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Background: In general, the identification of cholesterol-depleted lipid particles can be inferred from non-high-density lipoprotein cholesterol (non-HDL-C) concentration to apolipoprotein B (apoB) concentration ratio, which serves as a reliable indicator for assessing the risk of cardiovascular disease. However, the ability of non-HDL-C/apoB ratio to predict the risk of long-term mortality among the general population remains uncertain. The aim of this study is to explore the association of non-HDL-C/apoB ratio with long-term all-cause and cardiovascular mortality in adults of the United States. Methods: This retrospective cohort study was a further analysis of existing information from the National Health and Nutrition Examination Survey (NHANES). In the ultimate analysis, 12,697 participants from 2005 to 2014 were included. Kaplan-Meier (K-M) curves and the log-rank test were applied to visualize survival differences between groups. Multivariate Cox regression and restricted cubic spline (RCS) models were applied to evaluate the association of non-HDL-C/apoB ratio with all-cause and cardiovascular mortality. Subgroup analysis was conducted for the variables of age, sex, presence of coronary artery disease, diabetes and hypertriglyceridemia and usage of lipid-lowering drugs. Results: The average age of the cohort was 46.8 ± 18.6 years, with 6215 (48.9%) participants being male. During a median follow-up lasting 68.0 months, 891 (7.0%) deaths were documented and 156 (1.2%) patients died of cardiovascular disease. Individuals who experienced all-cause and cardiovascular deaths had a lower non-HDL-C/apoB ratio compared with those without events (1.45 ± 0.16 vs. 1.50 ± 0.17 and 1.43 ± 0.17 vs. 1.50 ± 0.17, both P values

Abstract Background Generally, low-density lipoprotein (LDL) particle size can be inferred from the LDL cholesterol concentration to total apolipoprotein B concentration ratio (LDL-C/ApoB ratio, hereinafter called LAR), which is a good predictor of cardiovascular disease. However, the predictive ability of LAR for mortality risk in the general population is still unclear. This study aimed to explore the association between LAR and cardiovascular as well as all-cause mortality among American adults. Methods The present study was a secondary analysis of existing data from the National Health and Nutrition Examination Survey (NHANES). The final analysis included 12,440 participants from 2005 to 2014. Survival differences between groups were visualized using Kaplan‒Meier curves and the log-rank test. The association of LAR with cardiovascular and all-cause mortality was evaluated using multivariate Cox regression and restricted cubic spline analysis. Age, sex, coronary artery disease, diabetes, lipid-lowering medication use and hypertriglyceridemia were analyzed in subgroup analyses. Results The median age in the study cohort was 46.0 years [interquartile range (IQR): 31.0–62.0], and 6,034 (48.5%) participants were male. During the follow-up period, there were 872 (7.0%) all-cause deaths and 150 (1.2%) cardiovascular deaths. Compared with individuals without cardiovascular events, those who experienced cardiovascular deaths had a lower LAR (1.13 vs. 1.25) (P

Abstract Tetralogy of fallot (TOF) in the fetus is a typical congential heart disease that occurs during the early embryonic period, being characterized by the abnormal development of conus arteriosus. The early diagnosis and prevention of fetal TOF is very important and there is a great need for exploring the pathogenesis of it in clinic. In this study, there were three cases being detected with TOF by fetal echocardiogram and confirmed by autopsy. We characterize the difference of expression of lncRNAs and mRNAs through sequencing analysis of 3 pairs of myocardial tissues of fetal TOF and those of age-matched controls. Compared with normal group, there were 94 differentially expressed lncRNAs and 83 mRNA transcripts in TOF (P

Abstract Background To analyze the ultrasound imaging and clinical characteristics of fetuses with umbilical artery thrombosis (UAT), explore the potential causes of UAT and construct a prognostic prediction model to guide clinical practice. Methods This was a retrospective cohort study of fetal UAT cases examined at two academic tertiary referral care centers from 2014 to 2020. The basic information of the participants was obtained by interview during follow-up, and data on clinical treatment, delivery conditions, diagnosis and confirmation were obtained through medical records. Probable causes of thrombosis were explored by comparative analysis of the UAT group to the control group and by further regression analysis. Multivariable logistic regression models were used to evaluate risk factors for adverse pregnancy outcomes. Receiver operating characteristic (ROC) curves were constructed to evaluate the diagnostic value of the prognostic prediction model. Results Thirty fetuses with UAT were included in this study. UAT occurred mostly in the third trimester of pregnancy, and there was an obvious predominance of right UAT. An abnormal pregnancy history (53.3%) was the most common comorbidity, followed by gestational diabetes mellitus (GDM) (20.0%). GDM and umbilical cord (UC) abnormalities were found to be independent risk factors for the development of UAT. After comprehensive decision-making, over two-thirds of the patients with UAT received urgent treatment, and less than one-third received expectant management. Surprisingly, there were no significant differences in fetal outcomes between the urgent treatment and expectant management groups. Multivariate logistic regression analysis showed that gestational age (GA) at clinical diagnosis and UC abnormalities were independent risk factors for adverse pregnancy outcomes (OR 0.781, p = 0.042; OR 16.779, p = 0.023, respectively). Based on this, we constructed a comprehensive prognostic prediction model. The area under the ROC curve (AUC) was 0.877 (95% CI 0.698–0.970; p

