detailed fetal echocardiography during the study period. The mean gestational age at examination was 26.5 weeks, ranging from 16 to 42 weeks. The most common indications for fetal echocardiography were advanced maternal age (31.7%), fetal arrhythmias (13.5%) and maternal infections (10.4%). Forty-three cases of fetal congenital heart disease were detected. The mean gestational age at prenatal diagnosis was 27.3 weeks ranging from 16 to 40 weeks. There were 3 false-negatives and 1 false-positive. The sensitivity, specificity, positive and negative predictive values were 92.1%, 99.9%, 97.2%, and 99.8%, respectively. Diagnostic accuracy was 86.1%. A cardiac defect suspected on routine prenatal sonography accounted for the highest proportion of abnormal cases (67.4%). As for pregnancy outcome, there were 24 (52.1%) terminations; 2.2% died in utero, 13% postnatally, and 28.3% survived.

CONCLUSIONS(1) Fetal congenital heart disease can be identified reliably by prenatal echocardiography. (2) Possible congenital heart disease or suspected heart defect noted on a screening obstetric sonogram is an important indication for fetal echocardiography. (3) A sequential segmental approach is critical for correct evaluation of the cardiac malformation. (4) The outcome of the patients with congenital heart disease is poor and a multidisciplinary approach is needed to the parental counseling and perinatal management planning.

China ; epidemiology ; Early Diagnosis ; Female ; Fetal Heart ; abnormalities ; diagnostic imaging ; pathology ; Fetus ; abnormalities ; Follow-Up Studies ; Gestational Age ; Heart Defects, Congenital ; diagnostic imaging ; epidemiology ; pathology ; Humans ; Mass Screening ; Pregnancy ; Prospective Studies ; Sensitivity and Specificity ; Ultrasonography, Prenatal

OBJECTIVETo evaluate the prenatal diagnostic accuracy of fetal echocardiography for congenital heart defects.

METHODSFetal echocardiographic databases from 2001 to 2007 were searched for patients with a prenatal diagnosis of congenital heart defect, medical records were obtained and the prenatal echocardiographic findings were correlated with postnatal echocardiography results or autopsy findings, if the pregnancy was terminated or the fetus died in utero.

RESULTSPrenatal diagnosis of congenital heart defects was made in 113 pregnancies at a mean gestational age of 26.8 weeks. Pathology or postnatal echocardiography was available in 79 cases (70%) and the accuracy of prenatal diagnosis was 86% (68/79). Prenatal diagnosis was accurate in 24 of 31 patients (77%) with conotruncal malformations, 26 of 27 patients (96%) with septal defects, 9 of 10 patients (90%) with valve abnormalities, and 5 of 6 patients (83%) with univentricular hearts. There were 4 false-positives and the positive predictive value was 95% (75/79).

CONCLUSIONFetal echocardiography is a reliable tool for prenatal diagnosis of congenital heart defects despite limitations for correctly diagnosing some specific fetal heart defects.

Echocardiography ; Female ; Fetal Heart ; diagnostic imaging ; Heart Defects, Congenital ; diagnostic imaging ; Humans ; Pregnancy ; Pregnancy Trimester, Second ; Pregnancy Trimester, Third ; Retrospective Studies ; Ultrasonography, Prenatal

Objective: To explore the pathogenic mechanism of the miR-340/high mobility group box 1 (HMGB1) axis in the formation of liver fibrosis. Methods: A rat liver fibrosis model was established by injecting CCl(4) intraperitoneally. miRNAs targeting and validating HMGB1 were selected with gene microarrays after screening the differentially expressed miRNAs in rats with normal and hepatic fibrosis. The effect of miRNA expressional changes on HMGB1 levels was detected by qPCR. Dual luciferase gene reporter assays (LUC) was used to verify the targeting relationship between miR-340 and HMGB1. The proliferative activity of the hepatic stellate cell line HSC-T6 was detected by thiazolyl blue tetrazolium bromide (MTT) assay after co-transfection of miRNA mimics and HMGB1 overexpression vector, and the expression of extracellular matrix (ECM) proteins type I collagen and α-smooth muscle actin (SMA) was detected by western blot. Statistical analysis was performed by analysis of variance and the LSD-t test. Results: Hematoxylin-eosin and Masson staining results showed that the rat model of liver fibrosis was successfully established. Gene microarray analysis and bioinformatics prediction had detected eight miRNAs possibly targeting HMGB1, and animal model validation had detected miR-340. qPCR detection results showed that miR-340 had inhibited the expression of HMGB1, and a luciferase complementation assay suggested that miR-340 had targeted HMGB1. Functional experiments results showed that HMGB1 overexpression had enhanced cell proliferation activity and the expression of type I collagen and α-SMA, while miR-340 mimics had not only inhibited cell proliferation activity and the expression of HMGB1, type I collagen, and α-SMA, but also partially reversed the promoting effect of HMGB1 on cell proliferation and ECM synthesis. Conclusion: miR-340 targets HMGB1 to inhibit the proliferation and ECM deposition in hepatic stellate cells and plays a protective role during the process of liver fibrosis.
Animals ; Rats ; Cell Proliferation ; Collagen Type I/metabolism* ; Fibrosis ; Hepatic Stellate Cells ; HMGB1 Protein/genetics* ; Liver Cirrhosis/pathology* ; MicroRNAs/metabolism*