Association between insulin resistance and uncontrolled hypertension and arterial stiffness among US adults: a population-based study.

BACKGROUND: Prior research has established the correlation between insulin resistance (IR) and hypertension. While the association between triglyceride-glucose (TyG) index, a reliable surrogate marker of IR, and uncontrolled hypertension as well as arterial stiffness among individuals with hypertension remains undisclosed. METHODS: In this study, a total of 8513 adults diagnosed with hypertension from the National Health and Nutrition Examination Survey 1999-2018 were included. The primary outcome of the study are arterial stiffness (represented with estimated pulse wave velocity, ePWV) and uncontrolled hypertension. Logistic regression model, subgroup analysis, restricted cubic spine, and smooth curve fitting curve were conducted to evaluate the association between the IR indicators and uncontrolled hypertension and arterial stiffness in individuals with hypertension. RESULTS: Among included participants, the overall prevalence of uncontrolled hypertension was 54.3%. After adjusting for all potential covariates, compared with the first quartile of TyG index, the risk of uncontrolled hypertension increased about 28% and 49% for participants in the third quartile (OR, 1.28; 95% CI 1.06-1.52) and the fourth quartile (OR, 1.49; 95% CI 1.21-1.89) of TyG index, respectively. The higher OR of TyG index was observed in participants taking antihypertensive medication [fourth quartile versus first quartile (OR, 2.03; 95% CI 1.37-3.11)]. Meanwhile, we explored the potential association between TyG index and arterial stiffness and found that TyG index was significantly associated with increased arterial stiffness (ß for ePWV, 0.04; 95% CI 0.00-0.08; P = 0.039). However, traditional IR indicator HOMA-IR showed no significant positive correlation to uncontrolled hypertension as well as arterial stiffness in US adults with hypertension. CONCLUSION: Elevated levels of the TyG index were positive associated with prevalence of uncontrolled hypertension and arterial stiffness among US adults with hypertension.

Association between periodontitis and the prevalence and prognosis of prediabetes: a population-based study.

BACKGROUND: Diagnosis and intervention of prediabetes is an emerging method for preventing diabetic progression and complications. Periodontitis has been reported to strongly correlate with the dysregulation of glucose metabolism. Nonetheless, the relationship between periodontal status and the prevalence of prediabetes as well as its prognosis remains elusive. This study aimed to investigate the association of periodontitis with the prevalence of prediabetes and furtherly explore the all-cause mortality of different periodontal status among patients with prediabetes. METHODS: The dateset from the National Health and Nutrition Examination Survey (NHANES) was utilized for our study. Participants were divided into two groups (with or without periodontitis) and further assigned into subgroups by different grades of periodontitis to analyze the association between periodontitis and prevalence of prediabetes. Then we analyzed the association between all-cause mortality and periodontitis among patients with prediabetes. Weighted multivariate logistic/Cox regression models were adopted in our study. RESULTS: A total of 15390 participants were included and divided into a periodontitis group (n = 5033) and a nonperiodontitis group (n = 10357). The results showed that participants with periodontitis had a higher risk of prediabetes. After adjusting for covariables, more severe periodontitis was positively related to prediabetes (moderate vs. no periodontitis: OR = 1.46, 95% CI: 1.29-1.65; severe vs. no periodontitis: OR = 1.62, 95% CI 1.31-2.01). Furtherly, we explored the association between all-cause mortality and periodontal status among patients diagnosed with prediabetes (n = 4518) and found that severe (HR = 1.806, 95% CI 1.19-2.74) and moderate periodontitis (HR = 2.42, 95% CI 1.95-3.01) were associated with elevated all-cause mortality among patients with prediabetes. CONCLUSIONS: In general, the results suggest that periodontitis is positively associated with the prevalence and mortality of prediabetes. These results suggest that good management of periodontal status could be a potential strategy to reduce the occurrence and development of prediabetes.

A national cross-sectional analysis of dietary copper intake and abdominal aortic calcification in the US adults: NHANES 2013-2014.

