MTHFR C677T gene polymorphism in patients with coronary heart disease and hypertension treated with enalapril and folic acid: implications for prognosis.

We aimed to investigate the effect of the methylenetetrahydrofolate reductase (MTHFR) C677T gene polymorphism on the prognosis of patients with coronary heart disease (CHD) and hypertension treated with enalapril and folic acid. A total of 540 CHD patients diagnosed by coronary angiography in our hospital were selected. According to whether there was folic acid intervention, they were divided into a folic acid group, a non-folic acid group and a control group. The genotypes of the MTHFR C677T locus were detected. Hcy concentration and the folate content were determined. In folic acid group, enalapril and folic acid tablets were used to reduce blood pressure, and clopidogrel or ticagrelor were selected according to CYP2C19 genotypes. In non-folic acid group, enalapril tablets were used, and clopidogrel or ticagrelor were selected based on CYP2C19 genotyping. Routine treatment without intervention was used in control group. Patients were prescribed standardized drug treatment and were followed up by an outpatient service or by telephone for 12 months after discharge. We found that the number and proportion of MTHFR C677T gene mutations in the folic acid group, non-folic acid group and control group were 150 (83.3%), 142 (78.9%) and 144 (80.0%), respectively. The recurrence rate of cardiovascular events in the folic acid and non-folic acid groups was significantly lower, and the degree of reduction in the recurrence rate of cardiovascular events in the folic acid and non-folic acid groups was significantly different. The concentrations of TG, TC, and LDL-C in folate and non-folic groups were lower, while HDL-C was higher than that in control group. To sum up, screening high-risk populations with genotypes has great significance in improving the clinical outcome of CHD patients with H-type hypertension. Folic acid supplementation improves the compliance rate of patients' blood pressure levels and improves their clinical prognosis as well.

GAS5 promotes glucose metabolism reprogramming and resistance to ferroptosis of endothelial progenitor cells through the miR-495-3p/SIX1 and IGF2BP2/NRF2 dual-regulatory pathways in coronary heart disease.

We aimed to explore the potential along with mechanism of lncRNA growth arrest-specific 5 (GAS5) in modulating glucose metabolism and ferroptosis of endothelial progenitor cells (EPCs) in coronary heart disease (CHD). CCK-8, flow cytometry, EdU, colony formation, scratch test as well as transwell assays were implemented to assess cell biological behaviors. Glucose uptake testing, lactic acid production assay, and detection of extracellular acidification rate (EACR) together with oxygen consumption rate (OCR) were used to assess glucose metabolism. Iron, GSH and MDA detection were used to measure ferroptosis. Besides, a series of mechanical experiments were implemented to clarify the modulatory relationship between GAS5 and nuclear factor erythroid 2-related factor 2 (NRF2) as well as sine oculis homeobox 1 (SIX1). We found that GAS5 was down-regulated in CHD patients relative to healthy controls. GAS5 depletion repressed EPCs proliferation, migration along with invasion while elevated cell apoptosis. GAS5 promoted the reprogramming of glucose metabolism and inhibited ferroptosis in EPCs. GAS5 affected glycometabolic reprogramming and ferroptosis resistance through regulating SIX1 and NRF2. On the one hand, GAS5 promoted NRF2 mRNA stability through IGF2BP2. On the other hand, GAS5 regulated the miR-495-3p/SIX1 axis in EPCs. To sum up, GAS5 promotes glucose metabolism reprogramming and resistance to ferroptosis of EPCs through the miR-495-3p/SIX1 and IGF2BP2/NRF2 dual-regulatory pathways in CHD.

Prognostic value of red blood cell distribution width-to-albumin ratio in ICU patients with coronary heart disease and diabetes mellitus.

