Assessment of Pulmonary Arterial Vascular Impedance in Fetuses With Tetralogy of Fallot.

OBJECTIVE: To evaluate the vascular impedance of the pulmonary arteries in fetuses with tetralogy of Fallot (TOF) by Doppler echocardiography. METHODS: A total of 42 fetuses with TOF (TOF group) and 84 gestational age-matched normal fetuses (control group) were prospectively collected from the Second Xiangya Hospital of Central South University from August 2022 to January 2023. The severity of TOF was classified into mild TOF (z score ≥-2), moderate TOF (-4 < z score < -2), or severe TOF (z score ≤-4) according to the z score value of the pulmonary annulus diameter. The pulsatility index (PI) of the main pulmonary artery (MPA), distal left pulmonary artery (DLPA), and distal right pulmonary artery (DRPA) were measured by pulsed-wave Doppler. The differences in clinical data and echocardiographic parameters between TOF group, control group, and TOF subgroups were compared. RESULTS: Compared with the control group, MPA-PI increased significantly, whereas DLPA-PI and DRPA-PI decreased in TOF group (all P < .001). There were no significant differences in MPA-PI and DRPA-PI among mild TOF, moderate TOF, and severe TOF (all P > .05). However, DLPA-PI decreased significantly in severe TOF compared with mild TOF (P < .05). CONCLUSION: Fetuses with TOF presented increased vascular impedance in the pulmonary trunk and decreased impedance in distal pulmonary artery branches. Further large and follow-up studies are needed to demonstrate the associations between those changed vascular impedances and the development of PA in patients with TOF.

Unusual presentation of a case of fetal hepatic mass: a case report.

BACKGROUND: Giant hepatic hemangiomas are rare and can cause serious complications that contribute to a high risk of perinatal mortality. The purpose of this article is to review the prenatal imaging features, treatment, pathology, and prognosis of an atypical fetal giant hepatic hemangioma and to discuss the differential diagnosis of fetal hepatic masses. CASE PRESENTATION: A gravida 9, para 0 woman at 32 gestational weeks came to our institution for prenatal ultrasound diagnosis. A complex, heterogeneous hepatic mass measuring 5.2 × 4.1 × 3.7 cm was discovered in the fetus using conventional two-dimensional ultrasound. The mass was solid and had both a high peak systolic velocity (PSV) of the feeding artery and intratumoral venous flow. Fetal magnetic resonance imaging (MRI) revealed a clear, hypointense T1-W and hyperintense T2-W solid hepatic mass. Prenatal diagnosis was very difficult due to the overlap of benign and malignant imaging features on prenatal ultrasound and MRI. Even postnatally, neither contrast-enhanced MRI nor contrast-enhanced computed tomography (CT) was useful in accurately diagnosing this hepatic mass. Due to persistently elevated Alpha-fetoprotein (AFP), a laparotomy was performed. Histopathological examination of the mass showed atypical features such as hepatic sinus dilation, hyperemia, and hepatic chordal hyperplasia. The patient was ultimately diagnosed with a giant hemangioma, and the prognosis was satisfactory. CONCLUSIONS: When a hepatic vascular mass is found in a third trimester fetus a hemangioma should be considered as a possible diagnosis. However, prenatal diagnosis of fetal hepatic hemangiomas can be challenging due to atypical histopathological findings. Imaging and histopathological assays can provide useful information for the diagnosis and treatment of fetal hepatic masses.

Heart-targeted amelioration of sepsis-induced myocardial dysfunction by microenvironment responsive nitric oxide nanogenerators in situ.

BACKGROUND: A balanced endogenous level of bioavailable nitric oxide (NO) plays a key role in maintaining cardiovascular homeostasis. The bioactive NO level in the cardiomyocytes was much reduced during sepsis. However, it is clinically challenging for the NO gas therapy due to the lack of spatial and temporal release system with precise control. The purpose of this study is to design a NO-releasing biomaterial with heart-targeted capability responsive to the infectious microenvironment, thus ameliorating lipopolysaccharide (LPS)-induced cardiac dysfunction. RESULTS: The heart-targeted NO delivery and in situ releasing system, PCM-MSN@LA, was synthesized using hollow mesoporous silica nanoparticles (MSN) as the carrier, and L-arginine (LA) as the NO donor. The myocardial delivery was successfully directed to heart by specific peptide (PCM) combined with low-intensity focused ultrasound (LIFU) guidance. The myocardial system synthesized NO from the LA released from PCM-MSN@LA in the presence of increased endogenous nitric oxide synthase (NOS) activity induced by LPS. This targeted NO release in situ achieved extraordinary protective effects against LPS-challenged myocardial injury by reducing the recruitment of inflammatory cells, inhibiting oxidative stress and maintaining the mitochondria integrity. In particular, this protection was not compromised by simultaneous circulation collapse as an adverse event in the context. CONCLUSIONS: PCM-MSN@LA + LIFU exhibited extraordinary cardioprotective effects against severe sepsis in the hearts of LPS-treated animals without the side effect of NO diffusion. This technology has great potential to be served as a novel therapeutic strategy for sepsis-induced myocardial injury.

