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.

Incorporating uric acid into the CHA2DS2-VASc score improves the prediction of new-onset atrial fibrillation in patients with acute myocardial infarction.

BACKGROUND: New-onset atrial fibrillation (NOAF) is a common cardiac arrhythmia observed in patients with acute myocardial infarction (AMI) and is associated with worse outcomes. While uric acid has been proposed as a potential biomarker for predicting atrial fibrillation, its association with NOAF in patients with AMI and its incremental discriminative ability when added to the CHA2DS2-VASc score are not well established. METHODS: We conducted a retrospective analysis of 1000 consecutive patients with AMI without a history of atrial fibrillation between January 2018 and December 2020. Continuous electrocardiographic monitoring was performed during the patients' hospital stay to detect NOAF. We assessed the predictive ability of the different scoring models using receiver operating characteristic (ROC) curves. In addition, we employed the area under the curve (AUC), integrated discrimination improvement (IDI), and net reclassification improvement (NRI) analyses to assess the incremental discriminative ability of uric acid when added to the CHA2DS2-VASc score. RESULTS: Ninety-three patients (9.3%) developed NOAF during hospitalisation. In multivariate regression analyses, the adjusted odds ratio (OR) for NOAF was 1.439 per one standard deviation increase in uric acid level (95% confidence intervals (CI):1.182-1.753, p < 0.001). The ROC curve analysis revealed that the AUC for uric acid was 0.667 (95% CI:0.601-0.719), while the AUC for the CHA2DS2-VASc score was 0.678 (95% CI:0.623-0.734). After integrating the uric acid variable into the CHA2DS2-VASc score, the combined score yielded an improved AUC of 0.737 (95% CI:0.709-0.764, p = 0.009). Furthermore, there was a significant improvement in both IDI and NRI, indicating an incremental improvement in discriminative ability (IDI = 0.041, p < 0.001; NRI = 0.627, p < 0.001). CONCLUSION: Our study suggests that uric acid level is an independent risk factor for the development of NOAF after AMI. Furthermore, the incorporation of uric acid into the CHA2DS2-VASc score significantly improves the discriminative ability of the score in identifying patients at high risk for NOAF.

Brain natriuretic peptide as a biomarker for predicting contrast-induced nephropathy in patients undergoing coronary angiography/intervention: A systematic review and meta-analysis.

BACKGROUND: Contrast-induced nephropathy (CIN) is associated with adverse events. As there are no effective treatments, the early identification of high-risk patients is required. Individual studies have suggested the utility of brain natriuretic peptide in predicting CIN. Therefore, this meta-analysis aimed to systematically investigate the value of brain natriuretic peptide in predicting CIN in patients undergoing coronary angiography (CAG) or percutaneous coronary intervention (PCI). METHODS: We searched PubMed, Embase, Cochrane Central Register of Controlled Trials Library, and Web of Science from inception date to March 9, 2022. Studies that evaluated the predictive value of brain natriuretic peptide for CIN outcomes in patients after CAG or PCI were included. The quality of the included studies was assessed using the QUADAS-2 tool. Diagnostic accuracy estimates were calculated using a random-effects model. Subgroup and meta-regression analyses were performed to identify the potential sources of heterogeneity. RESULTS: Twelve studies with 7789 patients were included in the meta-analysis. The pooled sensitivity and specificity of brain natriuretic peptide for the prediction of CIN were 0.73 (95% CI: 0.67-0.78) and 0.77 (95% CI: 0.71-0.82), respectively. The area under the summary receiver operating characteristic curve was 0.80 (95% CI: 0.77-0.84). Meta-regression analysis indicated that the sources of sensitivity heterogeneity may be the country, mean age, and study population. Additionally, country, study population, study design, and index text contributed to the specificity heterogeneity. CONCLUSION: This study demonstrated that brain natriuretic peptide could function as a novel potential marker for the early detection of CIN in patients undergoing CAG or PCI.

The Novel LncRNA AK035396 Drives Cardiomyocyte Apoptosis Through Mterf1 in Myocardial Ischemia/Reperfusion Injury.

Background: Myocardial ischaemia/reperfusion (I/R) injury is still a major challenge in clinical treatment. The role of long non-coding RNA (lncRNA) in the regulation of myocardial I/R injury still needs to be elucidated. Methods: The primary isolated neonatal mousse cardiomyocytes and adult mice were used to construct a myocardial ischemia-reperfusion model. qRT-PCR is used to verify gene expression in myocardial tissue and myocardial cells. The effect of AK035396 in primary cardiomyocytes and mouse myocardium was confirmed by TUNEL staining and in vitro flow cytometry experiments. RNA pulldown and Western blot were used to identify AK035396 interacting proteins. The expression of apoptosis-related proteins was identified by qRT-PCR and Western blot. Results: In vivo and in vitro MIRI models, AK035396 was up-regulated after myocardial infarction. Functional studies have shown that knockdown of AK035396 reduces the apoptosis of primary cardiomyocytes and mouse myocardial tissue. AK035396 directly interacts with Mterf1 and inhibits the level of Mterf1. Further experiments have shown that inhibiting Mterf1 will promote the expression of mitochondrial genes COXII and CYTb and cause cell apoptosis. Conclusion: AK035396 plays an important role in myocardial ischaemia-reperfusion injury by regulating the Mterf1-COXII/CYTb pathway.