Background: The red blood cell distribution width (RDW)-to-albumin ratio (RAR) has emerged as a potentially valuable prognostic indicator in diverse medical conditions. However, the prognostic significance of RAR in intensive care unit (ICU) patients with coronary heart disease (CHD) and diabetes mellitus (DM) remains uncertain and requires further investigation. Methods: This study aims to investigate the prognostic significance of RAR in ICU patients with coexisting CHD and DM through a retrospective cohort analysis using data from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database (version 2.2). The study population included patients aged 18 years or older who were diagnosed with both CHD and DM. The primary endpoint was 1-year mortality, and the secondary endpoints included 30-day mortality, 90-day mortality, hospital length of stay (LOS), and ICU LOS. Results: A total of 3416 patients, of whom 64.64% were male, were included in the study. The 30-day mortality, 90-day mortality, and 1-year mortality were 7.08%, 7.44%, and 7.49%, respectively. After adjusting for confounding factors, multivariate Cox proportional risk analysis demonstrated that high RAR levels were associated with an increased risk of 30-day mortality (HR, 1.53 [95% CI 1.17-2.07], P = 0.006), 90-day mortality (HR, 1.58 [95% CI 1.17-2.13], P = 0.003), and 1-year mortality (HR, 1.58 [95% CI 1.17-2.13], P = 0.003). Furthermore, the restricted cubic spline (RCS) model indicated a linear relationship between RAR and 1-year mortality. Conclusion: The results suggest that RAR holds potential as a valuable prognostic biomarker in ICU patients with both CHD and DM. Elevated RAR levels were found to be significantly associated with increased mortality during hospitalization, facilitating the identification of individuals at higher risk of adverse outcomes. These findings underscore the importance of incorporating RAR into risk stratification and overall management strategies for ICU patients with coexisting CHD and DM.

A Bidirectional Mendelian Randomization Study of the Causal Association Between Ischemic Stroke, Coronary Heart Disease, and Hydrocephalus.

BACKGROUND: The association among coronary heart disease, ischemic stroke, and hydrocephalus remains ambiguous. OBJECTIVES: There is a need for a Mendelian randomization study to evaluate the underlying causality between coronary heart disease, ischemic stroke, and hydrocephalus. METHODS: The data source utilized genome-wide association studies, employing a threshold of p < 5 × 10-8 to identify single nucleotide polymorphisms strongly linked to ischemic stroke and coronary heart disease as instrumental variables (IVs). Five methods-inverse variance weighted (IVW), Mendelian randomization (MR) Egger, Weighted Median, Weighted mode, and Simple mode-utilized the selected IVs to estimate the causality between ischemic stroke, coronary heart disease, and hydrocephalus. RESULTS: The IVW demonstrated that ischemic stroke and coronary heart disease serve as risk factors for hydrocephalus (odds ratio [OR] = 1.650, 95% CI: 1.066-2.554, p = 0.025; OR = 1.307, 95% CI: 1.023-1.668, p = 0.032). Both the MR-Egger intercept test and Cochran's Q test affirmed the relative reliability of the IVW analysis results. However, no evidence of a reverse causation was observed between hydrocephalus and coronary heart disease or ischemic stroke. CONCLUSIONS: Coronary heart disease and Ischemic stroke may increase the risk of hydrocephalus.

Cholesterol Levels and Lipid Lowering Treatment in Coronary Heart Disease Patients Hospitalized Because of Anginal Syndrome.

BACKGROUND: Coronary heart disease (CHD) patients are considered high cardiovascular risks. Guidelines recommend low-density lipoprotein cholesterol (LDL-C) target levels below 55 mg/dl with > 50% reduction from baselines. These levels can be reached by a combination of statins, ezetimibe, and anti-protein convertase subtilisin/kexin type 9 (anti-PCSK9) agents. Our clinical impression was that CHD patients do not reach LDL-C target levels, despite the wide availability. OBJECTIVES: To evaluate whether hospitalization would result in changes in lipid lowering regimens and short-term compliance. METHODS: We conducted a retrospective cohort study using data of CHD patients who were admitted to internal medicine wards at Clalit Health Services medical centers because of anginal syndrome during 2020-2022. The data were evaluated for demographic and clinical characteristics; LDL-C level at admission, 6 months previously, and 3 months and 6-9 months after discharge; rates of reaching LDL-C target levels; and lipid lowering treatment at admission, discharge, and 6-9 months after. RESULTS: The cohort included 10,540 patients. One-third and three-quarters did not have lipids level measurements up to 6 months before and during hospitalization, respectively. Only one-fifth of the patients reached LDL-C values before and during admission (median LDL-C 72 mg/dl; range 53-101). Approximately half were treated with high-dose potent statins. Only 10% were treated with ezetimibe. Hospitalization did not have a clinically significant effect on short-term lipid lowering treatment or LDL-C levels. CONCLUSIONS: Gaps were noted between guidelines and clinical practice for reaching LDL-C target levels. Further education and strict policy are needed.

