Dietary inflammatory potential is associated with sarcopenia in patients with hypertension: national health and nutrition examination study.

Background: Study has shown that sarcopenia increases the risk of poor outcomes in patients with hypertension. Inflammation is one of the important reasons for the occurrence and development of sarcopenia. Regulating systemic inflammation may be a potential intervention for sarcopenia in hypertensive patients. Diet is one of the important measures to improve systemic inflammation. The dietary inflammatory index (DII) is a tool designed to assess the inflammatory potential of the diet, the association between DII and sarcopenia in hypertensive patients is unclear. Objective: To explore the relationship between the DII and sarcopenia in patients with hypertension. Method: Data from the National Health and Nutrition Examination Survey (NHANES) 1999-2006 and 2011-2018. A total of 7,829 participants were evaluated. Participants were divided into four groups based on the quartile of the DII: Q1 group (n = 1,958), Q2 group (n = 1,956), Q3 group (n = 1,958) and Q4 group (n = 1,957). The relationship between the DII and sarcopenia was assessed by logistic regression analysis based on the NHANES recommended weights. Result: The DII was significantly associated with sarcopenia in patients with hypertension. After full adjustment, patients with higher DII (OR: 1.22, 95% CI: 1.13-1.32, p < 0.001) have a higher risk of sarcopenia. Compared with Q1 group, the group with higher DII levels had a higher risk of sarcopenia (Q2: OR: 1.23, 95%CI: 0.89-1.72, p = 0.209; Q3: OR: 1.68, 95%CI: 1.20-2.35, p = 0.003; Q4: OR: 2.43, 95%CI: 1.74-3.39, p < 0.001). Conclusion: High DII is associated with an increased risk of sarcopenia in hypertensive patients. The higher the level of DII, the higher the risk of sarcopenia in hypertensive patients.

Influence of sodium ferulate on miR-133a and left ventricle remodeling in rats with myocardial infarction.

To explore the influence of sodium ferulate (SF) on miR-133a and left ventricle remodeling (LVR) in rats with myocardial infarction (MI). The left coronary artery was ligated to create 36 ischemia-reperfusion (IR) rat models that were randomly divided into mock surgical group (MSG) (not ligated), model group (MG), and sodium ferulate group (SFG). After the successful modeling, SFG was intravenously injected with SF at the dose of 10 mg/kg, and the other two groups were injected with the same volume of normal saline. After 28 days, cardiac hemodynamic indices of all groups were measured; the myocardial infarction size (MIS), left ventricular mass index (LVMI), and collagen volume fraction (CVF) were calculated, the content of serum malondialdehyde (MDA) and activities of catalase (CAT), superoxide dismutase (SOD) and glutathione catalase (GSH-px) were detected by ELISA, and miR-133a expression in myocardial tissues of the left ventricle (LV) was detected by RT-qPCR. SF improved the cardiac hemodynamic indices of rat model and reduced the MIS, LVMI and CVF. SF decreased the serum MDA level and increased the serum CAT, SOD and GSH-px levels in rat model. SF increased the expression of miR-133a in myocardial tissue of rat model. Therefore, SF could effectively reduce the myocardial injury of IR rats and improve the LVR. Its mechanism may be related to the antioxygenation and upregulation of miR-133a.

Role of Diabetes Mellitus in Acute Coronary Syndrome Patients with Heart Failure and Midrange Ejection Fraction Who Have Undergone Percutaneous Coronary Intervention: A 3-Year Case-Series Follow-Up Retrospective Study.