BACKGROUND AND AIMS: Copper is an essential dietary element with a crucial role in physiological regulation. However, the relationship between dietary copper intake and abdominal aortic calcification (AAC) remains uncertain. METHODS AND RESULTS: This study encompassed a cohort of 2535 adults aged over 40 years, derived from the National Health and Nutrition Examination Survey 2013-2014. Dietary copper intake from both food sources and supplements was assessed through two 24-h dietary recall interviews. AAC was measured by dual-energy X-ray absorptiometry and classified into 3 groups using the Kauppila score system. Multivariable logistic regression models were constructed to evaluate the association between dietary copper intake and AAC. Among the participants, a total of 771 individuals (30.4%) were diagnosed with AAC, of which 239 (9.4%) exhibited severe AAC. Higher dietary copper intake was significantly associated with a lower incidence of severe AAC. Specifically, for each 1 mg/day increase in dietary copper intake, the incidence of severe AAC decreased by 38% (odds ratios [OR] 0.62, 95% confidence intervals [CI] 0.39-0.98) after adjustment for relevant covariates. Moreover, individuals in the third tertile of copper intake had a 37% lower incidence of AAC compared to those in the first tertile [OR 0.63, 95% CI (0.43-0.95)]. However, no significant associations were found between supplemental copper intake or serum copper levels and AAC. CONCLUSIONS: This study demonstrates that lower dietary copper intake, rather than serum copper levels or supplement copper intake, is significantly associated with a higher prevalence of AAC in adults ≥40 years old in the United States.

Association of iron status with non-alcoholic fatty liver disease and liver fibrosis in US adults: a cross-sectional study from NHANES 2017-2018.

Aims: Non-alcoholic fatty liver disease (NAFLD) is a widely prevalent hepatic disorder resulting in a high risk of adverse prognosis, and its presence has been considered a cause or an outcome of metabolic syndrome. But the relative factors and mechanism of NAFLD are still unclear. The aim of this study is to explore the association between iron status indicators and NAFLD as well as liver fibrosis. Methods: This study evaluated whether serum iron status indicators are independently related to the risk of NAFLD. The independent variable was each one of the iron status indicators (iron intake, ferritin, iron, unsaturated iron binding force (UIBC), total iron binding capacity (TIBC), transferrin saturation, transferrin receptor, hemoglobin, and mean cell hemoglobin), and the dependent variables were NAFLD and advanced liver fibrosis. A multivariable logistic regression analysis and subgroup analysis were performed to evaluate the association between iron status indicators and NAFLD as well as liver fibrosis. Results: A total of 3727 patients were included. After adjusting for other covariates in multiple logistic regression models, the serum ferritin, UIBC, TIBC, and hemoglobin had a significant positive association with the NAFLD (odds ratio [OR] = 1.16, 95% confidence interval [CI]: 1.09, 1.23; 1.31, 95% CI: 1.06, 1.62; 1.82, 95% CI: 1.23, 2.67; 2.67, 95% CI: 1.48, 4.82, separately), and the risk of NAFLD diagnosed by VCTE or ALT/AST further increased in the fourth quartile group of serum ferritin (diagnosed by VCTE OR = 1.93, 95% CI: 1.49, 2.50; diagnosed by ALT/AST OR = 5.76, 95% CI: 3.96, 8.38). Moreover, the main positive correlation between serum ferritin and NAFLD was found in females, participants aged >41 years, with no diabetes. Conclusion: Our results indicated that iron status indicators were closely associated with the occurrence of advanced liver fibrosis, which may indicate that iron status indicators could be potential biomarkers of NAFLD and advanced liver fibrosis.

Blood and urine manganese exposure in non-alcoholic fatty liver disease and advanced liver fibrosis: an observational study.