Network Pharmacology and Experimental Verification: SanQi-DanShen Treats Coronary Heart Disease by Inhibiting the PI3K/AKT Signaling Pathway.

Objective: To employee network pharmacology to predict the components and pathways of SanQi-DanShen (SQDS) in treating coronary heart disease, followed by in vitro experiments to validate the molecular mechanism of SQDS in treating coronary heart disease. Methods: We sourced the active ingredients and targets of Panax notoginseng and Danshen from the Traditional Chinese Medicine Systems Pharmacology database. Coronary heart disease related genes were retrieved from the OMIM, Genecards, and Therapeutic Target databases. Using Cytoscape 3.7.2 software, we constructed a network diagram illustrating the components and targets of SQDS. The associated targets were then imported into the STRING database to build a protein-protein interaction network. The Metascape database and WeChat software were utilized for Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. Lastly, we performed molecular docking between the key components and related targets using AutoDock Vina. To validate the potential mechanism of SQDS in treating coronary heart disease, we established an acute coronary heart disease rat model via tail vein injection of pituitrin. Results: Network pharmacology analysis revealed that 65 active ingredients and 167 targets of SQDS are implicated in the treatment of coronary heart disease. The key targets identified include AKT1, TNF, TP53, IL6, and VEGFA. Notably, the PI3K/AKT signaling pathway emerged as the primary pathway. Furthermore, animal experiments showed that, compared to the model group, SQDS significantly reduced levels of TNF-α, IL-6, Bax, and cardiac troponin I, while increasing Bcl-2 content. It also notably suppressed the expression of p-PI3K and p-AKT, thereby offering protection to myocardial tissue. Conclusion: Through the integrated approach of network pharmacology and molecular docking, we have established that SQDS exerts a multi-component, multi-target, and multi-pathway synergistic therapeutic effect on coronary heart disease. Its mechanism may involve the inhibition of the PI3K/AKT signaling pathway and the reduction of inflammatory factor expression.

Association between dietary inflammatory index and all-cause mortality risk in adults with coronary heart disease in the United States.

Diet and inflammation are crucial in the incidence and progression of coronary heart disease (CHD). This study aimed to investigate the correlation between the Dietary inflammatory index (DII) and all-cause mortality in CHD patients. A total of 1,303 CHD patients from the National Health and Nutrition Examination Survey (NHANES) between 2003 and 2018 were included. Multivariate Cox regression was used to explore the correlation between the DII and the risk of all-cause mortality in these patients. Restricted cubic spline (RCS) analysis was also utilized to examine the relationship between the DII and all-cause mortality risk in CHD patients. Additionally, subgroup analyses were conducted to determine how the correlation between the DII and all-cause mortality varied across different demographics. During a median follow-up period of 77 months among 1,303 CHD patients, 536 died from all causes. The DII scores were significantly higher in deceased patients compared to survivors. After adjusting for confounding factors, the multivariate Cox regression analysis indicated a strong positive correlation between the DII and all-cause mortality in CHD patients. RCS analysis suggested a non-linear relationship between the DII and all-cause mortality among CHD patients. Additionally, an increase in DII was more pronounced in its impact on female patients. The DII is strongly correlated with the risk of all-cause mortality among CHD patients, particularly among females. Thus, managing dietary inflammation is vital for the prevention and treatment of CHD, especially in female patients.

Multiple triglyceride-derived metabolic indices and incident cardiovascular outcomes in patients with type 2 diabetes and coronary heart disease.

