Asymmetric Occluder Occlusion of Outlet Ventricular Septal Defect Via a Subaxillary Approach.

BACKGROUND: Surgical transpleural minimally invasive occlusion of perimembranous and muscular ventral septal defects provides excellent results, but there is limited experience in outlet ventral septal defects (OVSDs) because of the specific anatomy and because OVSDs may occur with aortic valve prolapse. METHODS: The procedure was performed in 84 children (mean age, 2.5 ± 2.3 years; mean weight, 12.1 ± 10.3 kg) between July 2014 and December 2018 at the Children's Heart Center of Henan Provincial People's Hospital. An approximately 2-cm right subaxillary incision was made, and the right ventricle was punctured under transesophageal echocardiographic guidance. The OVSD was occluded under transesophageal echocardiographic guidance with an asymmetric occluder. RESULTS: Mean size of the OVSDs and the occluders was 4.6 ± 1.0 and 6.2 ± 1.2 mm, respectively. No patients died and no complications occurred, such as third-degree atrioventricular block, new aortic regurgitation, reoperation, or serious infection. All patients were observed for 32.1 ± 17.1 months. After surgery, there were 4 cases of residual shunt, which resolved spontaneously during follow-up. No complications, such as reoperation, aortic regurgitation, atrioventricular block, or occluder detachment, were observed during the follow-up period. CONCLUSIONS: Occluding OVSDs using an asymmetric occluder through the subaxillary approach was safe and effective, with satisfactory short-term and mid-term results. Further follow-up is required regarding the long-term results.

FOXD3-AS1 Knockdown Suppresses Hypoxia-Induced Cardiomyocyte Injury by Increasing Cell Survival and Inhibiting Apoptosis via Upregulating Cardioprotective Molecule miR-150-5p In Vitro.

Congenital heart disease (CHD) is the most common type of human innate malformation in fetuses. LncRNAs have been pointed to play critical regulatory roles in various types of cardiac development and diseases including CHD. Our study aimed to explore the effects of lncRNA forkhead box D3 antisense RNA 1 (FOXD3-AS1) on hypoxia-induced injury in AC16 cardiomyocytes and the related molecular mechanism. In vitro cell model of CHD was established by stimulating AC16 cells with hypoxia (1% O2). Expression of FOXD3-AS1 and miR-150-5p was detected by qRT-PCR. Hypoxia-induced injury was evaluated by detecting cell survival, lactate dehydrogenase (LDH) release, apoptosis, and caspase-3/7 activity using MTT, LDH assay, flow cytometry analysis, and caspase-3/7 activity assay, respectively. The regulatory relationship between FOXD3-AS1 and miR-150-5p was explored by luciferase reporter assay, RNA immunoprecipitation (RIP), and qRT-PCR. Results showed that hypoxia exposure caused an upregulation of FOXD3-AS1 and a downregulation of miR-150-5p in AC16 cells. Knockdown of FOXD3-AS1 attenuated reduction of cell survival and increase of LDH release, apoptosis, caspase-3/7 activity, and Bcl-2 associated X (Bax) expression induced by hypoxia in AC16 cells. Notably, we demonstrated that FOXD3-AS1 directly interacted with miR-150-5p to inhibit its expression. miR-150-5p knockdown reinforced the reduction of survival and induction of apoptosis by hypoxia and attenuated the effects of FOXD3-AS1 silencing on the same parameters in AC16 cells. In conclusion, FOXD3-AS1 knockdown protected AC16 cardiomyocytes from hypoxia-induced injury by increasing cell survival and inhibiting apoptosis through upregulating miR-150-5p.

Prenatal echocardiographic classification and prognostic evaluation strategy in fetal pulmonary atresia with intact ventricular septum.