Manganese was the key activator of biological enzymes-mediated metabolic diseases (Mets)-associated pathophysiological process. Non-alcoholic fatty liver disease (NAFLD), which was the hepatic manifestation of Mets, development remained a mystery. We aimed to explore the association between blood/urine manganese exposure and NAFLD and liver fibrosis diagnosed by vibration-controlled transient elastography (VCTE). All data were extracted from National Health and Nutrition Examination Survey database (2017-2018). A total of 3580 participants with blood manganese data were enrolled and divided into four groups according to the quartile of blood manganese exposure level. In multiple logistic regression models, the higher blood manganese exposure level (groups 2, 3, and 4) had a significant positive association with NAFLD (ß = 1.58, 1.30, and 1.69). In subgroup analysis, the main inversely correlation between blood manganese and NAFLD was found in participants with normal/high body mass index and high blood manganese exposure level. Moreover, in 1179 participants with urine manganese data, urine manganese exposure level presented as significantly associated with advanced liver fibrosis in models 1 and 2 (ß = 2.00 and 2.02). This study showed that manganese exposure level was positively associated with NAFLD and advanced liver fibrosis among the US population. We suggested that manganese exposure level was a biomarker of the development of NAFLD.

Outcomes of hyperlactatemia on admission in critically ill patients with acute myocardial infarction: A retrospective study from MIMIC-IV.

Background: It has not been verified whether there is a correlation between admission hyperlactatemia and outcomes in critically ill patients with acute myocardial infarction (AMI), especially in large data studies, which we aimed to do in this study. Methods: For this retrospective study, we extracted analysis data from a famous online intensive care unit database, the Medical Information Mart for Intensive Care (MIMIC)-IV. Included patients were divided into four groups according to the serum lactate level on admission. Hospital mortality and mortality over time were the main outcomes. To explore the relationship between admission hyperlactatemia and outcomes in critically ill patients with AMI, logistic regression, Cox regression, Kaplan-Meier curves, and subgroup analyses were used. Results: 2171 patients matching the selection criteria were enrolled in this study. After adjusting for potential confounding factors, hyperlactatemia on admission contributed to increased short-term mortality in critically ill patients with AMI. The adjusted odds ratio for hospital mortality were 1.62, 3.46 and 5.28 in the mild, moderate, and severe hyperlactatemia groups (95% CI: 1.20-2.18, 2.15-5.58, and 2.20-12.70, respectively). The adjusted hazard ratio for 7-day and 30-day mortality were 1.99 and 1.35 (95% CI: 1.45-2.73 and 1.09-1.67) in the mild hyperlactatemia group, 3.33 and 2.31 (95% CI: 2.22-4.99 and 1.72-3.10) in the moderate hyperlactatemia group, 4.81 and 2.91 (95% CI: 2.86-8.08 and 1.88-4.50) in the severe hyperlactatemia group. The adjusted hazard ratio for 1-year and 5-year mortality were 2.03 and 1.93 (95% CI: 1.58-2.62 and 1.52-2.47) in the moderate hyperlactatemia group, 1.92 and 1.74 (95% CI: 1.28-2.89 and 1.17-2.59) in the severe hyperlactatemia group. Subgroup analyses indicated that the positive correlation between serum lactate level on admission and short-term mortality of critically ill patients with AMI was similar in the subgroups of cardiogenic shock and acute heart failure (P for interaction > 0.05). Conclusion: Hyperlactatemia, especially moderate and severe hyperlactatemia, on admission is closely related to higher short-term mortality incidence in critically ill patients with AMI. The relationship between serum lactate level on admission and short-term mortality of critical AMI patients is stable in subgroups of cardiogenic shock and acute heart failure.

A novel cuproptosis-related gene signature for predicting prognosis in cervical cancer.

