Background: This study aimed to investigate the association between the triglyceride–glucose (TyG) index and left ventricular global longitudinal strain (GLS) in patients with coronary heart disease and to examine the role of left ventricular GLS in detecting early changes in cardiac function in patients with coronary heart disease in the subclinical stage. Methods: A cross-sectional study involving 178 participants with symptomatic coronary artery disease excluding myocardial infarction or left ventricular dysfunction was conducted in Jilin Province, China. Basic clinical, biochemical, and echocardiographic data were obtained from all participants. Myocardial strain parameters were compared between patients with higher TyG index and those with lower TyG index, and the association between the gradually elevated TyG index and on subclinical cardiac function in patients with coronary heart disease was evaluated. Results: The GLS of left ventricle was lower in the higher TyG index group than in the lower TyG index group. As the TyG index increases, the GLS progressively decreases. The results remained stable after adjusting for confounding factors. Conclusions: A higher TyG index maybe independently associated with subclinical left ventricular dysfunction in patients with coronary heart disease.

Yogurt consumption is a significant factor in reducing the risk of hypertension and preventing cardiovascular diseases. Although increasing evidence has emerged regarding the potential benefits of probiotics in hypertension, there is a lack of large, cross-sectional studies assessing the association between yogurt intake and blood pressure parameters. We aimed to evaluate the association between yogurt intake frequency and blood pressure. A cross-sectional study was designed using data from the National Health and Nutrition Examination Survey from 2003 to 2004 and 2005 to 2006. We included 3, 068 adults with blood pressure data and yogurt intake data. Multivariate regression analyses revealed significant inverse associations between yogurt and systolic blood pressure ( ), diastolic blood pressure ( ), and mean arterial pressure ( ) in nonhypertensive participants (n = 1 822) but not in hypertensive participants (n = 1 246). Furthermore, a high frequency of yogurt intake prevented hypertension; however, no additional antihypertensive effects were observed in patients already diagnosed with hypertension.

Background: Magnesium deficiency represents a prevalent electrolyte imbalance that notably heightens the risk of adverse cardiovascular incidents among individuals with heart failure. Research indicates that magnesium supplementation can diminish the frequency of negative events linked to hypomagnesemia in heart failure patients, while also enhancing the outcomes for critically ill individuals. Nevertheless, there remains a scarcity of studies investigating the effects of intravenous magnesium supplementation on mortality risk in those suffering from acute heart failure. This study aimed to explore the relationship between the administration of intravenous magnesium sulfate and the overall mortality risk in patients with acute heart failure who are admitted to intensive care units. Methods: This retrospective cohort study employed the Medical Information Mart for Intensive Care IV (MIMIC-IV) database (version 3.1), which encompasses the baseline clinical data of 10,031 patients diagnosed with acute heart failure. Propensity score matching and multivariate Cox regression analysis were utilized to assess the effects of intravenous magnesium sulfate on 28-day all-cause mortality. The evaluation of unmeasured confounding variables was undertaken through E-value calculations, while subgroup analyses were performed to ascertain the robustness of the results. Results: A total of 10,031 patients participated in the study, with 6240 belonging to the propensity-score matched group, which included 3120 subjects who received intravenous magnesium sulfate and 3120 who did not. The entire cohort consisted of 10,031 individuals, whereas the matched cohort specifically comprised 6240 patients. Within the matched group, the rates of 28-day all-cause mortality were observed to be 13.2% (413/3120) for those administered intravenous magnesium sulfate, compared to 15.8% (493/3120) for the control group. Administration of intravenous magnesium sulfate correlated with a significantly reduced risk of 28-day all-cause mortality (hazard ratio (HR), 0.81; 95% confidence interval (CI), 0.71–0.93; p = 0.004). A sensitivity analysis conducted on the entire cohort corroborated this association (HR, 0.77; 95% CI, 0.69–0.87; p < 0.001). Additional subgroup analyses and E-value assessments reinforced the relevance of these results. Furthermore, intravenous magnesium sulfate was linked to reduced all-cause mortality at both 90 and 365 days. Conclusions: Intravenous magnesium sulfate appears to decrease all-cause mortality in patients with acute heart failure, while further prospective studies are warranted to validate these results.

Background: Gut microbiota’s role in hypertension is emerging, but systematic studies on microbiota-linked dietary indices (DI-GM, BGMS, UGMS) remain limited.Methods: This study leveraged data from the National Health and Nutrition Examination Survey (NHANES) database spanning 1999–2020. A cross-sectional study design was employed to gather baseline information from 41,193 adult participants aged 20 years and older, encompassing sociodemographic characteristics and health-related factors. To investigate the associations between DI-GM, BGMS, UGMS, and the prevalence of hypertension, weighted logistic regression models, restricted cubic spline (RCS) analysis with three knots (positioned at the 10, 50, and 90th percentiles of the independent variables), and subgroup analyses were performed.Results: The study findings demonstrate that both DI-GM and BGMS are significantly and inversely associated with the prevalence of hypertension. Specifically, each one-unit increase in DI-GM was linked to a 4% reduction in hypertension risk (OR = 0.96, 95% CI: 0.94–0.98, p < 0.001), and each one-unit increase in BGMS was associated with a 5% decrease in hypertension risk (OR = 0.95, 95% CI: 0.92–0.97, p < 0.001). Further RCS analysis demonstrated a linear relationship between DI-GM and BGMS with hypertension risk. Additionally, subgroup analyses stratified by age, gender, BMI, and diabetes status exhibited robust results (P for interaction >0.05).Conclusion: DI-GM and BGMS exhibit significant inverse associations with hypertension prevalence, with BGMS displaying a stronger protective effect. No significant relationship was identified between UGMS and hypertension.

Considering the significance of lncRNA/miRNA axis in explaining atherosclerosis (AS) progression, this investigation was intended to clarify whether lncRNAs XIST/SNHG5 would regulate AS aetiology by sponging miR‐155, an AS‐promoting molecule. We altogether recruited 367 patients who were examined by coronary angiography, and meanwhile, human coronary artery endothelial cells (HCAECs) were purchased to establish cells models via ox‐LDL treatment. The study results indicated that lowly expressed XIST/SNHG5 and highly expressed miR‐155 were frequently detectable among AS patients who showed severe stenosis and possessed high triglyceride (TG), low‐density lipoprotein cholesterol (LDL‐C) and high‐sensitivity C‐reactive protein (hs‐CRP) levels. Besides, HCAECs treated by ox‐LDL released large amounts of inflammatory cytokines, and their apoptosis rate was also raised. Moreover, expressions of XIST and SNHG5 declined markedly within ox‐LDL‐treated HCAECs, whereas miR‐155 expression significantly ascended. Transfection of pcDNA‐XIST and pcDNA‐SNHG5 both reduced the expression of TNF‐α, IL‐6, IL‐8 and IL‐1β within HCAECs and also dampened the apoptotic tendency of HCAECs. Co‐treatment of pcDNA‐XIST and pcDNA‐SNHG5 produced a larger effect on HCAEC activity than pcDNA‐XIST or pcDNA‐SNHG5 alone. Furthermore, miR‐155, modified by XIST and SNHG5, was capable of reversing the impacts of XIST and SNHG5 on HCAEC activity. Eventually, CARHSP1 was activated by XIST and SNHG5, and its overexpression dwindled impacts of miR‐155 mimic on proliferation and inflammation response of HCAECs. In conclusion, targeting XIST and SNHG5 might be an ideal alternative in delaying AS progression, allowing for their repression of downstream miR‐155.