Fetal pulmonary atresia with intact ventricular septum (PA/IVS) is a rare congenital heart disease. The present study aimed to classify PA/IVS and determine the relationship between prenatal echocardiographic characteristics and postnatal biventricular or univentricular repair strategies.A total of 51 fetuses with PA/IVS were examined from 2012 to 2019. Data on prenatal echocardiography, associated anomaly, karyotype, and outcome were collected. Two-dimensional measurements included tricuspid valve (TV) z-score, mitral valve (MV) z-score, TV/MV ratio, and ratio of right to left ventricle (RV/LV) length, whereas color Doppler measurements included degree of tricuspid regurgitation (TR), ventriculo-coronary artery communication (VCAC), tricuspid inflow duration (TID), cardiac cycle duration (CCD), middle cerebral artery pulsatility index (MCA PI), and umbilical artery pulsatility index (UA PI). Diagnostic classification was based on the development of RV and the presence or absence of VCAC. Postnatal evaluation was divided according biventricular or univentricular repair.Of the 51 fetuses with PA/IVS, 20 were type I, 17 were type II, and 14 were type III. Only one fetus exhibited right aortic arch. The karyotype of all the fetuses was normal. Of the 28 patients who underwent postnatal surgery, 13 (46%) underwent biventricular repair and 15 (54%) underwent univentricular repair. TV z-score was significantly higher for the biventricular repair group compared with univentricular repair group (-1.20 ±â€Š0.98 vs -4.33 ±â€Š0.80, P = .000). TV/MV, RV/LV length, and TID/CCD were significantly higher for the biventricular repair group than the univentricular repair group (0.81 ±â€Š0.14 vs 0.54 ±â€Š0.09, 0.71 ±â€Š0.11 vs 0.49 ±â€Š0.09, 39.20 ±â€Š3.84 vs 29.16 ±â€Š4.58, P = .000). Moderate or severe TR and VCAC were significantly different between the 2 groups (P = .000). Gestational age, MCA PI, and UA PI did not differ between the 2 groups (P = .72, P = .36, P = .06). The cutoff values for the biventricular repair characteristic curves were TV z-score >-3.28, TV/MV ratio >0.71, RV/LV length >0.62, and TID/CCD >33.95%. The sensitivities of the TV z-score, TV/MV, RV/LV length, and TID/CCD were 100%, 77%, 85%, and 92%, respectively. The specificities of the TV z-score, TV/MV, RV/LV length, and TID/CCD were 94%, 100%, 100%, and 94%, respectively.Fetal echocardiography was able to classify PA/IVS according to variable degree of RV and VCAC. In fetal PA/IVS, TV z-score >-3.28, TV/MV >0.71, RV/LV length >0.62, TID/CCD >33.95%, moderate and severe TR, and the absence of VCAC were associated with postnatal biventricular repair strategy. These findings may have implications for prenatal counseling and prediction of fetal outcome.

miR-9 knockdown inhibits hypoxia-induced cardiomyocyte apoptosis by targeting Yap1.

AIMS: Aberrantly expressed miRNAs are demonstrated to be involved in the development of congenital heart disease (CHD). miR-9 was proposed to be upregulated in cardiac tissues from CHD cases. However, the role of miR-9 in hypoxia-induced cardiomyocytes and the potential mechanism are far from being addressed. MAIN METHODS: qRT-PCR and western blot analysis were performed to detect miR-9 and Yes-associated protein 1 (Yap1) expressions in hypoxic H9c2 cells. CCK-8, flow cytometry analysis, caspase-3/7 activity assay were applied to evaluate cell proliferation, apoptosis, and caspase-3/7 activity, respectively. The interaction between miR-9 and Yap1 was explored by luciferase reporter assay, qRT-PCR and western blot. KEY FINDINGS: miR-9 was upregulated and Yap1 was downregulated in H9c2 cells in response to hypoxia in a time-dependent manner. Knockdown of miR-9 promoted cell proliferation, and inhibited apoptosis and caspase-3/7 activity in hypoxic H9c2 cells, while miR-9 overexpression exerted the opposite effects on hypoxic H9c2 cells. In addition, Yap1 was a direct target of miR-9 in H9c2 cells. Yap1 knockdown suppressed cell proliferation and promoted apoptosis in hypoxia-exposed H9c2 cells. Yap1 knockdown attenuated the effect of anti-miR-9 on cell proliferation and apoptosis in hypoxia-exposed H9c2 cells. SIGNIFICANCE: miR-9 knockdown inhibited hypoxia-induced cardiomyocyte apoptosis by targeting Yap1. Our study provided a novel insight into the mechanism of the adaptation of cardiomyocytes to chronic hypoxia.