Purpose: Cuproptosis, a form of copper-induced cell death, can be a promising therapeutic target for refractory cancers. Hence, we conducted this research to explore the association between cuproptosis and prognosis in cervical cancer (CC). Methods: For constructing a prognostic signature based on cuproptosis-related genes from TCGA database, the least absolute shrinkage and selection operator Cox regression was utilized. The GSE44001 cohort was utilized for validation. Results: A total of nine cuproptosis-related genes showed distinct expression in CC and normal samples in TCGA-GTEx cohort. Two risk groups were identified based on a seven-gene signature. A significant decrease in overall survival was observed in the high-risk group (p < 0.001). The risk score (HR = 2.77, 95% CI = 1.58-4.86) was an autocephalous predictor with a better predictive ability than the clinical stage. Functional analysis indicated that immune activities were suppressed more in the high-risk group than in the low-risk group. A total of 11 candidate compounds targeting the signature were identified. Conclusion: A total of seven cuproptosis-related gene signatures were constructed to predict prognosis and propose a new therapeutic target for patients with CC.

The association between non-alcoholic fatty liver disease (NAFLD) and advanced fibrosis with blood selenium level based on the NHANES 2017-2018.

BACKGROUND & OBJECTIVE: Selenium was one of the essential trace elements that played a pivotal role in human health. Although previous studies have investigated the relationship between selenium and non-alcoholic fatty liver disease (NAFLD) and fibrosis, these findings were still inconclusive. Our study was aimed to explore the association between blood selenium level and NAFLD and advanced liver fibrosis diagnosed by vibration controlled transient elastography (VCTE) in US adults. METHODS: All data were extracted from National Health and Nutrition Examination Survey database (2017-2018). Participants were divided into four groups according to quartile of blood selenium level. Liver stiffness and controlled attenuation parameter (CAP) were measured by VCTE. Multiple logistic regression models and subgroup analyses were conducted to determine the association between blood selenium level and NAFLD and advanced liver fibrosis diagnosed by a variety of methods. RESULTS: A total of 3336 participants were enrolled in main analysis. In multiple logistic regression models, the higher blood selenium level (>205.32, ≤453.62 µg/L) had a significant positive association with NAFLD (ß = 1.31). Moreover, high blood selenium level had significantly inversely association to advanced liver fibrosis (ß = 0.61). In subgroup analysis, the main inversely correlation between blood selenium and advanced liver fibrosis was found in males with high blood selenium level. Despite dietary selenium intake being adjusted or in different subgroups, the associations between blood selenium level and NAFLD/advanced liver fibrosis remained significant. CONCLUSIONS: This study showed that blood selenium level were positively association with NAFLD among US population. Participants with lower blood selenium level showed a higher percentage of advanced liver fibrosis. Blood selenium is more likely to cause NAFLD and liver fibrosis due to imbalances in selenium homeostasis rather than dietary selenium intake.Key messagesHigh blood selenium level was association with NAFLD diagnosed by vibration controlled transient elastography.Participants with lower blood selenium level had high percentage of advanced liver fibrosis.NAFLD and liver fibrosis are caused by an imbalance of selenium homeostasis, not by dietary selenium intake.

A Nomogram for Predicting Hospital Mortality in Intensive Care Unit Patients with Acute Myocardial Infarction.

