The clinical role and regulatory mechanism of KMT2E-AS1 in coronary heart disease.

Objective To explore the predictive effect of negative emotions such as anxiety and depression on the poor prognosis of coronary heart disease (CHD) patients with stent implantation and to seek the improvement of clinical intervention measures. Methods A total of 303 patients with CHD and PCI were recruited from February 2019 to April 2021. The risk factors of CHD such as anxiety and depression, age, sex, smoking and drinking, BMI, hypertension, diabetes, dyslipidemia, and family history of CHD were collected. Meanwhile, clinical data such as laboratory examination, angiography, diseased vessels, and stent types were collected. The patients were followed up for 1 year, and the medical records, hospitalization records, or death records were checked by telephone interview once a month. Major adverse cardiovascular events (MACE) such as emergency and causes, readmission times and causes, new nonfatal myocardial infarction, stent restenosis, heart failure, arrhythmia, and death were recorded. The incidence of anxiety and depression in patients after PCI was counted, and Cox regression was applied to analyze the influence and prediction of anxiety and depression on MACE in patients with CHD stent implantation and improve clinical intervention measures. Results Compared with those without MACE, anxiety (56.25% vs 30.63%), depression (62.5% vs 22.88%, P < 0.01), anxiety combined with depression (46.88% vs 15.50%, P < 0.01), and hypertension history (71.8% vs 39.11%, P < 0.01) were more common in patients with MACE. Uncorrected Cox proportional hazard regression found that people with anxiety had a higher risk of developing MACE than those without anxiety (HR 3.181, P < 0.01). Multiple Cox proportional hazard regression analysis of anxiety showed that anxiety was an independent predictor of cumulative MACE (P < 0.01). The risk of developing MACE in patients with anxiety was 3.742 times higher than that in patients without anxiety (P < 0.01). Uncorrected Cox hazard regression analysis showed that people with depression had a higher risk of developing MACE than those without depression (HR 5.434, P < 0.01). Furthermore, the results also uncovered that depression was an independent predictor of cumulative MACE (P < 0.01). The risk of MACE in patients with depression was 3.087 times higher than that in patients without depression (P < 0.01). Cox hazard regression showed that the risk of MACE in patients with anxiety and depression was significantly higher than that in patients without anxiety and depression (HR 4.642, P < 0.01). After screening, it was found that anxiety with depression could predict the occurrence of MACE (P < 0.01). The risk of MACE in patients with anxiety and depression was 3.702 times higher than that in patients without anxiety and depression (P < 0.01). Cox regression analysis showed that the risk of MACE with only anxiety and depression was 2.793 times higher than that without anxiety and depression (95% CI 0.914 8.526), with no statistical significance (P > 0.05), and the risk of MACE with depression without anxiety was significantly higher than that without anxiety and depression (P < 0.01). The risk of MACE in patients with anxiety and depression was 7.303 times higher than that in patients without anxiety and depression (P < 0.01). Conclusion Negative emotions such as anxiety and depression can increase the risk of poor prognosis of patients with CHD. Therefore, in clinical work, in addition to routine treatment and nursing during hospitalization, it is recommended to screen patients with depression in CHD patients. Medical staff should use simple and effective assessment tools in time and take active measures to improve the depression of patients. This trial is registered with ChiCTR2200055645.

Our previous study finds that exosomal microRNA (miR)-186-5p promotes viability and invasion of vascular smooth muscle cells to accelerate atherosclerosis via inactivating phosphoinositide 3 kinase/protein kinase B/mammalian target of rapamycin pathway. Subsequently, this study aimed to identify the linkage of serum exosomal miR-186-5p with clinical features and major adverse cardiovascular events (MACE) in coronary heart disease (CHD) patients. Serum exosomal miR-186-5p was quantified in 175 CHD patients and 50 healthy controls (HCs) via reverse transcription quantitative polymerase chain reaction. Our study revealed that serum exosomal miR-186-5p was enhanced in CHD patients vs. HCs (P < 0.001). In CHD patients, serum exosomal miR-186-5p was positively correlated with total cholesterol (P = 0.002) and low-density lipoprotein cholesterol (P = 0.003). Elevated serum exosomal miR-186-5p was linked with increased Gensini score (P = 0.028) and stenosis degree categorized by the Gensini score (P = 0.018). Regarding MACE, the 1-year and 2-year accumulating MACE rate was 6.6% and 15.6%, respectively. Serum exosomal miR-186-5p was elevated in CHD patients with MACE vs. those without (P = 0.042). By Kaplan-Meier curves and log-rank analyses, serum exosomal miR-186-5p > 1.000 (P = 0.404) and > 1.610 (P = 0.328) was not related to accumulating MACE. While serum exosomal miR-186-5p > 3.390 exhibited a correlative trend with increased accumulating MACE, but not achieving statistical significance (P = 0.071). The 1-year and 2-year accumulating MACE rate of patients with serum exosomal miR-186-5p > 3.390 was 11.5% and 21.5%, respectively; while the rate was 3.3% and 11.5% in patients with serum exosomal miR-186-5p ≤ 3.390, accordingly. Conclusively, serum exosomal miR-186-5p positively associates with lipid level, coronary stenosis degree, and the risk of MACE in CHD patients.