Short-Term and Mid-Term Results of Minimally Invasive Occlusion of Ventricular Septal Defects via a Subaxillary Approach in a Single Center.

This retrospective, single-center study evaluated short-term and mid-term results of minimally invasive surgery to occlude ventricular septal defects (VSDs) using a subaxillary approach. The procedure was performed on 429 children (224 boys, 205 girls; age 2.4 ± 2.5 years; mean weight 12.7 ± 10.1 kg) between January 2014 and December 2016 at the Children's Heart Center of Henan Province People's Hospital. An approximately 2-cm subaxillary incision was made between the third and fifth ribs, and the appropriate right atrium or ventricle was punctured under the guidance of transencephalographic echocardiography (TEE). The VSD was then occluded under TEE guidance. The mean size of the VSDs was 4.2 ± 1.0 mm, and the occluder measured 5.3 ± 1.3 mm. Asymmetrical occluders were used in 44 patients and symmetrical occluders in 385 patients. The operative time was 60.7 ± 21.3 min, and time in the intensive care unit was 20.9 ± 6.5 h. Blood loss was 12.4 ± 14.4 ml. There were no deaths among these patients. Occluder displacement occurred in two cases. There were no complications (e.g., third-degree atrioventricular block, new aortic regurgitation, reoperation for massive bleeding, serious infection). All patients were followed for 6-48 months, during which time there were ten cases of a postoperative residual shunt, which self-closed in eight during follow-up. The other two cases are still being followed. No complications occurred during follow-up (e.g., reoperation, aortic regurgitation, atrioventricular block, occluder abscission). Occluding VSDs using the subaxillary approach is safe and effective. Short-term and mid-term results are satisfactory. Further follow-up is required regarding long-term results.

Investigating the characteristics of echocardiogram, surgical treatment, chromosome and prognosis for fetal right heart enlargement: A STROBE-compliant article.

The prognosis of right heart enlargement varies according to different etiologies. The purpose of this study was to investigate the characteristics of echocardiogram, surgical treatment, chromosome and prognosis for fetal right heart enlargement.The foetal echocardiogram was performed on 3987 pregnant women, and then 88 fetuses with right heart enlargement were identified. The data about prenatal and postnatal echocardiograms, postnatal cardiac surgical treatment, karyotype analysis and autopsy after induced labor were analyzed in the 88 fetuses.Except the 1111 cases that had loss of follow-up, 2876 cases had complete data. Among the 2876 cases, right heart enlargement was identified in 88 fetuses. Of the 88 fetuses, 15 had total atrioventricular septal defect (unbalanced type: right ventricular dominance), 15 Ebstein's anomaly, 18 fallot tetrad, 14 double outlet right ventricle, 13 total anomalous pulmonary venous drainage, and 13 premature closure of ductus arteriosus. Chromosomal abnormality was found in 12 cases.There are many etiological factors causing right heart enlargement. The prognosis is better in the fetuses with single heart malformation than in the fetuses who have extracardiac malformation or/and chromosomal abnormality besides heart malformation. Fetal echocardiography combined with karyotype analysis can provide important bases for evaluating the prognosis of fetuses with right heart enlargement.