BACKGROUND: This study aims to construct and validate an early-stage nomogram for predicting hospital mortality of ICU patients with acute myocardial infarction (AMI), to help clinicians determine the appropriate intervention. METHODS: The primary cohort of 2704 patients diagnosed with acute myocardial infarction in admission records from eICU-Collaborative Research Database (eICU-CRD) v2.0. Univariate logistic regression analysis and multivariate logistic regression analysis were enrolled for the construction of the predictive nomogram. Demographic factors, history of clinical cardiovascular disease, vital signs, the use of vasopressors, urine output, and serum variables in the first 24 hours were included in this analysis. The nomogram was evaluated by performance traits including Harrell's concordance index (C-index) and area under the receiver operating characteristic (AUC) analysis, calibration curve, and decision curve analysis (DCA). The nomogram was validated in a different cohort containing 1026 subjects collected from MIMIC-III Database v1.4. Finally, in order to compare the performance with other classic prediction models, AUC analysis, calibration curve, DCA and accuracy analysis (net reclassification improvement (NRI)) were conducted for three ICU scores in validated cohort. RESULTS: The nomogram revealed 14 predictors of the first 24 hours derived from univariate and multivariable analyses, including age, history of peripheral vascular disease, atrial fibrillation, cardiogenic shock and cardiac arrest, the use of norepinephrine, urine output, white blood cell (WBC), hemoglobin (Hb), red blood cell (RBC), red cell distribution width (RDW), glucose, bicarbonate and magnesium. The C-index of this nomogram was 0.834 (95% CI 0.812 to 0.856). Then, the result of AUC analysis, the DCA and calibration curve indicated that our nomogram was feasible for clinical prediction. The predictive ability and clinical use of the nomogram were verified in the validated cohort. The AUC analysis of ICU scores showed that the AUC of these score systems was ranged from 0.811 to 0.860 (the AUC of nomogram: 0.885). Moreover, our nomogram also showed a better performance in calibration curve and DCA NRI. CONCLUSION: The study presents a prediction nomogram incorporating 14 variables that could help identify AMI patients admitted in ICU who might have a high risk of hospital mortality in the first hospitalized 24 hours. This nomogram showed a better performance than normal ICU score systems.

Association Between the Admission Serum Bicarbonate and Short-Term and Long-Term Mortality in Acute Aortic Dissection Patients Admitted to the Intensive Care Unit.

OBJECTIVE: Serum bicarbonate (HCO3-) level is strongly related to multiple cardiovascular complications. Currently, there is no study evaluating the prognostic ability of serum HCO3- level in intensive care unit (ICU) patients with acute aortic dissection (AAD). Hence, this study was to assess the relationship between admission serum HCO3- level and clinical outcomes in patients with AAD. DESIGN SETTINGS AND PARTICIPANTS: Clinical data were extracted from the MIMIC-III database. Cox proportional hazards models and Kaplan-Meier (KM) survival curve were used to evaluate the association between serum HCO3- levels and short- and long-term mortality in ICU patients with AAD. The subgroup analysis and the receiver operating characteristic (ROC) curve analysis and further KM survival curve based on best cut-off value were applied to assessment of the performance of HCO3- in predicting the mortality in each period (30 days, 90 days, 1 year and 5 years). MAIN RESULTS: Firstly, 336 eligible patients were trisected to low-HCO3- level group (<22 mmol/L), mid-HCO3- level group (22-24 mmol/L) and high-HCO3- level group (>24 mmol/L). Then, in multivariate analysis, the serum HCO3- of low levels (<22 mmol/L) was a significant risk predictor of all-cause mortality in 30 days, 90 days, 1 year and 5 years. Subgroup analyses indicated that there is no interaction in most strata. Finally, areas under ROC curve ranged from 0.60 to 0.69. CONCLUSION: The low HCO3- serum level measured at ICU admission significantly predicts short-term and long-term mortality in AAD patients.

High-Normal Serum Magnesium and Hypermagnesemia Are Associated With Increased 30-Day In-Hospital Mortality: A Retrospective Cohort Study.

Background: Magnesium, the fourth most abundant mineral nutrient in our body, plays a critical role in regulating ion channels and energy generation, intracardiac conduction, and myocardial contraction. In this study, we assessed the association of admission serum magnesium level with all-cause in-hospital mortality in critically ill patients with acute myocardial infarction (AMI). Methods: Clinical data were extracted from the eICU Collaborative Research Database (eICU-CRD). Only the data for the first intensive care unit (ICU) admission of each patient were used, and baseline data were extracted within 24 h after ICU admission. Logistic regression, Cox regression, and subgroup analyses were conducted to determine the relationship between admission serum magnesium level and 30-day in-hospital mortality in ICU patients with AMI. Results: A total of 9,005 eligible patients were included. In the logistic regression analysis, serum magnesium at 2.2 to ≤2.4 and >2.4 mg/dl levels were both significant predictors of all-cause in-hospital mortality in AMI patients. Moreover, serum magnesium of 2.2 to ≤2.4 mg/dl showed higher risk of in-hospital mortality than magnesium of >2.4 mg/dl (adjusted odds ratio, 1.63 vs. 1.39). The Cox regression analysis yielded similar results (adjusted hazard ratio, 1.36 vs. 1.25). Conclusions: High-normal serum magnesium and hypermagnesemia may be useful and easier predictors for 30-day in-hospital mortality in critically ill patients with AMI.