Objective: To investigate the predictive value of cardiopulmonary exercise test (CPET) indexes for major adverse cardiovascular events (MACE) in patients with coronary heart disease (CHD). Methods: This study was a retrospective cohort study. CHD patients were consecutively enrolled who procedure CPET before discharge from the Department of Cardiology, General Hospital of Northern Theater Command from November 2015 to September 2021 were enrolled. Demographic information, past medical history, CPET indexes and other baseline data were collected and the patients were followed up. Patients were divided into a MACE group and a control group according to the presence or absence of MACE. A multivariate Cox proportional hazard regression model was used to analyze the CPET indexes with predictive value for MACE in CHD patients. Results: A total of 3 800 patients were eligible for the criterion, age (57.2±8.8) years, 2 920 (76.84%) males. During a follow-up of 1 237 (695, 1 596) days, 390 (10.26%) patients were in MACE group, and 3 410 (89.74%) patients were in control group. In adjusted multivariable analysis, higher metabolic equivalent of tasks (MET) at anaerobic threshold (AT) is an independent protective factor for MACE in patients with CHD (HR=0.75, 95%CI 0.62-0.90, P=0.002), higher VE/VCO2 is an independent risk factor for MACE in CHD patients (HR=1.05, 95%CI 1.02-1.07, P=0.001). Conclusion: In CPET, high MET at AT is an independent protective factor for MACE in patients with CHD, and high VE/VCO2 is an independent risk factor for MACE in CHD patients.

ObjectiveThis study aimed to investigate the role of long non‐coding RNA (lncRNA) THRIL in coronary heart disease (CHD) patients.MethodsA total of 420 patients who underwent coronary arteriography due to suspected symptoms of CHD were enrolled, in which 220 were diagnosed as CHD and 200 were set as control subjects. LncRNA THRIL in plasma samples of CHD patients and control subjects was detected by reverse transcription‐quantitative polymerase chain reaction. Gensini score and biochemical indexes were evaluated in CHD patients and control subjects. Plasma inflammatory cytokines were detected, and major adverse cardiovascular events (MACE) were recorded in CHD patients.ResultsBoth before and after adjustment by age/gender, lncRNA THRIL was increased in CHD patients compared with control subjects (both P < .001), and it well predicted enhanced CHD risk by receiver operating characteristic curves. For coronary artery stenosis, it was positively correlated with Gensini score (P < .001, r = .430). For clinical characteristics, lncRNA THRIL was positively correlated with diabetes mellitus occurrence (P < .001) and fasting blood glucose (FBG) level (P = .029, r = .147). For inflammation, it was positively associated with CRP (P < .001, r = .374), TNF‐α (P < .001, r = .249), IL‐1β (P = .001, r = .222), IL‐8 (P < .001, r = .254), and IL‐17 (P = .011, r = .172), while negatively correlated with IL‐10 (P < .001, r = −.244). For prognosis, lncRNA THRIL was positively associated with MACE accumulating rate (P = .037) in CHD patients.ConclusionLong non‐coding RNA THRIL was increased in CHD patients and well predicted elevated CHD risk. Moreover, it was correlated with enhanced coronary stenosis, systematic inflammation, FBG level, and MACE risk in CHD patients.

A microbiota pattern associated with cardiovascular events in secondary prevention: the CORDIOPREV study.