MiR-182 alleviates the development of cyanotic congenital heart disease by suppressing HES1.

miRNAs have been pointed to play critical roles in the protection and development of cyanotic congenital heart disease (CHD). MiR-182 is found to be associated with multiple heart diseases. However, little is known about the function and underlying mechanisms of miR-182 on cyanotic CHD. Here, H9c2 cells were exposed to hypoxia to construct the model of cyanotic CHD in vitro. qRT-PCR assay revealed that miR-182 expression was downregulated in serum samples from patients with cyanotic CHD and hypoxia-induced cardiomyocytes. Gain- and loss-of-function demonstrated that miR-182 overexpression promoted cell proliferation and suppressed apoptosis in hypoxia-induced H9c2 cells, while miR-182 knockdown repressed cell proliferation and promoted apoptosis. Dual-luciferase reporter assay verified that HES1 was a direct target of miR-182, and miR-182 repressed HES1 expression by binding to its 3'-UTR. Moreover, miR-182-mediated regulatory effect on cell proliferation and apoptosis was reversed by the restoration of HES1 expression. In conclusion, our study demonstrated that miR-182 exerted protection effect through suppressing HES1 in hypoxia-induced cardiomyocytes, highlighting its role as a potential therapeutic strategy for cyanotic CHD.

MiR-23a regulates the proliferation and migration of human pulmonary artery smooth muscle cells (HPASMCs) through targeting BMPR2/Smad1 signaling.

Pulmonary arterial hypertension (PAH) associated with congenital heart disease (CHD) (PAH-CHD) is a severe and progressive disease with a poor prognosis. MiR-23a, a member of miR-23a/24/27a cluster, has been reported to function as an important player in PAH. However, the detailed functions and molecular mechanisms of miR-23a in PAH-CHD are still not fully elucidated. Due to hypoxia is an important stimulus for pulmonary artery smooth muscle cells (PASMCs) proliferation and vascular remodeling, we assessed the expression and functions of miR-23a in hypoxia-induced HPASMCs. qRT-PCR assay revealed that miR-23a level was upregulated in plasma of PAH-CHD patients and hypoxia-induced HPASMCs. Loss-of-function experiments demonstrated that miR-23a depletion suppressed hypoxia-induced proliferation and migration in HPASMCs. Dual-luciferase reporter assay verified that bone morphogenetic protein receptor type 2 (BMPR2) was a direct target of miR-23a. Moreover, BMPR2 level was downregulated in plasma of PAH-CHD patients and hypoxia-induced HPASMCs. Additionally, BMPR2-mediated suppression on proliferation and migration of hypoxia-induced HPASMCs was abrogated by miR-23a overexpression. Furthermore, miR-23a directly affected BMPR2/Smad1 signaling in hypoxia-induced HPASMCs. In conclusion, miR-23a facilitated cell proliferation and migration by targeting BMPR2/Smad1 signaling in hypoxia-induced HPASMCs, providing a potential therapeutic target for PAH treatment.

Associations of GATA4 genetic mutations with the risk of congenital heart disease: A meta-analysis.

BACKGROUND: GATA4 gene is a cardiac transcriptional factor playing important role in cardiac formation and development. Three GATA4 gene mutations, 99 G>T, 487 C>T, and 354 A>C, have been reported in congenital heart disease (CHD). Therefore, a meta-analysis was performed to explore the associations between 99 G>T, 487 C>T, or 354 A>C mutations and the risk of CHD. METHODS: We searched the relevant studies in electronic databases, including ISI Science Citation Index, Embase, PubMed, CNKI, and Wan fang, from January 2006 to March 2016. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to estimate the associations between 99 G>T, 487 C>T, or 354 A>C mutations and the risk of CHD. RESULTS: A total of 11 studies including 2878 CHD cases and 3339 controls were evaluated. There was no significant association between GATA4 99 G>T (OR = 1.22, 95% CI = 0.74-2.01, P = .43) or 487 C>T (OR = 1.16, 95% CI = 0.48-2.78, P = .74) mutations and the risk of CHD, whereas GATA4 354 A>C (OR = 1.49, 95% CI = 1.15-1.93, P = .003) mutation was significantly associated with CHD risk. Subgroup analysis was further performed for GATA4 99 G>T, 487 C>T, and 354 A>C mutations based on sample size and ethnicity, and no significant association between GATA4 99 G>T or 487 C>T mutations and the risk of CHD was found in all subgroups, whereas GATA4 354 A>C mutation was significantly associated with CHD risk in large-sample-size and Asian subgroups. However, subgroup analysis by types of CHD indicated that there was no significant association between GATA4 354 A>C mutation and the risk of ventricular septal defects. CONCLUSIONS: Our findings suggested that GATA4 99 G>T and 487 C>T mutations may not be related to the incidence of CHD. However, GATA4 354 A>C mutation was significantly associated with CHD risk.