Bioinformatics analysis reveals the landscape of immune cell infiltration and immune-related pathways participating in the progression of carotid atherosclerotic plaques.

Atherosclerosis is a systemic disease associated with inflammatory cell infiltration and activation of immune-related pathways. In our study, we aimed to uncover immune-related changes and explore novel immunological features in the development of carotid atherosclerotic plaques. First, we applied integrated bioinformatics methods, including CIBERSORT and gene set enrichment analysis (GSEA). The gene expression matrices GSE28829, GSE41571, and GSE43292 were obtained from the Gene Expression Omnibus (GEO) dataset. After a series of data pre-processing steps, the resulting combined expression matrices were analysed using the CIBERSORT, GSEA, and Cluster Profiler packages. After the comparison and analysis between the carotid atherosclerotic plaques in the early and advanced stages, we discovered that there is a higher percentage of activated memory CD4 T cells and a lower percentage of resting memory CD4 cells in advanced-stage plaques. Moreover, activation of memory CD4 T cells can promote the development of carotid atherosclerotic plaques. Additionally, FOXP3+ Treg cell maturation can also participate in the progression of carotid plaques.

A prognostic nomogram based on lymph node ratio for postoperative vulvar squamous cell carcinoma from the Surveillance, Epidemiology, and End Results database: a retrospective cohort study.

BACKGROUND: Vulvar carcinoma is a rare gynecological malignancy. The most commonly used staging system for vulvar cancer is the 2009 International Federation of Gynecology and Obstetrics (FIGO) staging system. Nevertheless, it does not incorporate many indispensable prognostic parameters, which prominently influence vulvar cancer patient survival. Thus, the development of a prediction model for evaluating survival prognosis in postoperative vulvar squamous cell cancer patients is of vital importance. METHODS: Data from 2,166 patients with pathologically confirmed diagnosis of vulvar squamous cell carcinoma from 2004 to 2015 were acquired from the Surveillance, Epidemiology, and End Results (SEER) database. Thirty percent of the patients were randomly assigned to the validation group, and the remainder were used to develop the nomogram. Parameters that significantly correlated with overall survival (OS) were used to create the nomogram. Concordance index (C-index), calibration curve, and decision curve analysis (DCA) were used to assess the predictive accuracy and discriminability of the nomogram model. Additionally, the C-index and DCA of the nomogram and the FIGO staging system were compared. RESULTS: Following multivariate analysis of the training cohort, independent factors for OS, including race, age at diagnosis, marital status, FIGO stage, tumor diameter, and lymph node ratio (LNR), were included in the nomogram model. The calibration curve indicated a high correlation between the nomogram-predicted and observed survival probability. The C-index of the nomogram in the training cohort was 0.772 (95% CI: 0.752-0.792), statistically superior to the C-index value of the FIGO staging system (0.676, 95% CI: 0.654-0.698). In DCA, compared to the FIGO staging system, this nomogram showed a greater net benefit and a wider range of threshold probability. Results were verified by an internal validation cohort. CONCLUSIONS: Our nomogram, based on LNR, showed superior prognostic predictive accuracy compared with the FIGO staging system for predicting OS in postoperative vulvar squamous cell carcinoma patients.

Identification of Target Genes and Transcription Factors in Mice with LMNA-Related Dilated Cardiomyopathy by Integrated Bioinformatic Analyses.