Z-Score Reference Ranges for Umbilical Vein Diameter and Blood Flow Volume in Normal Fetuses.

OBJECTIVES: To establish Z-scores for the diameter and blood flow volume of the umbilical vein (UV) in normal fetuses. METHODS: This was a prospective study involving 907 normal fetuses. We measured the diameter (Duv) of two different segments of the UV (FUV: the free loop of the UV; FIUV: the fetal intra-abdominal UV). Next, we calculated the blood flow volume (Quv). Z-scores were created for both Duv and Quv using gestational age, femur length, and biparietal diameter as independent variables. RESULTS: We successfully acquired 858 (94.6%) normal fetal measurements. Between 20 and 39 weeks, the Duv of the FUV and FIUV increased from 0.38 to 0.80 cm and from 0.33 to 0.70 cm, respectively. The Quv of the FUV and FIUV increased from 32.66 to 381.88 ml/min and from 31.50 to 360.15 ml/min, respectively. Linear or quadratic regression models were best fitted between the parameters of UV and the independent variables. Z-scores were successfully determined for both the Duv and Quv. CONCLUSIONS: The calculation of Z-scores for the Duv and Quv is simple by applying standard statistical methods. These Z-scores may be useful to evaluate placental circulation and provide a rationale for monitoring and evaluating the prognosis of fetuses.

Evaluation of fetal foramen ovale blood flow by pulsed Doppler ultrasonography combined with spatiotemporal image correlation : To define the normal reference range of fetal foramen ovale blood volume for each gestational age: a cross-sectional study.

OBJECTIVE: The objective of this study was to determine fetal foramen ovale blood flow utilizing pulsed Doppler combined with spatiotemporal image correlation. METHODS: A cross-sectional study was performed in 440 normal fetuses between 20 and 40 weeks of gestation. In order to calculate foramen ovale blood flow, the foramen ovale flow velocity-time integral was obtained by pulsed Doppler ultrasonography, and the foramen ovale area was measured by using spatiotemporal image correlation rendering mode. Foramen ovale blood flow was calculated as the product of the foramen ovale area and the velocity-time integral. RESULTS: Gestational age-specific reference ranges are given for the absolute blood flow (ml/min) of foramen ovale, showing an exponential increase from 20 to 30 weeks of gestation, and a flat growth trend during the last trimester, while the weight-indexed flow (ml/min/kg) of foramen ovale decreased significantly. The median weight-indexed foramen ovale blood flow was 320.82 ml/min/kg (mean 319.1 ml/min/kg; SD 106.33 ml/min/kg). CONCLUSIONS: The reference range for fetal foramen ovale blood flow was determined from 20 to 40 weeks of gestation. The present data show that the volume of foramen ovale blood flow might have a limited capacity to increase during the last trimester.

MicroRNA-362-3p Targets PAX3 to Inhibit the Development of Glioma through Mediating Wnt/ß-Catenin Pathway.

BACKGROUND: Glioma is identified as a broad category of brain and spinal cord tumors. MiR-362-3p is important in regulating the genesis of different cancers; however, the mechanism of miR-362-3p in the progression of glioma remains largely unknown. OBJECTIVES: This study aimed to elucidate pathobiological functions of miR-362-3p by targeting PAX3 in glioma. METHOD: qRT-PCR and western blotting were used to examine miR-362-3p and PAX3 expression in glioma tissues and cells. CCK-8 assay and transwell assays were used to examine the functions of miR-362-3p on human glioma. Two bioinformatics analysis software and luciferase reporter assay were performed to analyze the relationship between miR-362-3p and PAX3. RESULTS: MiR-362-3p was downregulated, and PAX3 was upregulated in glioma tissues and cells. Functional assays revealed that ectopic expression of miR-362-3p inhibited glioma cell proliferation and migration. Further, PAX3 was confirmed as direct target gene of miR-362-3p, and downregulation of PAX3 reversed the suppressive effects of miR-362-3p in glioma. In addition, miR-362-3p also exhibited suppressive effect on epithelial-mesenchymal transition and Wnt/ß-catenin pathway. CONCLUSIONS: MiR-362-3p downregulation or PAX3 overexpression predicted poor prognosis in glioma. MiR-362-3p played a role in the suppressive effect on glioma by targeting PAX3 through suppressing Wnt/ß-catenin pathway.