BACKGROUND: Data are limited on the effect of diabetes mellitus (DM) on the prognosis of acute coronary syndrome (ACS) patients with heart failure with midrange ejection fraction (HFmrEF) who have undergone percutaneous coronary intervention (PCI). This study aimed to investigate the relationship between type 2 DM (T2DM) and 3-year outcomes in such a population. METHODS: A total of 377 ACS patients with HFmrEF (left ventricular EF 40%-49%) who had undergone PCI (132 diabetic and 245 nondiabetic patients) were included in the analysis. The primary outcome was a composite end point of all-cause death or HF rehospitalization. Cox proportional-hazard regression analysis and Kaplan-Meier tests were used to assess the effect of DM on the primary outcome. Sensitivity analysis was conducted with propensity score-matching analysis. RESULTS: During a follow-up of 3 years, diabetic patients had higher incidence of the primary outcome than nondiabetic patients (96.1 vs 44.6 per 1,000 patient-years, incidence ratio 2.301, 95% CI 1.334-3.969; P=0.002). Multivariate analysis showed that DM was associated with a significant increase in the composite outcome of all-cause death or HF rehospitalization (adjusted HR 2.080, 95% CI 1.115-3.878; P=0.021). Sensitivity analysis further confirmed that DM was an independent prognostic factor of long-term adverse outcomes for ACS patients with HFmrEF who had undergone PCI (adjusted HR 3.792, 95% CI 1.802-7.980; P<0.001). CONCLUSION: Among ACS patients with HFmrEF who had undergone PCI, T2DM comorbidity was significantly associated with worse long-term outcomes.

Berberine inhibits cardiac remodeling of heart failure after myocardial infarction by reducing myocardial cell apoptosis in rats.

The effects of berberine on cardiac function of heart failure after myocardial infarction and its possible mechanism were investigated. The anterior descending branches of 50 female Wistar rats were ligatured to establish the model of heart failure after myocardial infarction. At 4 weeks after successful modeling, the rats were randomly divided into two groups receiving 4-week gavage with saline (Sal group) and berberine (Ber group), while the sham-operation group (Sham group) was set up. After 4 weeks, the hemodynamics and serum BNP in rats were measured. The hearts of rats were taken to detect the degree of myocardial fibrosis. The myocardial cell apoptosis was detected. The expressions and changes in myocardial apoptosis-related proteins, including Bcl-2, Bax and caspase-3, were detected. The expression and changes in GRP78, CHOP and caspase-12 in myocardial tissue were detected. The results showed that Berberine improved the cardiac function of rats after myocardial infarction. After myocardial infarction, myocardial fibrosis and apoptosis were observed around the infarction area, berberine improved the myocardial fibrosis and reduced cell apoptosis. Furthermore, berberine alleviated endoplasmic reticulum stress (ERS) after myocardial infarction. In conclusion, Berberine can inhibit the myocardium cell apoptosis of heart failure after myocardial infarction, and its mechanism may be realized by affecting the ERS in myocardial tissue of heart failure after myocardial infarction and CHOP and caspase-12 apoptotic signaling pathway, upregulating Bcl-2/Bax expression and downregulating caspase-3 expression, thus inhibiting the cardiac remodeling and protecting the cardiac function.

Associations between ADRB1 and CYP2D6 gene polymorphisms and the response to ß-blocker therapy in hypertension.

OBJECTIVE: To investigate the associations between ß1-adrenergic receptor (ADRB1) and cytochrome P450 2D6 (CYP2D6) gene polymorphisms and ß-blocker treatment outcomes in patients with hypertension. METHODS: Chinese patients with essential hypertension were treated with the ß-blocker metoprolol and followed up for 12 weeks. xTAG® liquid-chip technology was used for CYP2D6 100 C > T and ADRB1 1165G > C genotyping. Associations between gene polymorphisms and antihypertensive therapy outcomes were assessed by generalized linear model fitting. A decrease of ≥ 10 mmHg in systolic blood pressure indicated an effective treatment outcome. RESULTS: A total of 93 patients were included in the study. Mutant allele frequencies of 61.29% and 58.60% were obtained for ADRB1 and CYP2D6, respectively. There was no significant interaction between the effects of ADRB1 and CYP2D6 gene polymorphisms on treatment outcome. Patients homozygous for the mutant ADRB1 genotype (CC) had better treatment outcomes than those heterozygous for the mutation (GC). Interestingly, ß-blocker treatment duration was an independent factor associated with treatment outcome. CONCLUSIONS: The ADRB1 1165G > C gene polymorphism and ß-blocker treatment duration are independent factors associated with ß-blocker treatment outcome. These findings suggest that the selection of antihypertensive therapy should take into consideration the patient's genotype.