Aim: This study aimed to investigate the correlation of ITIH4 with inflammatory cytokines, stenosis degrees and prognosis in coronary heart disease (CHD) patients. Methods: Serum ITIH4 levels of 300 CHD patients and 30 controls, together with levels of TNF-α, IL-6, IL-8 and IL-17A of CHD patients, were determined using ELISA. Results: Serum ITIH4 was reduced in CHD patientsversus controls (p<0.001). ITIH4 was negatively linked with TNF-α, IL-6, IL-8, IL-17A, C-reactive protein, serum creatinine and Gensini score in CHD patients (all p<0.050). ITIH4 quartile level negatively correlated with the cumulative major adverse cardiovascular event rate (p=0.041). Conclusion: Serum ITIH4 may serve as an anti-inflammatory biomarker that negatively associates with stenosis degree and major adverse cardiovascular event risk in CHD patients.

BackgroundBrain‐derived neurotrophic factor (BDNF) exerts protective roles against dyslipidemia, atherosclerosis, and inflammation in cardiovascular diseases; meanwhile, it retards CD4+ T cell differentiation into T helper (Th)1 and Th17 cells. Hence, this study aimed to investigate the linkage of serum BDNF with Th1/Th2 ratio, Th17/regulatory T (Treg) ratio, and major adverse cardiovascular events (MACE) risk in the coronary heart disease (CHD) patients.MethodsThis prospective study detected serum BDNF in 210 CHD patients, 50 disease controls (DCs), and 50 healthy controls (HCs) using an enzyme‐linked immunosorbent assay. For CHD patients only, the proportion of Th1, Th2, Th17, and Treg cells in blood CD4+ T cells was calculated by flow cytometry.ResultsThe BDNF varied among CHD patients, DC, and HC (p < 0.001). Specifically, BDNF was declined in CHD patients compared with DCs (p < 0.001) and HCs (p < 0.001). In CHD patients, BDNF was negatively related to Th1 cells (p = 0.031), Th1/Th2 ratio (p = 0.026), Th17 cells (p = 0.001), and Th17/Treg ratio (p = 0.002). Concerning the prognosis, BDNF was reduced in patients with MACE occurrence compared to patients without MACE occurrence (p = 0.006). Furthermore, BDNF showed a trend (lacked statistical significance) to relate to longer MACE‐free survival (p = 0.059). Besides, BDNF was related to the absence of obesity (p = 0.019), decreased total cholesterol (p = 0.043), low‐density lipoprotein cholesterol (p = 0.019), C‐reactive protein (p = 0.012), and Gensini score (p = 0.005).ConclusionSerum BDNF negatively correlates with Th1/Th2 ratio, Th17/Treg ratio, and estimates lower MACE risk in CHD patients.

Funding Acknowledgements Type of funding sources: None. Background Insomnia is highly prevalent in coronary heart disease (CHD) patients. However, the potential effect of insomnia on the risk of recurrent major adverse cardiovascular events (MACE) remains uncertain. Purpose To estimate the prospective association of insomnia and the risk of recurrent MACE in a CHD population from routine clinical practice. Methods This prospective cohort study included 1082 consecutive patients 2-36 (mean 16) months after a myocardial infarction and/or a coronary revascularization procedure. Data on insomnia, coronary risk factors and comorbidity were collected at baseline. Insomnia was assessed by Bergen insomnia scale (BIS), based on sleep symptoms per week during the past three months. BIS is constructed from the clinical diagnostic criteria for primary insomnia in DSM-IV TR. The primary composite endpoint of MACE defined as cardiovascular death, hospitalization due to myocardial infarction, revascularization, stroke or heart failure was obtained from the hospital records on average 4.2 (SD 0.3) years after the baseline study. Data were analysed using Cox proportional hazard regression on a multiple imputated dataset stratified by prior coronary events. Results At baseline, mean age was 62 (range 31-80) years, 21% were females, 90% were revascularized, 47% had participated in cardiac rehabilitation and the prescription rate of antiplatelets (97%) and statins (93%) were high. A total of 364 MACE (21%, 95% CI 19%-24%) occurred in 225 patients, including 39 CV deaths. Almost half of the patients (45%) suffered from insomnia at baseline and 24% used sleep medication the past week. For insomnia, the relative risk (RR) of recurrent MACE was 1.62 (95% confidence interval (CI) 1.24-2.11, p-value&amp;lt;0.001) in age and gender adjusted analysis, 1.49 (95% CI 1.14, 1.97, p-value=0.004) in analysis also adjusted for coronary risk factors and 1.48 (95% CI 1.12, 1.96, p-value=0.006) in a multi-adjusted analysis including age, gender, coronary risk factors and cardiovascular comorbidity. When also adjusted for symptoms of anxiety and depression the RR of insomnia on recurrent MACE remained significant at 1.41 (95% CI 1.05, 1.89, p-value=0.023). Insomnia accounted for 16% of the MACE in attributable risk fraction analyses, being third in importance after smoking (27%) and low physical activity (21%). Obstructive sleep apnea (Berlin Questionnaire) was not associated with recurrent MACE. Conclusions Insomnia was associated with increased risk of recurrent MACE in this prospective cohort following CHD patients from routine clinical practice. The association remained significant even after adjustments for the major coronary risk factors, comorbidity and symptoms of anxiety and depression, indicating that the effects of insomnia is not mediated through poor risk factor control and other psychosocial factors alone. These results emphasize the importance of identifying patients with insomnia as part of coronary rehabilitation.