Extracellular MicroRNAs Induce Potent Innate Immune Responses via TLR7/MyD88-Dependent Mechanisms.

Tissue ischemia, such as transient myocardial ischemia, leads to release of cellular RNA including microRNA(miRNA) into the circulation and extracellular (ex-) space, but the biological function of the ex-RNA is poorly understood. We recently reported that cardiac RNA of both human and rodent origins induced cytokine production and immune cell activation. However, the identity of the ex-RNA responsible for the proinflammatory effect remains unclear. In the current study, using an miRNA array, we profiled the plasma miRNAs 4 h after transient myocardial ischemia (45 min) or sham procedure. Among 38 plasma miRNAs that were elevated following ischemia, eight were tested for their ability to induce cytokine response in macrophages and cardiomyocytes. We found that six miRNA mimics (miR-34a, -122, -133a, -142, -146a, and -208a) induced cytokine production in a dose-dependent manner. The effects of miRNAs (miR-133a, -146a, and -208a) were diminished by uridine→adenosine mutation and by RNase pretreatment. The miRNA-induced cytokine (MIP-2, TNF-α, and IL-6) production was abolished in cells deficient of TLR7 or MyD88, or by a TLR7 antagonist, but remained the same in TLR3- or Trif-deficient cells. In vivo, mice i.p. injected with miR-133a or miR-146a had marked peritoneal neutrophil and monocyte migration, which was significantly attenuated in TLR7-/- mice. Moreover, locked nucleic acid anti-miRNA inhibitors of these six miRNAs markedly reduced cardiac RNA-induced cytokine production. Taken together, these data demonstrate that ex-miRNA mimics (miR-34a, -122, -133a, -142, -146a, and -208a) are potent innate immune activators and that the miRNAs most likely induce cytokine production and leukocyte migration through TLR7 signaling.

Splenic RNA and MicroRNA Mimics Promote Complement Factor B Production and Alternative Pathway Activation via Innate Immune Signaling.

Complement factor B (cfB) is an essential component of the alternative pathway (AP) and plays an important role in the pathogenesis of polymicrobial sepsis. However, the mechanism leading to cfB production and AP activation during sepsis remains poorly understood. In this study, we found that plasma cell-free RNA was significantly increased following cecal ligation and puncture (CLP), an animal model of polymicrobial sepsis, and was closely associated with sepsis severity. Quantitative RT-PCR and microRNA (miRNA) array analysis revealed an increase in bacterial RNA and multiple host miRNAs (miR-145, miR-146a, miR-122, miR-210) in the blood following CLP. Treatment with tissue RNA or synthetic miRNA mimics (miR-145, miR-146a, miR-122, miR-34a) induced a marked increase in cfB production in cardiomyocytes or macrophages. The newly synthesized cfB released into medium was biologically active because it participated in AP activation initiated by cobra venom factor. Genetic deletion of TLR7 or MyD88, but not TLR3, and inhibition of the MAPKs (JNK and p38) or NF-κB abolished miR-146a-induced cfB production. In vivo, CLP led to a significant increase in splenic cfB expression that correlated with the plasma RNA or miRNA levels. Peritoneal injection of RNA or miR-146a led to an increase in cfB expression in the peritoneal space that was attenuated in MyD88-knockout or TLR7-knockout mice, respectively. These findings demonstrate that host cellular RNA and specific miRNAs are released into the circulation during polymicrobial sepsis and may function as extracellular mediators capable of promoting cfB production and AP activation through specific TLR7 and MyD88 signaling.

[Blood flow parameters in fetal anterior cerebral artery during the second and third trimester of gestation].