Whole exome sequencing identifies novel mutation in eight Chinese children with isolated tetralogy of Fallot.

BACKGROUND: Tetralogy of Fallot is the most common cyanotic congenital heart disease. However, its pathogenesis remains to be clarified. The purpose of this study was to identify the genetic variants in Tetralogy of Fallot by whole exome sequencing. METHODS: Whole exome sequencing was performed among eight small families with Tetralogy of Fallot. Differential single nucleotide polymorphisms and small InDels were found by alignment within families and between families and then were verified by Sanger sequencing. Tetralogy of Fallot-related genes were determined by analysis using Gene Ontology /pathway, Online Mendelian Inheritance in Man, PubMed and other databases. RESULTS: A total of sixteen differential single nucleotide polymorphisms loci and eight differential small InDels were discovered. The sixteen differential single nucleotide polymorphisms loci were located on Chr 1, 2, 4, 5, 11, 12, 15, 22 and X. Among the sixteen single nucleotide polymorphisms loci, six has not been reported. The eight differential small InDels were located on Chr 2, 4, 9, 12, 17, 19 and X, whereas of the eight differential small InDels, two has not been reported. Analysis using Gene Ontology /pathway, Online Mendelian Inheritance in Man, PubMed and other databases revealed that PEX5, NACA, ATXN2, CELA1, PCDHB4 and CTBP1 were associated with Tetralogy of Fallot. CONCLUSIONS: Our findings identify PEX5, NACA, ATXN2, CELA1, PCDHB4 and CTBP1 mutations as underlying genetic causes of isolated tetralogy of Fallot.

Application of array-comparative genomic hybridization in tetralogy of Fallot.

To explore the underlying pathogenesis and provide references for genetic counseling and prenatal gene diagnosis, we analyzed the chromosome karyotypes and genome-wide copy number variations (CNVs) in 86 patients with tetralogy of Fallot (TOF) by G-banding karyotype analysis and array-comparative genomic hybridization (aCGH), respectively. And then quantitative polymerase chain reaction was used to validate these candidate CNVs. Based on their different properties, CNVs were categorized into benign CNVs, suspiciously pathogenic CNVs, and indefinite CNVs. Data analysis was based on public databases such as UCSC, DECIPHER, DGV, ISCA, and OMIM.The karyotype was normal in all the 86 patients with TOF. CNVs were detected in 11 patients by aCGH and quantitative polymerase chain reaction. Patient no. 0001, 0010, and 0029 had 2.52-Mb deletion in the chromosome 22q11.21 region; patient no. 0008 had both 595- and 428-kb duplications, respectively, in 12p12.3p12.2 and 14q23.2q23.3 regions; patient no. 0009 had 1.46-Mb duplication in the 1q21.1q21.2 region; patient no. 0016 had 513-kb duplication in the 1q42.13 region; patient no. 0024 had 292-kb duplication in the 16q11.2 region; patient no. 0026 had 270-kb duplication in the 16q24.1 region; patient no. 0028 had 222-kb deletion in the 7q31.1 region; patient no. 0033 had 1.73-Mb duplication in the 17q12 region; and patient no. 0061 had 5.79-Mb deletion in the 1p36.33p36.31 region.aCGH can accurately detect CNVs in the patients with TOF. This is conducive to genetic counseling and prenatal diagnosis for TOF and provides a new clue and theoretical basis for exploring the pathogenesis of congenital heart disease.

Downregulation of long non-coding RNA H19 promotes P19CL6 cells proliferation and inhibits apoptosis during late-stage cardiac differentiation via miR-19b-modulated Sox6.