BACKGROUND: Triglyceride (TG) and its related metabolic indices are recognized as important biomarker gauging cardiovascular diseases. This study aimed to explore the association between multiple TG-derived metabolic indices including the atherogenic index of plasma (AIP), triglyceride-glucose (TyG) index, triglyceride glucose-body mass index (TyG-BMI) and cardiovascular outcomes to identify valuable predictors for cardiovascular prognosis in patients with type 2 diabetes (T2DM) and coronary heart disease (CHD). METHODS: Data of 1034 patients with T2DM and CHD from China-Japan Friendship Hospital between January 2019 and March 2022 were collected and analyzed. Multivariate Cox proportional hazards models and restricted cubic spline (RCS) analysis were conducted to examine the associations between AIP, TyG index, TyG-BMI and major adverse cardiac and cerebrovascular events (MACCEs). The area under the receiver operating characteristic (ROC) curve (AUC) was used to screen the most valuable predictor. Kaplan-Meier curve analysis was employed to examine the relationship between the predictor and prognosis. The goodness-of-fit of models was evaluated using the calibration curve and χ2 likelihood ratio test. Subgroup analysis and interaction test were performed to control for confounding factors. RESULTS: The overall incidence of MACCEs was 31.04% during a median of 13.3 months of follow-up. The results showed that AIP, TyG index and TyG-BMI were all positively correlated with the risk of MACCEs in patients with T2DM and CHD (P < 0.05). Furthermore, ROC (AUC = 0.899) suggested that AIP had the strongest ability to predict the risk of MACCEs, and the highest AIP values enhanced the risk by 83.5% in the population. RCS model demonstrated that AIP was nonlinearly associated with the incident cardiovascular outcomes (P for nonlinear = 0.0118). The Kaplan-Meier analysis for MACCEs grouped by the AIP tertiles indicated that the probability of cumulative incidences of MACCEs was significantly higher in patients with a higher AIP (all Log rank P < 0.001). Meanwhile, the calibration curve demonstrated an excellent goodness-of-fit of the multivariate model (χ2 = 13.210, P = 0.105). Subgroup analysis revealed that the trend of positive association of AIP with cardiovascular risk was similar across subgroups except in non-hypertensive individuals. CONCLUSION: Our study, for the first time, may provide valuable information that multiple TG-derived metabolic indices play a crucial role in the risk of MACCEs and it is recommended to monitor the AIP for lipid management in patients with established T2DM and CHD.

The role of glycemic traits in the mediation of the causal effect of hypothyroidism on coronary heart disease.

Background: Hypothyroidism and coronary heart disease are both common diseases in life and both are increasing in prevalence. Many studies have found a strong association between the two. However, they have not been able to prove a causal relationship. Furthermore, numerous studies have demonstrated that glycemic traits play a role in both. Consequently, the objective of this study was to ascertain the causal estimation of the association between hypothyroidism and coronary heart disease and to quantify the potential mediating role of glycemic traits in this relationship. Methods: We used two-sample Mendelian randomisation (UVMR) to explore causality between hypothyroidism and coronary heart disease. Additionally, multivariate Mendelian randomisation (MVMR) was applied to quantify the potential mediation of glycemic traits in this relationship. A variety of Mendelian randomization methods were employed in this study, including the inverse variance weighting (IVW) method, weighted median method, and MR-Egger test. Heterogeneity and horizontal pleiotropy were evaluated through MR-Egger intercept test, Cochran's Q test, and leave-one-out analysis to ensure the robustness of the study results. Results: The results of the MR analyses indicated that hypothyroidism was associated with an increased risk of coronary heart disease (IVW: OR=2.75, 95% CI: 1.53-4.94). In mediation analyses, the proportion of HbA1c-mediated effects of hypothyroidism on coronary heart disease was 7.3% (2.2%-12.5%). Conclusion: The results of our study indicate a causal relationship between hypothyroidism and coronary heart disease. Furthermore, HbA1c partially mediated the causal effect of hypothyroidism on coronary heart disease. Consequently, intervention in this factor may reduce the risk of coronary heart disease associated with hypothyroidism.