OBJECTIVE: To investigate hemodynamic parameters in 2 anatomical segments (S1 and S2) of anterior cerebral artery (ACA) in normal pregnancy during the second and third trimester of gestation.
 Methods: The peak systolic velocity (PSV), end diastolic velocity (EDV), time-average maximum velocity (TAMAXV), peak systolic velocity/end diastolic velocity (S/D), resistance index (RI), and pulsation index (PI) in S1 and S2 of fetal anterior cerebral artery (ACA) in 288 normal pregnant women were detected by power Doppler and pulsed Doppler. Multiple regression models were fitted to estimate the relation between Doppler variables and gestational age. The differences of hemodynamic parameters between ACAS1 and ACAS2 were compared.
 Results: The PSV, EDV, and TAMAXV of ACAS1 and ACAS2 were positively correlated with the weeks of pregnancy (P<0.001), all fitted with the cubic curve. The S/D, PI, and RI values of ACAS1 and ACAS2 were not correlated with gestational ages (P>0.05). The PSV, TAMAXV, S/D, PI, and RI of ACAS1 were significantly higher than those of ACAS2, while EDV in ACAS1 was lower than that in ACAS2 (P<0.05).
 Conclusion: The velocity parameters (PSV, EDV, TAMAXV) of the 2 anatomical segments (ACAS1 and ACAS2) are increased with the increase of gestational age in normal pregnant fetus during the second and third trimester of gestation, and the resistance parameters (S/D, PI, RI) are not significantly correlated with gestational age. Distribution of blood flow is different in the blood supply territory between ACAS1 and ACAS2.

Cardiac RNA induces inflammatory responses in cardiomyocytes and immune cells via Toll-like receptor 7 signaling.

We have recently reported that extracellular RNA (exRNA) released from necrotic cells induces cytokine production in cardiomyocytes and immune cells and contributes to myocardial ischemia/reperfusion injury. However, the signaling mechanism by which exRNA exhibits its pro-inflammatory effect is unknown. Here we hypothesize that exRNA directly induces inflammation through specific Toll-like receptors (TLRs). To test the hypothesis, we treated rat neonatal cardiomyocytes, mouse bone marrow-derived macrophages (BMDM), or mouse neutrophils with RNA (2.5-10 µg/ml) isolated from rat cardiomyocytes or the hearts from mouse, rat, and human. We found that cellular RNA induced production of several cytokines such as macrophage inflammatory protein-2 (MIP-2), ILs, TNFα, and the effect was completely diminished by RNase, but not DNase. The RNA-induced cytokine production was partially inhibited in cells treated with TLR7 antagonist or genetically deficient in TLR7. Deletion of myeloid differentiation primary response protein 88 (MyD88), a downstream adapter of TLRs including TLR7, abolished the RNA-induced MIP-2 production. Surprisingly, genetic deletion of TLR3 had no impact on the RNA-induced MIP-2 response. Importantly, extracellular RNA released from damaged cardiomyocytes also induced cytokine production. Finally, mice treated with 50 µg of RNA intraperitoneal injection exhibited acute peritonitis as evidenced by marked neutrophil and monocyte migration into the peritoneal space. Together, these data demonstrate that exRNA of cardiac origin exhibits a potent pro-inflammatory property in vitro and in vivo and that exRNA induces cytokine production through TLR7-MyD88 signaling.

Complement Factor B Production in Renal Tubular Cells and Its Role in Sodium Transporter Expression During Polymicrobial Sepsis.