Anatomical Predictors of Valve Malposition During Self-Expandable Transcatheter Aortic Valve Replacement.

Background: The consequence of valve malposition (VM) during transcatheter aortic valve replacement (TAVR) can be severe, but the determinants of VM with self-expandable TAVR have not been thoroughly evaluated. We aimed to investigate the anatomical predictors of VM during self-expandable TAVR. Methods: In this multicenter retrospective study, TAVR was performed using the Venus A-Valve. The baseline, computed tomography, and procedural characteristics along with clinical outcomes were collected. Multivariate logistic regression model and receiver operating characteristic (ROC) curve analyses were performed. Results: A total of 84 consecutive patients (23 with VM) were included. Stepwise regression showed that annulus perimeter/left ventricular outflow tract perimeter (AL ratio) and sinotubular junction (STJ) height were predictors of VM. The ROC curve indicated a moderate strength of AL ratio [area under the curve (AUC) 0.71, cutoff 0.96] and a weak strength of STJ height (AUC 0.69, cutoff 23.8 mm) to predict VM. The combination of both predictors revealed a higher predictive value of VM (AUC 0.77). In multivariate analysis, AL ratio <0.96 [odds ratio (OR) 3.98, p = 0.015] and STJ height ≥23.8 mm (OR 4.63, p = 0.008) were strong independent predictors of VM. The presence of both predictors was associated with a very high risk of VM (OR 10.67, p = 0.002). The rate of moderate-to-severe paravalvular regurgitation was higher in patients with VM at 30 days (26.1 vs. 4.9%, p = 0.011). Conclusions: A conical left ventricular outflow tract and tall aortic sinuses were strong anatomical predictors of VM during self-expandable TAVR.

Study of the features of coronary artery atheromatous plaque using intravascular ultrasound in patients with impaired glucose tolerance.

OBJECTIVE: We used intravascular ultrasound (IVUS) to analyze the features of coronary artery atheromatous plaque in patients with impaired glucose tolerance and mild-to-moderate angiographic coronary stenosis. The aim was to determine the clinical significance of plaque characteristics as well as the relationship between hemoglobin A1c (HbA1c) levels and coronary artery lesions. METHODS: HbA1c levels were evaluated in 85 patients (96 lesions), of whom 46 had impaired glucose tolerance (IGT Group) and 39 had normal blood glucose (NBG Group). IVUS was used to analyze the lesion vessel of both groups qualitatively and quantitatively. The external elastic membrane area (EEMA), minimal lumen area (MLA), plaque area (PA), and plaque burden (PB) were measured for both the target lesion and the reference segments (reference external elastic membrane area (REEMA), reference minimal lumen area (RMLA), reference plaque area (RPA), and reference plaque burden (RPB), respectively). RESULTS: HbA1c levels were significantly higher in the IGT Group than in the NBG Group (P < 0.05). In the IGT Group there was more soft plaque, eccentric plaque, and positive remodeling, and less calcification, while in the NBG Group there was much harder plaque and calcification, no reconstruction, and negative remodeling (P < 0.05). MLA was smaller in the IGT Group than in the NBG Group, while EEMA, PA, and PB were clearly greater (P < 0.05). In the meantime, RMLA was clearly smaller in the IGT Group than in the NBG Group, while RPA and RPB were greater (P < 0.05). HbA1c levels were positively correlated with PA and PB, and negatively correlated with MLA. CONCLUSION: IVUS is very valuable for the evaluation of mild-to-moderate coronary lesions. The coronary artery lesions in patients with IGT are more serious and widespread than those in patients with NBG. HbA1c levels might be of some value in assessing the severity of coronary artery lesions.

[Relation of plasma brain natriuretic peptide to serum creatine kinase MB level in patients with acute myocardial infarction following primary percutaneous coronary intervention].

OBJECTIVE: To study the relation between plasma brain natriuretic peptide (BNP) and serum creatine kinase MB (CK-MB) level in patients with acute myocardial infarction (AMI) following primary percutaneous coronary intervention (PCI). METHODS: Sixty-three consecutive patients with AMI were divided into two groups according to the timing of PCI, namely direct PCI and indirect PCI groups. Plasma BNP levels were measured in all patients on admission and at 4, 24 and 48 h after admission. The CK-MB level was measured every 3 h on the first day of hospitalization, every 6 h on the second day and every 12 h on the third day. RESULTS: BNP level increased gradually following admission and began to decrease 48 h after admission in the two groups of patients. The peak BNP level occurred at 24 h after admission, and the BNP levels in patients of indirect PCI group were significantly higher than that of direct PCI group at 4, 24 and 48 h after admission. The peak CK-MB level of the direct PCI group occurred significantly earlier than that of the indirect group. CONCLUSION: Plasma BNP level may serve as an important objective indicator for recanalization of the infarct-related arteries following PCI in the early stage of AMI, which can help in the decision on clinical treatment plans for AMI.