BACKGROUND: Regulating cardiac differentiation to maintain normal heart development and function is very important. At present, biological functions of H19 in cardiac differentiation is not completely clear. METHODS: To explore the functional effect of H19 during cardiac differentiation. Expression levels of early cardiac-specific markers Nkx-2.5 and GATA4, cardiac contractile protein genes α-MHC and MLC-2v were determined by qRT-PCR and western lot. The levels of lncRNA H19 and miR-19b were detected by qRT-PCR. We further predicted the binding sequence of H19 and miR-19b by online softwares starBase v2.0 and TargetScan. The biological functions of H19 and Sox6 were evaluated by CCK-8 kit, cell cycle and apoptosis assay and caspase-3 activity. RESULTS: The expression levels of α-MHC, MLC-2v and H19 were upregulated, and miR-19b was downregulated significantly in mouse P19CL6 cells at the late stage of cardiac differentiation. Biological function analysis showed that knockdown of H19 promoted cell proliferation and inhibits cell apoptosis. H19 suppressed miR-19b expression and miR-19b targeted Sox6, which inhibited cell proliferation and promoted apoptosis in P19CL6 cells during late-stage cardiac differentiation. Importantly, Sox6 overexpression could reverse the positive effects of H19 knockdown on P19CL6 cells. CONCLUSION: Downregulation of H19 promoted cell proliferation and inhibited cell apoptosis during late-stage cardiac differentiation by regulating the negative role of miR-19b in Sox6 expression, which suggested that the manipulation of H19 expression could serve as a potential strategy for heart disease.

miR-20a regulates proliferation, differentiation and apoptosis in P19 cell model of cardiac differentiation by targeting Smoothened.

MicroRNA (miR)-20a, a member of the miR-17-92 cluster related to cardiac development, was obviously downregulated in myocardially differentiated P19 cells compared with normal P19 cells. Smoothened (SMO) is a member of the Hh pathway. Hh signaling induces cardiac differentiation in P19 cells, and SMO mediates the Hh pathway during embryonic development. Using bioinformatic prediction software Targetscan (http://www.targetscan.org/), PicTar (http://pictar.bio.nyu.edu), and miRBase (http://microrna.sanger.ac.uk/), miR-20a and the 3'-untranslated region (3'-UTR) of SMO mRNA were predicted to have complementary binding regions. Accordingly, we inferred that miR-20a might act as a regulator of SMO, and regulate proliferation, differentiation and apoptosis in P19 cells. We determined the expression of miR-20a, SMO and marker proteins of cardiomyocytes (cTnT, GATA4 and desmin) by quantitative real-time PCR (qRT-PCR) and western blot assays, and found that P19 cells had differentiated into cardiomyocytes successfully at differentiation day 10, and downregulation of miR-20a and upregulation of SMO existed in myocardially differentiated P19 cells. Cell proliferation, differentiation and apoptosis detection showed that miR-20a upregulation inhibited proliferation and differentiation and enhanced apoptosis in P19 cells. Moreover, we verified that miR-20a directly targeted SMO and knockdown of SMO and miR-20a overexpression had similar effects on P19 cell proliferation, differentiation and apoptosis, which verified the speculation that miR-20a inhibits proliferation and differentiation and enhances apoptosis in P19 cells by directly targeting SMO. Our results suggest that miR-20a may be a potential target against congenital heart diseases.

Restoration of miR-98 relieves the inhibitory effect of nicotine on the differentiation of P19 cells into cardiomyocytes.