OBJECTIVES: Toll-like receptors and complement are two components of the innate immunity. Complement factor B is essential for the alternative pathway of complement activation. We have recently reported that complement factor B is significantly up-regulated in the kidney and may contribute to acute tubular injury in an animal model of sepsis. This study investigates the mechanisms responsible for the complement factor B up-regulation and its role in sodium transporter expression in tubular cells during sepsis. DESIGN: Animal study. SETTING: Laboratory investigation. SUBJECTS: C57BL/6 J wild-type, complement factor B(-/-), and Nfkb1(tm1Bal) p50(-/-) mice. INTERVENTIONS: Human proximal tubular cells and mouse tubular epithelial cells were stimulated with Toll-like receptor agonists. Bay 11-7082 was used to block nuclear factor-κB pathway. Alternative pathway activation was detected by C3 zymosan deposition. Polymicrobial sepsis was created by cecal ligation and puncture. Sodium transporter gene expression was determined by quantitative reverse transcriptase-polymerase chain reaction. MEASUREMENTS AND MAIN RESULTS: The agonists for Toll-like receptor 4 (lipopolysaccharide) or Toll-like receptor 3 (polyinosinic-polycytidylic acid) induced a marked increase in complement factor B expression in human proximal tubular cells and mouse tubular epithelial cells both at gene and protein levels. The Toll-like receptor 1/2 agonist, Pam3cys, induced complement factor B production only in human proximal tubular cells, not in mouse tubular epithelial cells. The Toll-like receptor 9 ligand, CpG oligodeoxynucleotides failed to induce complement factor B production either in human proximal tubular cells or in mouse tubular epithelial cells. Lipopolysaccharide/polyinosinic-polycytidylic acid-induced complement factor B up-regulation was blocked by Bay 11-7082, a potent inhibitor of nuclear factor-κB signaling, and in mouse tubular epithelial cells deficient in p50 subunit of nuclear factor-κB. Media from the lipopolysaccharide-treated mouse tubular epithelial cell cultures contained de novo synthesized complement factor B and led to functional alternative pathway activation. In a cecal ligation and puncture model, wild-type septic mice had down-regulated expression of sodium transporters in the kidney compared with the sham. In comparison, complement factor B mice or mice treated with anti-complement factor B displayed preserved levels of Na⁺/K⁺ ATPase-α1 following sepsis. CONCLUSIONS: 1) Toll-like receptor 3/4 activation is sufficient to induce complement factor B production via nuclear factor-κB pathway and to enhance alternative pathway activation in the kidney tubular epithelial cells. 2) Complement factor B may contribute to the down-regulation of certain sodium transporter expression during sepsis.

Imaging Lymphoid Cell Death In Vivo During Polymicrobial Sepsis.

OBJECTIVES: Cell death in lymphatic organs, such as the spleen, is in part responsible for immunosuppression and contributes to mortality during sepsis. An early and noninvasive detection of lymphoid cell death could thus have significant clinical implications. Here, we tested in vivo imaging of lymphoid cell death using a near-infrared annexin V (AV-750). DESIGN: Animal study. SETTING: Laboratory investigation. SUBJECTS: C57BL/6J wild-type and toll-like receptor 3 knockout mice. INTERVENTIONS: Mild and severe polymicrobial sepsis was induced with cecum ligation and puncture. Serum cytokines and acute kidney injury markers were tested by immunoassay and quantitative reverse transcription-polymerase chain reaction, respectively. Sepsis-induced lymphoid cell death was detected by fluorescent AV-750 accumulation in the thorax and abdomen (in vivo), in isolated organs (ex vivo), and in isolated cells (flow cytometry). Caspase-3 cleavage/activity and terminal deoxynucleotidyl transferase dUTP nick-end labeling staining were tested for apoptosis. MEASUREMENTS AND MAIN RESULTS: Severe sepsis induced marked apoptosis in the thymus, spleen, and liver as demonstrated by cleaved caspase-3 and an increase in caspase-3 activity and terminal deoxynucleotidyl transferase dUTP nick-end labeling-positive cells. A significant increase in fluorescent AV-750 signal was seen in the thoracic and upper abdominal fields and associated with the severity of sepsis. The in vivo thoracic and abdominal AV-750 fluorescent signal was attributed to the thymus, liver, and spleen as determined by ex vivo imaging and highly correlated with the levels of cell death in thymocytes and splenocytes, respectively, as measured by flow cytometry. Compared with wild-type septic mice, toll-like receptor 3 septic mice had attenuated abdominal AV-750 fluorescent signal, reduced ex vivo fluorescence in the spleen, and decreased splenocyte cell death. CONCLUSIONS: In vivo AV-750 fluorescent imaging provides spatially resolved and organ-specific detection of lymphoid cell death during polymicrobial sepsis. The AV-750 fluorescent intensity in the thoracic and abdominal fields is associated with sepsis severity and well correlated with sepsis-induced cell death in the thymus and spleen, respectively.

[3-vessel subsequence view in prenatal screen and diagnosis of fetal congenital heart disease].

OBJECTIVE: To investigate the clinical significance of 3-vessel subsequence view in prenatal screening and diagnosis of fetal congenital heart disease. METHODS: The 3-vessel subsequence view of 231 fetuses with congenital heart disease was obtained with Sequoia 512, Voluson 730 and E8 color Doppler ultrasonographic diagnostic system. RESULTS: Of the 231 consecutive fetuses with congenital heart defects (CHD), 169 (73%) had at least 1 abnormality on the 3-vessel subsequence view. When ventricl septal defects and so on were excluded, the detection rate increased to 91%. Some defects had several abnormalities visualized at the 3-vessel subsequence view. CONCLUSION: The 3-vessel subsequence view has high detection rate in identifying the presence of CHD.

