Background: Quercetin, a major flavonol, wildly exists in plantage, which has been reported to have an anti-apoptosis and anti-inflammation effects on vascular endothelial cells, but its underlying molecular mechanisms remain unclear. Objective: The aim of this study was to investigate the mechanisms of how quercetin inhibits tumor necrosis factor alpha (TNF-α) induced human umbilical vein endothelial cells (HUVECs) apoptosis and inflammation. Methods and Results: HUVECs were preconditioned with quercetin for 18 hours, and subsequently treated with TNF-α for 6 hours to induce apoptosis. The expression of intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), E-selectin, β-actin mRNA was then detected by RT-PCR. Flow cytometry was used to estimate the apoptosis rates, and the expression of activator protein 1 (AP-1) and nuclear factor kappa B (NF-κB) was measured by Western blot. TNF-α induced elevated apoptosis rates and upregulation of VCAM-1, ICAM-1, and E-selectin were meaningfully reduced in HUVECs by pretreatment with quercetin. In addition, quercetin also inhibited the activation of AP-1and NF-κB. Conclusion: Results indicate that quercetin could suppress TNF-α induced apoptosis and inflammation by blocking NF-κB and AP-1 signaling pathway in HUVECs, which might be one of the underlying mechanisms in treatment of coronary heart disease.

Aim: Inflammation-based Glasgow Prognostic Scores (GPS) have been reported to predict the prognosis of patients with acute ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). The goal of this study was to investigate whether three kinds of GPSs can effectively predict major cardiovascular adverse events (MACEs) in STEMI or non-ST-segment elevation myocardial infarction (NSTEMI) patients undergoing PPCI, elective PCI (EPCI) or conservative drug therapy during hospitalization. Methods: In this retrospective cohort study, patients with acute myocardial infarction (AMI) were divided into 0, 1 or 2 score according to the GPSs. Logistic regression and receiver operating characteristic (ROC) curve analysis were performed to assess the predictive value of GPSs for MACE and all-cause mortality during hospitalization. Three kinds of GPSs, Inflammation-based Glasgow Prognostic Score (GPS), modified GPS (MGPS) and high-sensitivity CRP-modified GPS (HS-MGPS) and Global Registry of Acute Coronary Events (GRACE) score were applied in this study. Results: A total of 188 patients were enrolled. The ROC curve with MACE showed that the AUC of GPS (0.820 (95% confidence interval (CI) [0.754–0.885]), P < 0.001) was larger than that of MGPS (0.789 (95% CI [0.715–0.863]), P < 0.001), HS-MGPS (0.787 (95% CI [0.717–0.856]), P < 0.001) and GRACE score (0.743 (95% CI [0.672–0.814]), P < 0.001). The ROC curve with all-cause mortality showed that the AUC of GPS (0.696 (95% CI [0.561–0.831]), P = 0.005) was similar to the HS-MGPS (0.698 (95% CI [0.569–0.826]), P = 0.005) and higher than the MGPS (0.668 (95% CI [0.525–0.812]), P = 0.016), but lower than the GRACE score (0.812 (95% CI [0.734–0.889]), P < 0.001). Multivariate logistic regression analysis showed that the GPS was an independent risk factor for the incidence of MACE during hospitalization. Compared with the odds ratio (OR) value for a GPS of 0, the OR for a GPS of 1 was 7.173 (95% CI [2.425–21.216]), P < 0.001), and that for a GPS of 2 was 18.636 (95% CI [5.813–59.746]), P < 0.001), but not an independent risk factor for all-cause mortality (P = 0.302). GRACE score was an independent risk factor for MACE (1.019 (95% CI [1.004–1.035]), P = 0.015) and all-cause mortality (1.040 (95% CI [1.017–1.064]), P = 0.001). In the subgroups classified according to the type of AMI, the presence of disease interference GPSs and the type of PCI, the ability of GPS to predict the occurrence of MACE seemed to be greater than that of MGPS and HS-MGPS. Conclusion: The GPS has a good predictive value for the occurrence of MACE during hospitalization in patients with AMI, regardless of STEMI or NSTEMI, the choice of PCI mode and the presence or absence of diseases that interfere with GPS. However, GPS is less predictive of all-cause mortality during hospitalization than GRACE score, which may be due to the interference of patients with other diseases.

Atherosclerotic cardiovascular disease (ASCVD) is a leading cause of mortality, and while the association between the urinary albumin-to-creatinine ratio (UACR) and cardiovascular risk is recognized, the specific impact of UACR on the long-term survival of ASCVD patients remains not fully understood. The aim of this study is to investigate the influence of UACR on the long-term risk of all-cause mortality in patients with ASCVD. This study included ASCVD patients from the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2018. Mortality outcomes were ascertained by linkage to the National Death Index as of December 31, 2019. UACR risk was stratified into three levels: Group 0 (UACR < 30 mg/g), Group 1 (30–300 mg/g), and Group 2 (>300 mg/g). The primary outcome was all-cause mortality, with cardiovascular mortality as a secondary outcome. Cox proportional hazards, adjusted for demographic factors, traditional cardiovascular risk factors, and secondary prevention medications for ASCVD, were used to analyze the cumulative risk of outcomes. Propensity score matching was employed for risk adjustment, and sensitivity analyses were conducted based on cohorts with chronic coronary syndrome (CCS), stroke, heart failure, and non-heart failure. Among the 1,737 patients with a median follow-up of 10 years, 1,026 all-cause deaths and 351 cardiovascular deaths were recorded. After full model adjustment, higher UACR levels were associated with increased risks of all-cause mortality (Group 1: hazard ratio (HR), 1.601; 95 % confidence interval (CI), 1.382–1.855; Group 2: HR, 2.378; 95 % CI, 1.884–3.001; both P < 0.001 for trend) and cardiovascular mortality (Group 1: HR, 2.080; 95 % CI, 1.631–2.652; Group 2: HR, 2.883; 95 % CI, 1.951–4.260; both P < 0.001 for trend). Propensity score matching confirmed these findings, showing significantly elevated all-cause mortality risks in high-risk UACR groups (with a cutoff of 30 mg/g: HR, 1.468 (95 %CI, 1.254–1.719), P < 0.001; with a cutoff of 300 mg/g: HR, 1.935 (95 %CI, 1.399–2.675), P < 0.001). All sensitivity analyses were consistent with the results of the overall cohort. UACR is an important prognostic indicator for predicting the long-term outcomes of ASCVD patients, with its impact being independent of eGFR.