BackgroundGenetic, observational, and clinical intervention studies indicate that circulating levels of remnant cholesterol (RC) are associated with cardiovascular diseases. However, the predictive value of RC for cardiovascular mortality in the general population remains unclear.MethodsOur study population comprised 19,650 adults in the United States from the National Health and Nutrition Examination Survey (NHANES) (1999–2014). RC was calculated from non-high-density lipoprotein cholesterol (non-HDL-C) minus low-density lipoprotein cholesterol (LDL-C) determined by the Sampson formula. Multivariate Cox regression, restricted cubic spline analysis, and subgroup analysis were applied to explore the relationship of RC with cardiovascular mortality.ResultsThe mean age of the study cohort was 46.4 ± 19.2 years, and 48.7% of participants were male. During a median follow-up of 93 months, 382 (1.9%) cardiovascular deaths occurred. In a fully adjusted Cox regression model, log RC was significantly associated with cardiovascular mortality [hazard ratio (HR) 2.82; 95% confidence interval (CI) 1.17–6.81]. The restricted cubic spline curve indicated that log RC had a linear association with cardiovascular mortality (p for non-linearity = 0.899). People with higher LDL-C (≥130 mg/dL), higher RC [≥25.7/23.7 mg/dL in males/females corresponding to the LDL-C clinical cutoff point (130 mg/dL)] and abnormal HDL-C (

Background: Patients with deletions involving the long arm of chromosome 1 are rare, and the main aim of this study was to refine the genotype-phenotype correlation.Case Report: In this report, a 28-year-old pregnant woman, gravida 2 para 1, at 25+4 weeks of gestation underwent ultrasound examination in our institute. The ultrasonographic findings of the fetus were as follows: (1) fetal growth restriction; (2) cleft lip and palate; (3) bilateral renal hypoplasia; (4) lateral ventriculomegaly; (5) single umbilical artery; (6) absent stomach; (7) coronary sinus dilatation with persistent left superior vena cava, ventricular septal defect and unroofed coronary sinus syndrome. Chromosomal microarray analysis of amniotic fluid from the fetus revealed a 28.025 Mb deletion in 1q23.3q31.2, spanning from position 164,559,675 to 192,584,768 (hg19).Conclusion: Genotype-phenotype correlation might improve prenatal diagnosis of fetuses with chromosome 1q deletion. PBX1 could be a candidate gene for fetal growth restriction, renal hypoplasia and congenital heart disease. Fetal growth restriction was accompanied by decreased renal volume in the fetus. Combined with ultrasonic examination, the application of chromosomal microarray analysis will provide accurate prenatal diagnosis.

Objectives: The size of cardiovascular structures in fetuses with congenital heart disease (CHD) is variable, and current reference structures used for comparative purposes are suboptimal: There are no known cardiovascular structures that are reliably normal in size. We sought to evaluate whether the aortic diameter at the diaphragmatic hiatus (ADDH) is affected in CHD. Methods: The ADDH was evaluated by sonography in both study subjects (CHD group, n = 506) and age-matched normal controls (normal group, n = 506). The CHD group was divided into different subgroups according to evident anomalies in the cardiovascular system. ADDH differences between CHD subgroups and their controls were calculated with a paired Student's t-test. Possible sex differences were determined by an unpaired Student's t-test on the whole group. Results: There were no significant differences in the ADDH between all CHD subgroups and age-matched controls (p > 0.05). No difference was found in the ADDH between female and male fetuses (p > 0.05). Conclusion: The ADDH in fetuses with CHD is similar to that in controls. Hence, ratios between size of involved cardiovascular structures and ADDH may be a useful parameter for monitoring fetuses with CHD .

Abstract Background FGF21 is a critical endogenous regulator in energy homeostasis and systemic glucose and lipid metabolism. Despite intensive study of the metabolic functions of FGF21, its important role in heart disease needs further exploration. Apoptosis induced by ox-LDL in vascular endothelial cells is an important step in the progress of atherosclerosis. Methods The effects of FGF21 treatment on apoptosis induced by ox-LDL were tested in HUVECs. The role of FGF21 in atherosclerosis was studied by evaluating its function in apolipoprotein E double knockout (apoE−/−) mice. Results We found that apoptosis in HUVECs was alleviated by FGF21 treatment. The effects of FGF21 were independent of the ERK1/2 pathway and were mediated through inhibition of the Fas signaling pathway. FGF21 suppressed the development of atherosclerosis, and the administration of FGF21 ameliorated Fas-mediated apoptosis in apoE−/− mice. Conclusion FGF21 protects against apoptosis in HUVECs by suppressing the expression of Fas; furthermore, FGF21 alleviated atherosclerosis by ameliorating Fas-mediated apoptosis in apoE−/− mice.

Aim: To investigate the types, associated anomalies and postnatal outcomes of fetal hepatic venous system (HVS) variants by ultrasound in China.Material and Methods: A large-scale and prospective investigation of HVS variants for low-risk singleton pregnant women was performed in three academic tertiary referral care centers in China. Ultrasound imaging wasused for the identification and follow-up of anatomical variants. Follow-up was conducted once every four weeks prenatally and every two months postnatally, mainly concerned on the adverse events that may appear.Results: There were 20848 cases with anatomical variants of fetal HVS identified from 46179 candidates during the study period. Following the anatomical position of variants occurring, four main divisions were present: main portal vein variants (17.9%), intrahepatic portal vein variants (21.30%), intrahepatic persistent right umbilical vein (0.27%) and hepatic vein variants (5.67%). In the fetal period, the pregnancy of all cases was normally continued, except that the pregnancy of two cases, which were associated with multiple anomalies and were terminated by their parents. After birth, approximately 99.47% of the cases with isolated variants orbeing associated no clinic significant anomalies were normally alive. Approximately 0.50% cases were associated with simple ventricular septum defect or tetralogy of Fallot and further treatment was needed.Conclusion: The anatomical variants of fetal HVS may appear as numerical, morphological or positional variants of MPV, intrahepatic PV branches, intrahepatic PRUV and HVs. The majority of cases are isolated or their associated anomalies are not clinically significant and have normal lifeafter birth. [ABSTRACT FROM AUTHOR]