Biomechanical properties of the ascending aorta in patients with arterial hypertension by velocity vector imaging.

Aortic stiffness is an important risk factor for cardiovascular events and morbidity. Increased aortic stiffness is associated with an increase in cardiac and vascular hypertension-related organ damage. To evaluate the biomechanical properties of the ascending aorta (AA) in patients with arterial hypertension (AH) by velocity vector imaging (VVI). Ninety-five patients with AH and 53 normal healthy control participants were prospectively enrolled. AA biomechanical properties, i.e., ascending aortic global longitudinal strain (ALS), ascending aortic global circumferential strain (ACS), and fractional area change (FAC), were evaluated by VVI. Relative wall thickness (RWT) and left ventricular mass (LVM) were calculated. Pulsed Doppler early transmitral peak flow velocity (E), early diastolic mitral annular velocity (e'), left ventricular global longitudinal strain (GLS), distensibility (D) and stiffness index (SI) of AA were also obtained. The ALS, ACS and FAC were significantly lower in the AH patients, especially in those with ascending aorta dilatation (AAD), than in the normal healthy control subjects. The patients with AAD had a higher E/e' ratio, RWT, LVM and SI and a lower GLS and D than patients without AAD and normal healthy volunteers (p < 0.05). There were significant associations between biomechanical properties and D, SI, E/e' and GLS (ALS and D: r = 0.606, ALS and SI: r = - 0.645, ALS and E/e': r = - 0.489, ALS and GLS: r = 0.466, ACS and D: r = 0.564, ACS and SI: r = - 0.567, ACS and E/e': r = - 0.313, ACS and GLS: r = 0.320, FAC and D: r = 0.649, FAC and SI: r = - 0.601, FAC and E/e': r = - 0.504, FAC and GLS: r = 0.524, respectively, p < 0.05). The biomechanical properties of AA were impaired in patients with AH, especially patients with ascending aorta dilatation. Hypertension is associated with a high prevalence of diastolic and systolic dysfunction and increased arterial stiffness. Further study is needed to evaluate the clinical application of AA biomechanical properties by VVI.

Pulmonary artery stiffness in fetuses with tetralogy of Fallot.

PURPOSE: This study evaluated the elastic characteristics of the pulmonary trunk and distal branches in fetuses diagnosed with tetralogy of Fallot (TOF) using Doppler echocardiography. METHODS: Data on 42 fetuses diagnosed with TOF and 84 gestational age-matched normal fetuses were prospectively collected from the Second Xiangya Hospital of Central South University between August 2022 and January 2023. The severity of TOF was classified into three categories based on the z-score of the pulmonary annulus diameter: mild (z-score ≥-2), moderate (-40.05). CONCLUSION: Fetuses diagnosed with TOF exhibited increased vascular stiffness in the MPA and reduced stiffness in the distal pulmonary artery (PA). Larger-scale follow-up studies are required to elucidate the relationships between these changes in vascular stiffness and PA development in patients with TOF.

Impaired Distensibility of the Proximal Aorta in Fetuses With Tetralogy of Fallot.

Background Increased aortic wall stiffness, which even persists after repair, has been reported in patients with tetralogy of Fallot (TOF). We aimed to observe the distensibility of the ascending aorta and descending aorta in fetuses with TOF and explore its relation with aortic blood flow volume and aortic and pulmonary annular size. Methods and Results Twenty-three fetuses with TOF and 23 gestational age-matched normal fetuses were included in this prospective cross-sectional study. The distensibilities of the ascending aorta and descending aorta were assessed by aortic strain (AS), which was defined as follows: 100×(maximum internal diameter in the systolic phase-minimum internal diameter in the diastolic phase)/minimum internal diameter in the diastolic phase. The maximum internal diameter in the systolic phase and minimum internal diameter in the diastolic phase of the ascending aorta and descending aorta were measured by M-mode echocardiography. Associations between AS and aortic blood flow volume and aortic and pulmonary valve diameters were assessed in both groups. AS of the ascending aorta in TOF group was lower than that in controls (20.48%±4.19% versus 28.17%±4.54%; P<0.001), whereas there was no significant difference in the descending aorta. The multivariate regression model demonstrated that AS was significantly related to aortic valve size (P=0.014) and aortic blood flow volume (P=0.022) in fetuses with TOF, whereas only aortic blood flow volume was significantly correlated with AS in the control group (P=0.01). No significant association was found between AS and pulmonary valve size. Conclusions Impaired distensibility of proximal aorta was observed in fetuses with TOF. Both intrinsic abnormalities of the aortic wall and aortic volume overload probably play roles in the altered aortic distensibility.