[Effect of Trichosanthis Pericarpium extract on bile acid metabolism in coronary heart disease model rats].

This study aims to explore the potential mechanism of action of Trichosanthis Pericarpium(TP) in improving coronary heart disease(CHD) based on a CHD rat model and metabolomics. The rat model of CHD was built by subcutaneous injection of high-fat diet combined with isoprenaline hydrochloride(ISO). To compare the expression level of lactate dehydrogenase, cardiac troponin Ⅰ(cTnⅠ), creatine kinase-MB(CK-MB), creatine kinase(CK), tumor necrosis factor-α(TNF-α), interleukin-1ß(IL-1ß),interleukin-6(IL-16), hypersensitive C-reactive protein(hs-CRP) in serum and cardiac pathological changes of model animals after administration of TP, LTQ-Orbitrap-MS analysis was combined with principal component analysis. The effect of TP on endogenous metabolites in the feces of CHD rats was studied. In addition, biomarkers were identified using the HMDB database and metabolic pathway enrichment analysis was performed using the MetaboAnalyst online pathway enrichment tool. The content of bile acid was further determined in the feces and serum of different groups of rats. Compared with blank group, the myocardial injury markers(CK,LDH, cTnⅠ, CK-MB) and inflammatory factors(TNF-α, IL-1ß, IL-6, hs-CRP) in serum of CHD rats were significantly increased.Myocardial injury and inflammatory infiltration in CHD rats were significantly improved by TP extract. The primary bile acid biosynthetic metabolism pathway was enriched by non-targeted metabolome analysis. The levels of total bile acid, primary bile acid,secondary bile acid, and unconjugated bile acids in the feces of CHD rats were significantly lower than those of control rats. Fecal excretion of total bile acid, primary bile acid, and unconjugated bile acid was significantly improved by TP extract. The levels of total bile acid, primary bile acid, secondary bile acid, and unconjugated bile acids in the serum of CHD rats were significantly higher than those of control rats. Circulating blood levels of total bile acids, primary bile acids, secondary bile acids, and unconjugated bile acids were significantly reduced by TP extract. Increasing fecal excretion of bile acid and decreasing the level of bile acid in blood circulation can improve CHD, and maintaining proper bile acid metabolism is one of the mechanisms of TP to improve CHD.

Sleep disorders are closely associated with coronary heart disease in US adults (≥20 years): A cross-sectional study.

The purpose of this research was to assess the association between sleep disorders and coronary heart disease (CHD) using data from the National Health and Nutrition Examination Survey (NHANES) database. This cross-sectional study included 9886 eligible participants with valid data on sleep disorders and CHD from the NHANES from 2011 to 2014. The complex NHANES sampling led to use of sample weights in analyses. Various statistical methods and covariates were utilized. Significance was set at P < .05. Receiver operating characteristic curves were used to assess the diagnostic efficacy of sleep disorders in relation to CHD. Sleep disorders were significantly associated with CHD (P < .001). In the model corrected for age, sex, race, hypertension, diabetes, and uric acid as covariates, sleep disorders and CHD remained significantly associated (P < .001, odds ratio = 1.83 [95% confidence interval: 1.31-2.58]). The correlation between sleep disorders and CHD varies by age and gender. Sleep disorders have some predictive value for CHD (0.5 < area under curve ≤ 0.7). Sleep disorders were associated with and predictive of CHD risk, warranting consideration in clinical assessments.

Prevalence and management of depressive symptoms in coronary heart disease patients and relationship with cardiovascular prognosis: a prospective cohort study.