ObjectiveYKL-40, previously known as chitinase-3-like protein 1 (CHI3L1), is an inflammation-related glycoprotein that promotes atherosclerosis, but its application and optimal cut-off value as a prognostic biomarker in coronary heart disease (CHD) require more clinical evidence. Thus, this prospective study aimed to evaluate the linkage of serum YKL-40 with disease features, inflammatory cytokines, and major adverse cardiovascular events (MACEs) in CHD patients.MethodsA total of 410 CHD patients were enrolled for serum YKL-40 determination via enzyme-linked immunosorbent assay. Meanwhile, serum YKL-40 levels in 100 healthy controls (HCs) were also quantified.ResultsYKL-40 level was higher in CHD patients compared with that in HCs (P < 0.001). YKL-40 was positively linked with hyperlipidemia (P = 0.014), diabetes mellitus (P = 0.001), fasting blood glucose (P = 0.045), C-reactive protein (P < 0.001), the Gensini score (P < 0.001), and stenosis degree (graded by the Gensini score) (P < 0.001) in CHD patients. In addition, an elevated YKL-40 level was associated with increased levels of tumor necrosis factor alpha (P = 0.001), interleukin (IL)-1β (P = 0.001), IL-6 (P < 0.001), and IL-17A (P = 0.002) in CHD patients. The 1-/2-/3-year cumulative MACE rates of CHD patients were 5.5%, 14.4%, and 25.0%, respectively. Regarding the prognostic capability, YKL-40 ≥100 ng/ml (the median cut-off value) (P = 0.003) and YKL-40 ≥150 ng/ml (the third interquartile cut-off value) (P = 0.021) reflected an elevated accumulating MACE rate, whereas accumulating MACE was not different between CHD patients with YKL-40 ≥80 and <80 ng/ml (the first interquartile cut-off value) (P = 0.083).ConclusionSerum YKL-40 is positively linked with inflammatory cytokines and the Gensini score, whose high expression cut-off by 100 and 150 ng/ml estimates a higher MACE risk in CHD patients.

Objective This study aimed to evaluate the diagnostic performance, risk assessment, and treatment-guiding value of coronary computed tomographic angiography (CCTA) in patients with coronary heart disease (CHD). Methods The diagnostic value of CCTA for CHD was assessed by analyzing key parameters including sensitivity, specificity, accuracy, positive predictive value, and negative predictive value. Additionally, the diagnostic relevance of specific CCTA-derived metrics was explored. Patients with confirmed CHD underwent percutaneous coronary intervention (PCI), and the occurrence of major adverse cardiovascular events (MACE) within one year after PCI were recorded. Differences in CCTA parameters between patients with and without MACE were compared. Multivariate logistic regression was conducted to identify independent risk factors for post-PCI MACE. Results CCTA demonstrated high diagnostic value for CHD. Compared to the control group, patients with CHD exhibited significantly greater plaque length, total plaque volume, calcified plaque volume, lipid plaque volume, plaque burden, and coronary diameter stenosis, along with a smaller minimum lumen area. These imaging features were predictive of CHD. Relative to the non-MACE group (n = 69), the MACE group (n = 56) had higher plaque length, total plaque volume, plaque burden, and coronary diameter stenosis rate, and smaller minimum lumen area. Multivariate logistic regression analysis identified plaque burden, coronary diameter stenosis, and hypertension serve as independent predictors for adverse cardiovascular events following PCI in CHD patients. Conclusion CCTA is a valuable noninvasive modality for the diagnosis of CHD, risk assessment, and optimization of treatment strategies, particularly in predicting adverse outcomes following PCI.