Aortic Elasticity and Cardiac Function in Fetuses With Aortic Coarctation.

Objective: The purpose of the study was to observe the elasticity of the ascending aorta (AAo) in normal fetuses and fetuses with coarctation of the aorta (CoA) by M-mode echocardiography. Methods: This was a prospective clinical study performed on 16 fetuses with CoA and 48 gestational-age matched normal fetuses. The minimum internal diameter in the diastolic phase (Dmin) and the maximum internal diameter in the systolic phase (Dmax) of the AAo were measured by M-mode echocardiography. The aortic strain was calculated using the formula 100 × (Dmax-Dmin)/Dmin). Doppler echocardiography was performed to measure the cardiac function parameters. Correlations between aortic strain and cardiac function were assessed in fetuses with CoA. Results: The aortic strain of the ascending aorta in the fetuses with CoA was significantly lower than that in normal fetuses (18.12 ± 4.88% vs. 25.22 ± 4.92%, p < 0.01). The fetuses with CoA showed significantly higher combined cardiac output than the controls (471.89 ± 93.98 vs. 411.57 ± 46.35 ml/min/kg, p < 0.05). Compared with the normal group, the early diastolic velocities (E') and peak systolic velocities (S') of the left side were obviously decreased in the CoA group (p < 0.05), while the left early diastolic velocity ratio (E/E') was significantly increased in the fetuses with CoA (p < 0.01). For the fetuses with CoA, the aortic strain of the AAo was correlated with the left E/E' and S' (r = -0.522 and 0.504, respectively, P < 0.05). Conclusions: The aortic strain of the ascending aorta was significantly decreased in fetuses with CoA in middle-late gestation. The impaired strain of the ascending aorta was correlated with the left ventricle function in the fetuses with CoA. These findings imply that the abnormalities of the intrinsic aortic wall of CoA might develop early in utero.

Case Report: Prenatal Diagnosis of Nemaline Myopathy.

Nemaline myopathy (NM) is a rare, hereditary heterogeneous myopathy. Fetal NM has a more severe disease course and a poorer prognosis and is usually lethal during the first few months of life. Hence, early prenatal diagnosis is especially important for clinical interventions and patient counseling. We report the case of a fetus with NM due to KLHL40 gene variation leading to arthrogryposis multiplex congenita (AMC). The ultrasonography and histopathology results revealed an enhanced echo intensity and decreased muscle thickness, which may be novel features providing early clues for the prenatal diagnosis of NM. Moreover, to our knowledge, this article is the first report to describe a case of NM associated with complex congenital heart disease (CHD).

Chinese Expert Consensus on Protection for Ultrasound Healthcare Workers against COVID-19.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has caused a worldwide pandemic and poses a serious public health risk. It has been proven that lung ultrasound can be extremely valuable in the diagnosis and treatment of the disease, which could also minimize the number of exposed healthcare workers and equipment. Because healthcare workers in ultrasound departments are in close contact with patients who might be infected or virus carriers, it is extremely important that they be provided sufficient protection. Extremely aggressive protection should be avoided because it might lead to a lack of protection equipment for the hospital. Guidance on proper protection management should be provided in detail, for example, how to choose personal protective equipment, how to disinfect the environment. To address these problems, on behalf of the Chinese Ultrasound Doctors Association, Chinese PLA Professional Committee of Ultrasound in Medicine, Beijing Institute of Ultrasound in Medicine and Chinese Research Hospital Association Ultrasound Professional Committee, the authors have summarized the recommendations for effective protection according to existing hygienic standards, their experience and available literature. After the recommendations were completed, two online conferences were held on January 31, 2020 and February 7, 2020, at which the recommendations were discussed in detail. A modified version of the work was circulated and finally approved by all authors, and is the present Chinese Expert Consensus on Protection for Ultrasound Healthcare Workers against COVID-19.