AIMS: Depressive symptoms are comorbid with coronary heart disease (CHD). There is a controversial debate about whether screening and intervention for depressive symptoms could improve cardiovascular prognosis. This study characterizes the prevalence, characteristics, cardiovascular prognosis and management need of depressive symptoms among CHD patients. METHODS: CHD patients were recruited between November 18, 2020 and November 26, 2021. Depressive symptoms were evaluated with the Patient Health Questionnaire (PHQ-9). During the 12-month follow-up, cardiovascular disease (CVD) was the endpoint. Time-to-event data were estimated by Kaplan-Meier curves and Cox models. RESULTS: Of 582 patients (25% women), 21.0% had mild depressive symptoms, and 7.5% had moderate-to-severe depressive symptoms during hospitalization. Mild and moderate-to-severe depressive symptoms were risk factor-adjusted predictors of the primary composite endpoints (adjusted HR = 2.20; 95%CI 1.19-4.03, and adjusted HR = 2.70; 95%CI 1.23-5.59, respectively). Platelet count and low-density lipoprotein were higher in mild depressive symptoms compared to no depressive symptoms. CONCLUSION: Depressive symptoms are prevalent in CHD patients. Mild and moderate-to-severe depressive symptoms are associated with higher risk of further CVD in CHD patients. Platelet function and behavioral mechanisms may contribute to this association. TRIAL REGISTRATION: This research was registered at https://www.chictr.org.cn . Full data of first registration is 11/09/2020. The registration number is ChiCTR2000038139.

Association between Type D personality, illness perception, and coping strategies in patients undergoing open-heart surgery.

BACKGROUNDS: A combination of social inhibition and negative affectivity characterizes Type D personality. Type D, or distressed personality, is an established risk factor for the development and prognosis of coronary heart disease. It occurs in approximately 1 in 4 patients with coronary heart disease. This study aimed to investigate the relationship between Type D personality, illness perception, and coping strategies in patients undergoing open-heart surgery. METHODS: This retrospective and cross-sectional study was conducted in a university hospital psychiatry and cardiovascular surgery clinics between February 2022 and April 2022. Seventy-one volunteered patients over the age of 18 who underwent open-heart surgery in the cardiovascular surgery clinic were included in the study. Cardiovascular surgeons recorded the sociodemographic and clinical data of the patients and referred them to the psychiatry clinic for further evaluation. Subsequently, patients underwent psychiatric evaluation and were assessed using the Type D Personality Scale, Coping Attitudes Assessment Scale, Hospital Anxiety and Depression Scale, and Illness Perception Questionnaire. RESULTS: According to this study, individuals with Type D personality tended to have higher scores on the Hospital Anxiety and Depression Scale. Analysis of the subdimensions of the Stress Coping Styles Scale revealed that individuals with Type D personalities showed a significantly lower optimistic approach and a considerably higher helpless approach. In terms of the subdimensions of the Illness Perception Questionnaire, it was found that individuals with Type D personality had a statistically lower treatment control approach and a statistically higher emotional representations approach. CONCLUSIONS: Identifying Type D personality traits in patients undergoing open-heart surgery can help manage negative illness perceptions through effective coping mechanisms.

An 8-SNP LDL Cholesterol Polygenic Score: Associations with Cardiovascular Risk Traits, Familial Hypercholesterolemia Phenotype, and Premature Coronary Heart Disease in Central Romania.

Familial hypercholesterolemia (FH) is the most significant inherited risk factor for coronary heart disease (CHD). Current guidelines focus on monogenic FH, but the polygenic form is more common and less understood. This study aimed to assess the clinical utility of an 8-SNP LDLC polygenic score in a central Romanian cohort. The cohort included 97 healthy controls and 125 patients with premature (P)CHD. The weighted LDLC polygenic risk score (wPRS) was analyzed for associations with relevant phenotypic traits, PCHD risk, and clinical FH diagnosis. The wPRS positively correlated with LDLC and DLCN scores, and LDLC concentrations could be predicted by wPRS. A trend of increasing LDLC and DLCN scores with wPRS deciles was observed. A +1 SD increase in wPRS was associated with a 36% higher likelihood of having LDLC > 190 mg/dL and increases in LDLC (+0.20 SD), DLCN score (+0.16 SD), and BMI (+0.15 SD), as well as a decrease in HDLC (-0.14 SD). Although wPRS did not predict PCHD across the entire spectrum of values, individuals above the 90th percentile were three times more likely to have PCHD compared to those within the 10th or 20th percentiles. Additionally, wPRS > 45th percentile identified "definite" clinical FH (DLCN score > 8) with 100% sensitivity and 45% specificity. The LDLC polygenic score correlates with key phenotypic traits, and individuals with high scores are more likely to have PCHD. Implementing this genetic tool may enhance risk prediction and patient stratification. These findings, the first of their kind in Romania, are consistent with the existing literature.