BackgroundAt present, the relationship among inflammatory markers [monocytes/HDL-c (MHR), neutrophils/HDL-c (NHR) and lymphocytes/HDL-c (LHR)] and long-term prognosis of coronary heart disease (CHD) is still unclear. Therefore, this study explores the relationship between inflammatory indicators and the risk of long-term major adverse cardiovascular events (MACE) in elderly patients with CHD.MethodsA retrospective analysis was conducted on 208 elderly patients who underwent coronary angiography at Wuhan Fourth Hospital from August 2022 to August 2023. They were divided into the CHD group (N = 116) and control group (N = 92). Patients in the CHD group were followed up for 1 year and divided into the MACE group (N = 36) and the non-MACE group (N = 80) according to whether MACE occurred.ResultsIn elderly patients, logistic regression analysis shows that MHR is an independent risk factor for CHD (OR = 3.050, 95% CI 1.318–1.772). ROC curve analysis found that MHR (AUC = 0.865, 95% CI 0.811–0.919, p < 0.001) is higher than NHR and LHR. In patients with CHD, the spearman analysis show that MHR is positively correlated with Gensini score (R = 0.266, p = 0.004). The logistic regression analysis found that MHR is independent risk factors for MACE (OR = 6.048, 95% CI 1.224–1.941, p = 0.002). ROC analysis showed that the critical value of MHR to predict MACE was 0.651, the sensitivity of 58.3% and specificity of 90.0% could predict MACE, and the AUC was 0.793 (95% CI 0.702–0.884, p < 0.001) is higher than LHR.ConclusionIn elderly patients, MHR is an independent predictor of CHD and long-term MACE and is positively correlated with the severity of coronary artery lesions.

Cell division control 42 (CDC42) regulates blood lipids, atherosclerosis, T cell differentiation and inflammation, which is involved in the process of coronary heart disease (CHD). This study aimed to evaluate the CDC42 level and its correlation with clinical features, the T-helper 17 (Th17)/regulatory-T (Treg) cell ratio and prognosis in CHD patients. In total, 210 CHD patients, 20 healthy controls and 20 disease controls were enrolled. Serum CDC42 levels of all participants were measured by enzyme-linked immunosorbent assay. In CHD patients, Th17 and Treg cells were discovered by flow cytometry; CHD patients were followed-up for a median of 16.9 months (range of 2.5–38.2 months). CDC42 level was lowest in CHD patients (median (interquartile range (IQR)): 402.5 (287.3–599.0) pg/mL), moderate in disease controls (median (IQR): 543.5 (413.0–676.3) pg/mL) and highest in healthy controls (median (IQR): 668.0 (506.5–841.3) pg/mL) (p < .001). Moreover, in CHD patients, lower CDC42 level was related to more prevalent diabetes mellitus (p = .021), and higher levels of C-reactive protein (p = .001), Gensini score (p = .006), Th17 cells (p = .001) and Th17/Treg ratio (p < .001) but was associated with lower Treg cells (p = .018). Furthermore, CDC42 low level [below the median level (402.5 pg/mL) of CDC42 in CHD patients] was correlated with higher accumulating major adverse cardiovascular event (MACE) risk (p = .029), while no correlation was found between the quartile of CDC42 level and accumulating MACE risk in CHD patients (p = .102). The serum CDC42 level is decreased and its low level is related to higher Th17/Treg ratio and increased accumulating MACE risk in CHD patients.

This research aimed to evaluate the influence of the systemic immunoinflammatory index (SII) on the development of major adverse cardiovascular events (MACE) in individuals with coronary heart disease (CHD) and heart failure (HF), as determined by propensity score matching (PSM). The 218 patients with CHD and HF were divided into the MACE group and the non-MACE group. After balancing the baseline data of the two groups by PSM (76 cases in each group after matching, total sample 152 cases), the diagnostic value of SII for MACE was analyzed using the ROC curve to determine the optimal threshold value. The independent risk factors for MACE were analyzed using multifactorial Cox regression. Kaplan-Meier curves were employed to compare the MACE-free survival rates of patients with varying SII levels. PSM effectively balanced the baseline characteristics of the two groups, with absolute values of standardized mean difference for all variables < 0.1. Platelet counts, neutrophil counts, neutrophil-to-lymphocyte ratio, SII, C-reactive protein (CRP), and NT-proBNP levels were significantly higher in the MACE group than in the non-MACE group (P < 0.05). The ROC curve showed that the area under the curve (AUC) of SII after PSM was 0.788 (95% CI 0.714-0.860, P < 0.001), with an optimal threshold of 589.31 (sensitivity 81.58%, specificity 65.79%). Multifactorial Cox analysis showed that SII ≥ 589.31 (HR 1.92, 95% CI 1.18-3.14, P = 0.009), elevated CRP (HR 1.12, 95% CI 1.03-1.23, P = 0.010), and NT-proBNP (HR 1.01, 95% CI 1.01-1.01, P < 0.001) were independent risk factors for MACE. Kaplan-Meier analysis showed that the incidence of MACE was significantly higher in the high SII (≥ 589.31) group than in the low SII group (69.30% vs 23.40%, P < 0.05). Elevated SII increases the risk of MACE in patients with CHD with HF and is associated with poor survival.

