Left atrial size modify the association between uric acid and atrial fibrillation in patients with coronary artery disease.

BACKGROUND AND AIMS: The potential influence of left atrial size on the relationship between uric acid and atrial fibrillation has not been fully investigated. This study aims to evaluate the interaction effect of left atrial size on the association between uric acid and atrial fibrillation in patients with coronary artery disease. METHODS AND RESULTS: This retrospective cohort study, conducted from January 2018 to October 2022, included 2004 patients undergoing Drug-Eluting Stent implantation for coronary artery disease. Utilizing logistic regression models with the product of left atrial enlargement (LAE) and uric acid, interaction effects were assessed. Among the participants, 383 had LAE, and 159 experienced atrial fibrillation. After adjusting for covariates, continuous uric acid levels were associated with an increased risk of atrial fibrillation in patients without LAE (OR:1.631, 95% CI: 1.284-2.072), but not in those with LAE (OR:1.069, 95% CI: 0.848-1.348). A significant interaction of uric acid levels was observed between groups with and without LAE (p = 0.046). Restricted cubic spline curves indicated a J-shaped relationship between uric acid and atrial fibrillation in the absence of LAE. However, the association between uric acid levels and atrial fibrillation in the LAE group remained unchanged with increasing uric acid levels. CONCLUSION: The study suggested that left atrial size modified the association between uric acid and atrial fibrillation in patients with coronary artery disease. Uric acid serves as a potential biomarker for atrial fibrillation risk, especially in individuals without LAE.

Research Progress in the Relationship Between Trimethylamine Oxide and Coronary Heart Disease.

Objective: To provide a theoretical basis for intestinal intervention in the treatment of coronary heart disease. Methods: Summarizing the mechanism of trimethylamine oxide (TMAO) inducing coronary heart disease and discussing the target of clinical intervention including TMAO generation, metabolism, and other links. The authors also clarified the potential clinical value of TMAO as a predictor of cardiovascular disease．. Results: The intestinal microbiota metabolite TMAO is closely related to the occurrence and development of coronary heart disease. TMAO can induce the development of coronary heart disease by promoting endothelial cell dysfunction, promoting foam cell formation, affecting cholesterol and bile acid metabolism, and promoting platelet activation and thrombosis. Diet, physical exercise, and other ways can reshape intestinal flora, inhibit TMAO generation, and help to prevent and cure coronary heart disease. In addition, TMAO has important clinical value in predicting risk stratification and evaluating the prognosis of coronary heart disease. Conclusion: TMAO can induce and assist in the development of coronary heart disease by promoting endothelial cell dysfunction, foam cell formation, and other mechanisms. At present, diet and physical exercise can reduce the production of TMAO to a certain extent, to prevent the occurrence and development of coronary heart disease. Furthermore, TMAO is a promising predictive marker for risk stratification and evaluating the prognosis of coronary heart disease.TMAO can not only directly induce coronary heart disease by promoting endothelial cell dysfunction, foam cell formation and other mechanisms, but also promote the occurrence and development of coronary heart disease by affecting the risk factors related to coronary heart disease (such as hypertension and diabetes). It has been confirmed that diet and physical exercise can reduce the production of TMAO to a certain extent and prevent the occurrence and development of coronary heart disease. In addition, TMAO is a valuable indicator for assessing risk stratification and prognosis of coronary heart disease.

Application of atomic-scale mechanistic insights into carbon-catalyzed N2O reduction for kinetic modeling construction.

To achieve the collaborative elimination of N2O and carbon of potent greenhouse pollutants from automotive mobile sources, a chemical kinetic model is developed to accurately track the heterogeneous process of carbon-catalyzed N2O reduction based on density functional theory, with experimental data used to validate the model's reliability. The influence of carbon structure, site density, and surface chemical properties on N2O catalytic reduction can be analyzed within this system. Results reveal that the free-edge site of carbon accurately describes the catalytic reduction process of N2O. Adsorption of N2O to carbon edges in O-down, N-down, or parallel orientations exhibits an exothermic process with energy barriers. The N2O with O-down reduction pathway predominates due to the limitations imposed by the unitary carbon site. As the number of active carbon atoms at carbon edges increases, the N2O reaction mode tends towards parallel and N-down pathways, resulting in a significant enhancement of N2O conversion rates and a reduction in catalytic temperatures, with the lowest achievable temperature being 300 K. Furthermore, the triplet carbon structure exhibits higher efficiency in N2O catalytic reduction compared to the singlet carbon structure, achieving a remarkable N2O conversion rate of 93.8 % within the typical temperature exhaust window of diesel engines. This study supplies a breakthrough for carbon materials as catalysts for achieving high N2O conversion rates at low cost, which is important for the collaborative catalytic elimination of N2O and carbon black pollutants.

Compound Danshen Dripping Pills pretreatment protects the heart from ischemia/reperfusion injury by enhancing autophagic flux

Abstract Compound Danshen Dripping Pills (CDDPs) have been used in clinical treatment to protect the heart from ischemia/reperfusion (IR) injury for many years. However, the underlying mechanism implicated in the protective effects remains to be explored. Here, we determined the effects of CDDPs in Sprague-Dawley rats with the IR model. Cardiac function in vivo was assessed by echocardiography. Transmission electron microscopy, histological and immunohistochemical techniques, Western blotting and recombinant adeno-associated virus 9 transfection were used to illustrate the effects of CDDPs on IR and autophagy. Our results showed that pretreatment with CDDPs decreased the level of serum myocardial enzymes and infarct size in rats after IR. Apoptosis evaluation showed that CDDPs significantly ameliorated the cardiac apoptosis level after IR. Meanwhile, CDDPs pretreatment increased myocardial autophagic flux, with upregulation of LC3B, downregulation of p62, and increased autophagosomes and autolysosomes. Moreover, the autophagic flux inhibitor chloroquine could increase IR injury, while CDDPs could partially reverse the effects. Furthermore, our results showed that the activation of AMPK/mTOR was involved in the cardioprotective effect exerted by CDDPs. Herein, we suggest that CDDPs partially protect the heart from IR injury by enhancing autophagic flux through the activation of AMPK/mTOR.