Coronary Disease Risk Prediction, Risk Reduction, and Postoperative Myocardial Injury.

For patients considering surgery, the preoperative evaluation allows physicians to identify and treat acute cardiac conditions before less-urgent surgery, predict the benefits and harms of a proposed surgery, and make temporary management changes to reduce operative risk. Multiple risk prediction tools are reasonable for use in estimating perioperative cardiac risk, but management changes to reduce risk have proven elusive. For all but the most urgent surgical procedures, patients with active coronary syndromes or decompensated heart failure should have surgery postponed.

ZNF429 Participates in the Progression of Coronary Heart Disease through Regulating Inflammatory and Adhesive Factors.

BACKGROUND: Coronary heart disease (CHD) is an intricate and multifaceted cardiovascular disorder that contributes significantly to global morbidity and mortality. Early and accurate identification and diagnosis of CHD are paramount to ensuring patients receive optimal therapeutic interventions and satisfactory outcomes. METHODS: Data on CHD gene expression were obtained from the Gene Expression Omnibus (GEO) repository and potential hub genes were screened through gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), weighted gene co-expression network analysis (WGCNA), and least absolute shrinkage and selection operator (LASSO) analyses. Functional validation of these hub genes was conducted by interfering with them in human umbilical vein endothelial cells (HUVECs). Cell proliferation and apoptosis were assessed through cell counting kit-8 (CCK-8) and flow cytometry assays, respectively, while enzyme-linked immunosorbent assay (ELISA), quantitative polymerase chain reaction (qPCR), Western blot, and immunofluorescence were used to measure the expression of key indicators. RESULTS: We identified 700 upregulated differentially expressed genes (DEGs) and 638 downregulated DEGs in CHD, and utilized LASSO analyses to screen disease potential biomarkers, such as zinc finger protein 429 (ZNF429). Interference with ZNF429 in HUVECs mitigated the CHD-induced decrease in cell proliferation and increase in apoptosis. Moreover, the expression of interleukin-1ß (IL-1ß), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), cluster of differentiation 62E (CD62E), and cluster of differentiation 62P (CD62P) was reduced, leading to decreased cellular inflammation and adhesion. CONCLUSIONS: CHD-associated biomarker ZNF429 was identified through bioinformatics analysis to potentially regulate the expression of inflammatory factors IL-6, IL-1ß, and TNF-α, along with adhesion molecules ICAM-1, VCAM-1, CD62E, and CD62P. This modulation influence was subsequently found to impact the progression of CHD. These findings offered valuable insights into potential targets for further investigation and therapeutic interventions for CHD management.

Current Status and Factors Influencing Mental Health Literacy in Patients With Coronary Heart Disease: A Cross-Sectional Study.

This study aimed to investigate the current status of mental health literacy and related influencing factors in patients with coronary heart disease. Four hundred and thirty-five patients with coronary heart disease were recruited in this survey. Data collection was conducted using the General Information Questionnaire, the Chinese version of the Mental Health Literacy Scale, Coronary Artery Disease Self-Management Scale, Social Support Rating Scale, and Coronary Heart Disease Self-Efficacy Scale. Descriptive methods, independent samples t-test or one-way ANOVA, Pearson's correlation analysis, and multiple linear regression were used for data analysis. The results showed that the mean total mental health literacy score of patients with coronary heart disease was 96.42 ± 8.40; gender, age, education level, monthly per capita family income, first diagnosed with coronary heart disease, cardiac function classification, self-management ability, social support, and self-efficacy were the factors influencing the level of mental health literacy in patients with coronary heart disease (all p < 0.05). The study suggests that mental health literacy can improve patients' self-management ability and self-efficacy, and healthcare professionals should emphasize the strengthening of this aspect of health education in order to better improve patient's prognosis.

Metagenomic Study of the MESA: Detection of Gemella Morbillorum and Association With Coronary Heart Disease.

