Background: Sepsis is a systemic inflammatory disease, and Brevilin A (BA) has a powerful anti-inflammatory effect. However, whether BA has a similar effect on septic cardiomyopathy remains unclear. This study aimed to investigate the effect and mechanism of BA in septic cardiomyopathy. Methods: First, a model of septic cardiomyopathy was constructed in vitro and vivo. The expression of the cardiac injury markers, NOD–like receptor family pyrin domain–containing 3(NLRP3) inflammation factors and its upstream modulator NF-κB was detected by Real-time Polymerase Chain Reaction (RT-PCR) and western blotting. Cardiac function was measured using Echocardiography, Cell viability was detected using the methyl thiazolyl tetrazolium assay (MTT). To further investigate the effects of BA on septic cardiomyopathy, different concentrations of BA were used, the experiment was divided into Control group, LPS induced- group, LPS+2.5, 5.0, 10.0 μM BA treatment group of the vitro model, and Sham, CLP, CLP+10, 20, 30 mg/kg BA treatment group of the rat vivo model. Lastly, cardiac injury, NLRP3 inflammation, and cardiac function were assessed in each group. Results: The mRNA and protein expression of cardiac inflammation and injury genes were significantly increased in the in vitro and in vivo sepsis cardiomyopathy models. When different concentrations of BA were used in sepsis cardiomyopathy in vivo and in vitro, the above-mentioned myocardial inflammation and injury factors were suppressed to varying degrees, cell viability increased, cardiac function improved, and the survival rate of rats also increased. Conclusion: BA ameliorated sepsis cardiomyopathy by inhibiting NF-κB/ NLRP3 inflammation activation. Export

Background: The monocyte-to-lymphocyte ratio (MLR) has emerged as a novel marker of inflammation. Nevertheless, its potential utility in predicting the development of left ventricular aneurysm (LVA) remains unexplored. This study aims to investigate the association between MLR and the risk of LVA in patients presenting with acute ST segment elevation myocardial infarction (STEMI). Methods: A total of 551 patients were enrolled in the first cohort, and 471 patients were included in the validation cohort. To evaluate the predictive value of MLR for LVA, multivariable logistic regression analysis, restricted cubic splines (RCS) analysis, and receiver operating characteristic (ROC) analysis were employed. Results: The prevalence of LVA was 14.5% in the first cohort and 13.6% in the validation cohort. The multivariable logistic regression analysis revealed that individuals in the highest quartile of MLR (Q4) exhibited a significantly increased risk of LVA formation compared to those in the lowest quartile (Q1) in both cohorts (first cohort: OR = 3.07, 95% CI = 1.33–7.08, P = 0.009; validation cohort: OR = 3.55, 95% CI = 1.34–9.42, P = 0.011). The RCS analysis identified a positively nonlinear association in the first cohort and a positively linear association in the validation cohort between MLR and the risk of LVA (overall P < 0.05). Furthermore, the discriminative ability of MLR for LVA is 0.69 in the first cohort and 0.71 in the validation cohort, exceeding that of both monocyte and lymphocyte alone. The subgroup analyses further substantiated the robustness of our findings. Conclusion: An elevated MLR was independently linked to an increased risk of LVA development in patients with STEMI who received primary PCI. This readily available inflammatory index may offer supplementary prognostic information and could be considered for inclusion in future risk stratification models.