OBJECTIVE: To study whether miR-98 participates in the effects of nicotine on myocardial differentiation. RESULTS: By western blot, MTT and flow cytometry assays, we found that nicotine suppresses P19 cell differentiation into cardiomyocytes and apoptosis, and promotes proliferation, while restoration of miR-98 relieves the inhibitory effect of nicotine on the P19 cell differentiation. By target prediction analysis and luciferase reporter assay, we observed that miR-98 inhibits the protein expression of Wnt1 by directly acting on the 3'-UTR of Wnt1 mRNA. We assumed that the effect of miR-98 on Wnt1 might alter the activity of the Wnt1/ß-catenin signaling pathway and be associated with myocardial differentiation. In summary, nicotine restrains differentiation of P19 cells into cardiomyocytes and decreases the level of miR-98. CONCLUSIONS: Restoration of miR-98 relieves the inhibitory effect of nicotine on differentiation of P19 cells via targeting the 3'-UTR of Wnt1, which offers novel insights into our understanding of underlying molecular mechanisms of congenital heart defects.

Analysis of etiology, chromosome and prognosis for small left heart system development in 69 fetuses.

OBJECTIVE: To provide a basis for evaluating the prognosis of small left heart system development in fetuses, we analyzed its related factors. METHODS: The fetal echocardiogram was performed in 3859 pregnant women, and then small left heart system development was identified in 69 fetuses. The data of prenatal and postnatal echocardiograms, postnatal cardiac surgical treatment, chromosome and autopsy after induced labor were analyzed in the 69 fetuses. RESULTS: Except 1320 cases losing follow-up, 2539 cases had complete data. Among the 2539 cases, small left heart system development was identified in 69 fetuses. Of the 69 fetuses, 12 had hypoplastic left heart syndrome, 20 premature closure of foramen ovale, 13 total anomalous pulmonary venous drainage, 2 common pulmonary vein lumen atresia, 21 aortic coarctation or interruption and 1 right pulmonary hypoplasia. Among the 69 fetuses, chromosome abnormality was found in 7. CONCLUSION: There are many etiological factors causing small left heart system development. The prognosis is poor in the fetuses with hypoplastic left heart syndrome, common pulmonary vein lumen atresia, pulmonary hypoplasia, other malformations or/and chromosome abnormality. Fetal echocardiography combined with chromosome examination can provide important bases for making diagnosis and evaluating the prognosis regarding small left heart system development.

Level of perioperative B-type natriuretic peptide associates with heart function after on-pump coronary artery bypass graft surgery on a beating heart.

OBJECTIVE: To explore the relationship of the perioperative B-type natriuretic peptide (BNP) level with heart function among patients undergoing on-pump coronary artery bypass graft surgery on a beating heart. METHODS: Total 90 patients expected to undergo coronary artery bypass graft surgery were selected and their left ventricular ejection fraction (LVEF) were examined before operation. Patients with LVEF greater than or equal to 50% were selected as the A group (n=46), and those less than 50% formed the B group (n=44). BNP levels of the patients were examined and its relationship with cardiac function was analyzed. RESULTS: BNP levels of group A was lower than that in group B pre-and post-operatively (until 7 days after the surgery), the difference is statistically significant (p<0.05). Pearson analysis showed that the BNP level was negatively correlated with the LVEF (r = 0.767, p< 0.05). The area under the Roc curve is 0.865. CONCLUSION: BNP level was negatively correlated with the LVEF. Perioperative BNP level can be used as the prediction for heart function of patients with on-pump coronary artery bypass graft surgery on a beating heart.

[The effect of anticoagulant therapy on coagulation and inflammation markers in sepsis patients and its significance].