BACKGROUND: Inflammation is a feature of coronary heart disease (CHD), but the role of proinflammatory microbial infection in CHD remains understudied. METHODS AND RESULTS: CHD was defined in the MESA (Multi-Ethnic Study of Atherosclerosis) as myocardial infarction (251 participants), resuscitated arrest (2 participants), and CHD death (80 participants). We analyzed sequencing reads from 4421 MESA participants in the National Heart, Lung, and Blood Institute Trans-Omics for Precision Medicine program using the PathSeq workflow of the Genome Analysis Tool Kit and a 65-gigabase microbial reference. Paired reads aligning to 840 microbes were detected in >1% of participants. The association of the presence of microbe reads with incident CHD (follow-up, ~18 years) was examined. First, important variables were ascertained using a single regularized Cox proportional hazard model, examining change of risk as a function of presence of microbe with age, sex, education level, Life's Simple 7, and inflammation. For variables of importance, the hazard ratio (HR) was estimated in separate (unregularized) Cox proportional hazard models including the same covariates (significance threshold Bonferroni corrected P<6×10-5, 0.05/840). Reads from 2 microbes were significantly associated with CHD: Gemella morbillorum (HR, 3.14 [95% CI, 1.92-5.12]; P=4.86×10-6) and Pseudomonas species NFACC19-2 (HR, 3.22 [95% CI, 2.03-5.41]; P=1.58×10-6). CONCLUSIONS: Metagenomics of whole-genome sequence reads opens a possible frontier for detection of pathogens for chronic diseases. The association of G morbillorum and Pseudomonas species reads with CHD raises the possibilities that microbes may drive atherosclerotic inflammation and that treatments for specific pathogens may provide clinical utility for CHD reduction.

Quantifying Triglyceride-Rich Lipoprotein Atherogenicity, Associations With Inflammation, and Implications for Risk Assessment Using Non-HDL Cholesterol.

BACKGROUND: Triglyceride-rich lipoproteins and remnants (TRL/remnants) have a causal, but not yet quantified, relationship with coronary heart disease (CHD): myocardial infarction plus revascularization. OBJECTIVES: The authors sought to estimate TRL/remnant per-particle atherogenicity, investigate causal relationships with inflammation, and determine whether differences in the atherogenicity of TRL/remnants and low-density lipoprotein (LDL) impact the causal association of non-high-density lipoprotein cholesterol (non-HDL-C) with CHD. METHODS: Single nucleotide polymorphisms (SNPs) (N = 1,357) identified by genome-wide association in the UK Biobank were ranked into 10 clusters according to the effect on TRL/remnant-C vs LDL-C. Mendelian randomization analysis was used to estimate for each SNP cluster CHD ORs per 10 mg/dL apolipoprotein B (apoB) and per 0.33 mmol/L non-HDL-cholesterol, and to evaluate association of TRL/remnants with biomarkers of systemic inflammation. RESULTS: SNPs in cluster 1 predominantly affected LDL-C, whereas SNPs in cluster 10 predominantly affected TRL/remnant-C. CHD risk per genetically predicted increase in apoB and in non-HDL-C rose across clusters. ORs per 10 mg/dL higher apoB was 1.15 (95% CI: 1.11-1.19) in cluster 1 vs 1.70 (95% CI: 1.52-1.90) in cluster 10. Comparing ORs between these TRL/remnant-predominant and LDL-predominant clusters, we estimated that TRL/remnants were at least 3.9 (95% CI: 2.8-5.4) times more atherogenic than LDL on a per-particle basis. For non-HDL-C, CHD ORs per 0.33 mmol/L rose from 1.15 (95% CI: 1.11-1.19) for cluster 1 to 1.40 (95% CI: 1.30-1.50) for cluster 10. TRL/remnants exhibited causal relationships with inflammation, but this did not explain their greater atherogenicity. CONCLUSIONS: TRL/remnants are about 4 times more atherogenic than LDL. Variation in the causal association of non-HDL-C with CHD indicates that adjustment for percentage TRL/remnant-C may be needed for accurate risk prediction.