ObjectiveTo explore the correlation between triglyceride-to-glucose (TyG) ratio and major adverse cardiovascular events (MACE) risk in coronary artery disease complicated with human immunodeficiency virus (CAD-HIV) patients, and assess its predictive value.MethodsA single-center retrospective cohort study was conducted. A total of 103 CAD-HIV patients admitted to the First Affiliated Hospital of Xinjiang Medical University from January 2020 to June 2025 were enrolled, with a follow-up of 5–49 months (median 22.00 months). Patients were grouped by MACE occurrence. Baseline data and TyG index were collected, with MACE as the primary endpoint. Cox regression, restricted cubic spline (RCS), ROC curve and subgroup analysis were performed.ResultsForty-one patients (39.81%) developed MACE, with significantly higher TyG index in the MACE group (P < 0.001). Multivariate Cox analysis showed each 0.1-unit elevation in TyG index increased MACE risk by 42% (HR = 1.42, 95% CI: 1.16–1.74, P < 0.001). Compared with Q1, Q3 and Q4 had 4.42-fold (95% CI: 1.17–16.68, P = 0.028) and 6.17-fold (95% CI: 1.77–21.54, P = 0.004) higher risk. RCS verified linear positive correlation (P for overall = 0.006, P for nonlinear = 0.387). AUC for 1-year and 3-year MACE prediction was 0.745 and 0.805, respectively. The association was stronger in non-smokers (P for interaction = 0.006).ConclusionTyG index is linearly associated with MACE risk in CAD-HIV patients and shows favorable predictive performance for 1-year and 3-year MACE, which can be used as a simple biomarker for cardiovascular risk stratification.

Long non-coding RNA activated by DNA damage (lnc-NORAD) modulates inflammation, lipid level, and atherosclerosis in various cardiovascular diseases. This study intended to investigate the dysregulated expression of lnc-NORAD, and its linkage with clinical characteristics, inflammatory cytokines, and accumulating major adverse cardiovascular events (MACE) in coronary heart disease (CHD) patients. Totally, 160 CHD patients, 30 disease controls (DCs), and 30 healthy controls (HCs) were included. The reverse transcription-quantitative polymerase chain reaction was used to detect lnc-NORAD expression in peripheral blood mononuclear cell samples from all participants. Enzyme-linked immunosorbent assay was applied to detect proinflammatory cytokines and adhesion molecules in CHD patients. Then, MACE was recorded during a median follow-up of 12 (range: 1.0-27.0) months. Lnc-NORAD was highest in CHD patients, followed by DCs, and lowest in HCs (p < 0.001). In CHD patients, lnc-NORAD was positively linked with Gensini score (p=0.001). Meanwhile, lnc-NORAD was positively linked to C-reactive protein (p=0.023), tumor necrosis factor-alpha (p=0.016), interleukin (IL)-6 (p=0.003), IL-8 (P=0.018), and IL-17A (p=0.029). No relation of lnc-NORAD with vascular cell adhesion molecule-1 (p=0.094) and intercellular adhesion molecule-1 (p=0.060) was found. Furthermore, lnc-NORAD was positively related to total cholesterol (p=0.014) and low-density lipoprotein cholesterol (p=0.004), whereas lnc-NORAD was not linked to triglyceride (p=0.103) and high-density lipoprotein cholesterol (p=0.533). However, lnc-NORAD (high vs. low), and its higher quartiles were both not linked to accumulating MACE rate (p > 0.05). Increased lnc-NORAD is linked with aggravated stenosis degree, inflammation status, and blood lipid in CHD patients. However, further validation is required.