Background: Heart failure (HF) is a prevalent cardiovascular disease exhibiting a complex interplay with dietary vitamin intake. This study employed a comprehensive methodology to investigate the association between exposure to single and multiple dietary vitamins and the risk of HF, with the ultimate goal of providing an evidence-based framework for HF prevention and management strategies. Methods: Data on subjects over the age of 18 years were extracted from the 2009 to 2014 National Health and Nutrition Examination Survey (NHANES). Three different covariate-adjusted models were constructed to analyze the single effects of dietary vitamins A, C, D, K, B6, B12, B1 and B2 intake on HF. The dose-response relationship between each vitamin and HF risk was analyzed via a restricted cubic spline (RCS). Results: This study enrolled 13,025 subjects and categorized them into the non-HF (N=12,623) and the HF (N=402) groups. The HF group exhibited a lower intake of vitamins A, K, B6, B1 and B2 compared with the non-HF group (P<0.05). The fully adjusted model demonstrated a negative association of the intake of vitamins A [odds ratio (OR): 0.750, 95% confidence interval (CI): 0.565, 0.997], K (OR: 0.702, 95% CI: 0.523, 0.942), D (OR: 0.715, 95% CI: 0.535, 0.955), B12 (OR: 0.703, 95% CI: 0.533, 0.927), B1 (OR: 0.680, 95% CI: 0.489, 0.946), and B2 (OR: 0.673, 95% CI: 0.490, 0.925) with HF. An obvious association of high levels of vitamins A, K, B1 and B2 with a reduced probability of HF was found across the three models (all P0.05, P for overall <0.05). Conclusions: HF risk was found to decrease with increasing intake of dietary vitamins A, K, B1 and B2. There was a negative correlation of vitamins K, B6, B1, B2 intake with HF.

Background: Left ventricular aneurysm (LVA) is a major mechanical complication following acute ST-segment elevation myocardial infarction (STEMI). This study aimed to evaluate the predictive ability of the lactate dehydrogenase to albumin ratio (LAR) for the risk of LVA among STEMI patients. Methods: The study was conducted from July 2018 to 2025 across three medical centers in China. The study cohort comprised STEMI patients who underwent primary percutaneous coronary intervention across three medical centers. Multivariate logistic regression analysis and Restricted cubic spline plots were employed to assess the association between different LAR levels and LVA risk. Subgroup analyses were conducted to assess the consistency of the result. Results: The study included 551, 471, and 1384 eligible participants from the first, second, and third cohort, respectively. After adjusting for potential confounders, individuals in the highest quartile of LAR (Q4) demonstrated a significantly elevated risk of developing LVA compared to those in the lowest quartile (Q1) across all cohorts (First cohort: OR = 3.63, 95% CI = 1.65 - 7.96, P = 0.001; Second cohort: OR = 6.01, 95% CI = 2.22 - 16.26, P< 0.001; Third cohort: OR = 2.41, 95% CI = 1.47 - 3.96, P< 0.001). RCS analysis revealed a positive linear association between LAR and the risk of LVA across the three cohorts (overall P> 0.05). The predictive capacity of LAR for assessing LVA risk exceeded that of both lactate dehydrogenase and albumin (P< 0.05). Subgroup analyses further reinforced the robustness of these findings. Conclusion: An elevated LAR was independently associated with an increased risk of LVA development in patients with STEMI who underwent primary PCI.

The C-reactive protein (CRP) to albumin ratio (CAR) has emerged as a novel marker of inflammation. However, its potential predictive value for the development of left ventricular aneurysm (LVA) has not yet been evaluated. This study aims to explore the association between CAR and the risk of LVA in patients experiencing acute ST-segment elevation myocardial infarction (STEMI). This study recruited 551 patients in the first cohort and 471 patients in the validation cohort. Multivariable logistic regression analysis, restricted cubic splines (RCS) analysis, and receiver operating characteristic were conducted to assess the predictive value of CAR for LVA. The prevalence of LVA were 14.5% in the first cohort and 13.6% in the validation cohort. Multivariable logistic regression analysis indicated that individuals in the highest quartile of CAR (Q4) were significantly associated with the risk of LVA formation compared to those in the lowest quartile (Q1) in both cohorts (First cohort: OR = 3.26, 95% CI = 1.51–7.05, P = 0.003; Validation cohort: OR = 4.05, 95% CI = 1.71–9.60, P = 0.002). RCS analysis demonstrated a positive and nonlinear association between CAR and the risk of LVA (overall P < 0.05, nonlinear P < 0.05). Furthermore, the discriminative ability of CAR for LVA is 0.72 in the first cohort and 0.74 in the validation cohort, exceeding that of both CRP and albumin alone. Subgroup analyses further corroborated the robustness of our findings. Elevated CAR was independently linked to an increased risk of LVA development in patients with STEMI who received primary PCI. This finding may hold considerable significance for clinical practice and could aid in the development of a personalized prevention strategy that incorporates the monitoring of CAR.