OBJECTIVE: To study the effect of anticoagulant therapy with low molecular weight heparin (LMWH) on coagulation and inflammation markers in sepsis patients. METHODS: A prospective randomized controlled trial ( RCT ) was conducted. Eighty-seven patients suffering from septic shock undergoing mechanical ventilation in Department of Critical Care Medicine of Subei People's Hospital from June 2012 to September 2014 were enrolled. The hemodynamic changes before and after PLR were monitored by pulse indicated continuous cardiac output ( PiCCO ) and PVI monitoring. Responsive group: positive fluid response was defined as an increase in cardiac index ( CI )≥10% after PLR. Unresponsive group: negative fluid response was defined as an increase in CI<10% after PLR. The hemodynamic parameters, including heart rate ( HR ), mean arterial pressure ( MAP ), central venous pressure ( CVP ), stroke volume variation ( SVV ), CI and PVI, and the changes in cardiac parameters (ΔHR, ΔMAP, ΔCVP, ΔSVV, ΔCI, and ΔPVI ) before and after PLR were determined. The relations between hemodynamic parameters and their changes with ΔCI were analyzed by the Pearson analysis. The role of the parameters for volume responsiveness prediction was evaluated by receiver operating characteristic ( ROC ) curves. RESULTS: There were no significant differences in values of all parameters, including CD62p, D-dimmer, IL-6, TNF-α, and APACHE II score at 1 day of treatment. The values of all parameters in observation group were gradually decreased. CD62p at 3 days of treatment and D-dimmer, IL-6, TNF-α, and APACHE II score at 5 days of treatment were significantly lower than those at 1 day of treatment. The values in the control group were decreased at first and then increased, as D-dimmer, IL-6 and TNF-α were significantly higher on the 5th day than those at 1 day of treatment. Compared with control group, CD62p, D-dimmer, IL-6, TNF-α and APACHE II score on the 7th day of treatment were significantly lowered in observation group [CD62 (µg/L): 22.64±2.88 vs. 31.52±2.81, D-dimmer (g/L): 1.32±0.46 vs. 4.79±0.82, IL-6 (ng/L): 5.84±1.87 vs. 49.64±3.12, TNF-α (ng/L): 21.04±3.15 vs. 130.58±6.26, APACHE II score: 9.71±2.02 vs. 14.17±2.38, all P < 0.05]. Correlation analysis showed that in observation group, CD62p, D-dimmer, IL-6, and TNF-α were positively correlated with APACHE II score (r value was 0.907, 0.868, 0.880, 0.693, respectively, all P=0.000). The incidence of MODS in observation group was significantly lower than that in the control group [26.7% (8/30) vs. 46.7% (14/30), χ (2)=3.943, P = 0.028]. CONCLUSIONS: LMWH, which was given early in sepsis, can significantly down-regulate the expression of CD62p, D-dimmer, IL-6 and TNF-α, and reduce the incidence of MODS. Some indicators regarding coagulation and inflammation can be used as supplementary indicators to severity scores, and it may be able to improve the accuracy of scoring systems for sepsis.

Application of Real-Time Three-Dimensional Echocardiography to Evaluate the Pre- and Postoperative Right Ventricular Systolic Function of Patients with Tetralogy of Fallot.

UNLABELLED: Tetralogy of Fallot (ToF) can be challenging for clinicians to both diagnose and treat, given the multiple heart defects that are by definition associated with the illness. This study investigates the value of real-time three- dimensional echocardiography (RT-3DE) in evaluating the pre-and postoperative right ventricular systolic function of patients with tetralogy of Fallot. A total of 41 ToF patients were divided into two groups: the child group (CG) and the adult group (AG) according to age. The right ventricular end-diastolic volume (RVEDV), right ventricular end-systolic volume (RVESV), and the right ventricular ejection fraction (RVEF) of ToF patients were measured before surgery, 7 days, and 3 months after the surgery. The correlation between the preoperative Nakata index and RVEF was then analyzed. Compared with the RVEDV and RVESV prior to surgery, those of the postoperative 7-day and 3-month were not statistically significant (p > 0.05). However, RVEF decreased, and the difference was statistically significant (p < 0.05). The differences in RVEDV, RVESV, and RVEF between postoperative 3-month and 7-day were not significant (p > 0.05). Compared with the pre-and postoperative RVEDV and RVESV of CG, those of AG increased. However, RVEF decreased, and the differences were statistically significant (p < 0.05). Our study indicated that the correlation between preoperative Nakata index and RVEF was good. Ultimately, we did confirm that RT-3DE can quantitatively evaluate the right ventricular volume and systolic function of ToF patients, thereby providing clinical significance in determining postoperative efficacy and prognosis evaluation. KEY WORDS: Echocardiography; Right; Tetralogy of Fallot; Three-dimensional; Ventricular function.