BACKGROUND Dilated cardiomyopathy (DCM), which is characterized by enlarged ventricular dimensions and systolic dysfunction, is the most common type of cardiomyopathy. Mutations in the LMNA gene are reported in approximately 10% of familial DCM cases. However, the mechanism of LMNA mutations in human DCM remains unclear. MATERIAL AND METHODS We used the GSE36502 and GSE123916 datasets to obtain gene expression profiles from LMNA-related DCM mice and to identify differentially expressed genes (DEGs). Crucial function and pathway enrichment analyses of DEGs were performed. Protein-protein interaction (PPI) network analysis was carried out to identify the top 10 hub genes, which were validated using reverse transcription-polymerase chain reaction (RT-PCR) to find target genes. Weighted gene co-expression network analysis (WGCNA) was used to explore the module relevant to external traits of LMNA-related DCM mice. Transcription factors (TFs) for the selected genes were analyzed using NetworkAnalyst. RESULTS A total of 156 common DEGs (co-DEGs) were identified, including 80 up-regulated and 76 down-regulated genes. The enriched biological functions and pathways were oxidative stress, regulation of apoptosis, regulation of fibrosis, and MAPK pathways. Five target genes (Timp1, Hmox1, Spp1, Atf3, and Adipoq) were verified after RT-PCR. Most co-DEGs were discovered to be related to the development of external traits. Three TFs (ELF1, ETS1, and NRF1) showed close interactions with the hub genes. CONCLUSIONS Our study used integrated bioinformatic analyses and revealed some important genes in mice with LMNA-related DCM, which could provide novel insights into the mechanism underlying human LMNA-related DCM.

Identification of key genes and pathways affected in epicardial adipose tissue from patients with coronary artery disease by integrated bioinformatics analysis.

BACKGROUND: Coronary artery disease (CAD) is a common disease with high cost and mortality. Here, we studied the differentially expressed genes (DEGs) between epicardial adipose tissue (EAT) and subcutaneous adipose tissue (SAT) from patients with CAD to explore the possible pathways and mechanisms through which EAT participates in the CAD pathological process. METHODS: Microarray data for EAT and SAT were obtained from the Gene Expression Omnibus database, including three separate expression datasets: GSE24425, GSE64554 and GSE120774. The DEGs between EAT samples and SAT control samples were screened out using the limma package in the R language. Next, we conducted bioinformatic analysis of gene ontology terms and Kyoto Encyclopedia of Genes and Genomes pathways to discover the enriched gene sets and pathways associated with DEGs. Simultaneously, gene set enrichment analysis was carried out to discover enriched gene functions and pathways from all expression data rather than DEGs. The PPI network was constructed to reveal the possible protein interactions consistent with CAD. Mcode and Cytohubba in Cytoscape revealed the possible key CAD genes. In the next step, the corresponding predicted microRNAs (miRNAs) were analysed using miRNA Data Integration Portal. RT-PCR was used to validate the bioinformatic results. RESULTS: The three datasets had a total of 89 DEGs (FC log2 > 1 and P value < 0.05). By comparing EAT and SAT, ten common key genes (HOXA5, HOXB5, HOXC6, HOXC8, HOXB7, COL1A1, CCND1, CCL2, HP and TWIST1) were identified. In enrichment analysis, pro-inflammatory and immunological genes and pathways were up-regulated. This could help elucidate the molecular expression mechanism underlying the involvement of EAT in CAD development. Several miRNAs were predicted to regulate these DEGs. In particular, hsa-miR-196a-5p and hsa-miR-196b-5p may be more reliably associated with CAD. Finally, RT-PCR validated the significant difference of OXA5, HOXC6, HOXC8, HOXB7, COL1A1, CCL2 between EAT and SAT (P value < 0.05). CONCLUSIONS: Between EAT and SAT in CAD patients, a total of 89 DEGs, and 10 key genes, including HOXA5, HOXB5, HOXC6, HOXC8, HOXB7, COL1A1, CCND1, CCL2, HP and TWIST1, and miRNAs hsa-miR-196a-5p and hsa-miR-196b-5p were predicted to play essential roles in CAD pathogenesis. Pro-inflammatory and immunological pathways could act as key EAT regulators by participating in the CAD pathological process.