Background: Despite statins and other medications central to atherosclerotic cardiovascular disease (ASCVD) secondary prevention, stable coronary artery disease (SCAD) patients remain at significant cardiovascular risk, partly due to residual inflammation risk (RIR). This study aims to assess if adding Guanxinning to standard ASCVD therapy further mitigates RIR in SCAD patients. Methods: In a prospective, randomized, single-blind endpoint design, 50 patients with SCAD who received ASCVD standardized treatment strategy were randomly assigned to either take Guanxinning tablets (4 tablets, thrice daily) or no Guanxinning tablets and were followed up for an average of 12 weeks. The primary outcomes were changes in inflammation-related indicators, including interleukin-2 (IL-2), IL-4, IL-6, tumor necrosis factor-α (TNF-α), and high sensitivity C-reactive protein (hs-CRP). Results: Compared with the control group, the intervention group showed significantly greater decreases in the levels of IL-2, IL-6, TNF-α, and hs-CRP (all P < 0.05). However, there was no significant difference in the IL-4 level between the two groups (P > 0.05). Compared with the control group, there were also significant improvements in endothelial function-related indicators (vascular endothelial growth factor (VEGF), nitric oxide (NO), and peroxisome proliferator-activated receptor-γ (PPAR-γ)), blood lipid profile (total cholesterol (Tch), low-density lipoprotein cholesterol (LDL-C)), and chest pain related scores (angina and Traditional Chinese medicine syndrome scores) in the intervention group (all P< 0.05). There was no significant difference in the triglyceride (TG) and carotid intima-media thickness between the two groups (P< 0.05). Compared to the control group, there was no significant difference in the white blood cell line, liver and kidney function, anemia, and bleeding in the intervention group (all P< 0.05). Conclusion: The addition of Guanxinning tablets (4 tablets, thrice daily) to the standard treatment strategy for ASCVD was associated with a reduction in the RIR in patients with SCAD and demonstrated good safety. Plain Language Summary: In the quest for a heart-healthy life, even with statins at our side, some folks with stable heart troubles still face a sneaky foe: lingering inflammation. Our study explored whether adding Guanxinning, a traditional Chinese medicine, to the standard treatment might help. Over 12 weeks, patients who took Guanxinning along with their usual heart meds showed promising signs of reduced inflammation and improved heart health markers. These preliminary positive signs hint at the potential benefits of Guanxinning, which, however, need further studies to confirm. Fortunately, it appears to be safe to use Guanxinning alongside conventional treatments for now. As we delve deeper into the mysteries of heart health, every promising discovery brings us one step closer to developing better therapeutic strategies.

Background: This study aimed to investigate whether nutrition levels in patients with active pulmonary tuberculosis (TB) affect their risk of all-cause mortality during hospitalization and to further evaluate the predictive ability of Geriatric Nutritional Risk Index (GNRI) and Body Mass Index (BMI) for risk of all-cause mortality. Methods: Patients from January 1, 2020 to December 31, 2021 were retrieved, and a total of 1847 were included. The primary outcome was all-cause mortality. Propensity score matching (PSM) was performed for risk adjustment, and receiver operating characteristic (ROC) curve analysis was performed to assess the predictive ability of GNRI and BMI for all-cause mortality. Results: Malnourished TB patients were older, had more congestive heart failure, and had more chronic obstructive pulmonary disease or asthma. Under the nutrition level grouping defined by GNRI, the all-cause mortality in the malnourished group did not appear to reach a statistical difference compared with the nonmalnourished group (P = 0.078). When grouped by level of nutrition as defined by BMI, the all-cause mortality was higher in the malnourished group (P = 0.009), and multivariate logistic regression analysis revealed that malnutrition was an independent risk factor for all-cause mortality. After propensity score matching, the results showed that the all-cause mortality was higher in the malnutrition group, regardless of BMI or GNRI defined nutrition level grouping, compared with the control group (both P < 0.001). The ROC curve analysis revealed that the area under the curve (AUC) was 0.811 ([95% confidence interval (CI) 0.701– 0.922], P < 0.001) for GNRI and 0.728 ([95% CI 0.588– 0.869], P = 0.001) for BMI. Conclusion: In the clinical treatment of patients with active TB, more attention should be paid to the management of nutritional risk. GNRI may be a highly effective and easy method for predicting short-term outcomes in patients with active pulmonary TB.