Clinical and Experimental Hypertension最新文献

Objective: This study aimed to investigate the prevalence of hypertension among young adults with MAFLD, assess the association between the presence and severity of MAFLD and hypertension, and explore potential mediating mechanisms linking MAFLD and hypertension in this population.

Methods: A total of 5,327 individuals aged 18-45 years from the National Health and Nutrition Examination Survey (2017-2023) were included. Multivariable logistic regression analysis was performed to evaluate the independent associations of MAFLD and its severity with hypertension and isolated diastolic hypertension. Mediation analysis assessed the mediating effects of inflammatory markers, including white blood cell (WBC) count, neutrophil count, and systemic immune-inflammation index (SII).

Results: The prevalence of MAFLD in the study population was 44.05%. Hypertension prevalence in the MAFLD group was significantly higher than in the non-MAFLD group (37.68% vs. 15.19%, P < 0.001). After adjusting for sex, age, race, alcohol consumption, and comorbidities such as diabetes and renal insufficiency, individuals with MAFLD and moderate-to-severe fibrosis exhibited a significantly higher risk of hypertension compared to non-MAFLD individuals (OR = 3.414, 95% CI: 2.522-4.622), P < 0.001). Mediation analysis demonstrated that WBC, neutrophils, and SII mediated 7.62% (95% CI: 2.75-15.00), 6.71% (95% CI: 2.48-12.65), and 5.90% (95% CI: 2.40-10.88) of the association between MAFLD and hypertension, respectively.

Conclusion: MAFLD, particularly in the presence of advanced liver fibrosis, is strongly and independently associated with hypertension in young adults. Systemic inflammation acts as a key mediator in this relationship, highlighting its potential as a therapeutic target for precision antihypertensive strategies in this population.

Pulmonary arterial hypertension (PAH) is a group of complex vasculopathies characterized by increased pulmonary arterial pressure and subsequent pulmonary vascular remodeling. However, the underlying pathogenesis of PAH has not been fully elucidated. In the present study, we employed bioinformatics technology to investigate the pathogenesis of PAH. Microarray datasets related to PAH were retrieved from the Gene Expression Omnibus database to screen for ER stress-related genes (ERSRGs) between normal control and PAH samples. The differentially expressed genes (DEGs) were analyzed for functional enrichment and protein‒protein interaction (PPI) networks. DEG-related miRNAs and transcriptional factor (TF) were predicted to construct the miRNA-TF-hub gene network. The diagnostic accuracy of the hub genes was assessed via receiver operating characteristic (ROC) curve analysis. The relative abundances of different types of immune cells were determined via immune infiltration analysis. The screening detected 20 ERSRGs between normal and PAH samples, nine of which (HIF1A, BCL2L1, TLR4, HMOX1, VCAM1, EGR1, MAPK8, LCN2, and CEBPB) were further identified as hub genes via the PPI network. To construct a regulatory network analysis of the Hub genes, 57 miRNAs and 35 TFs were subsequently predicted. There was a significant difference in the infiltration of 17 types of immune cells between the two groups. These results suggest that the nine hub genes might play crucial roles in the development of PAH. These findings might provide new therapeutic targets for PAH or potential biomarkers for its diagnosis.

With rapid advancements in genomics, proteomics, and metabolomics researchers have gained significant insights into ACS (ACS) pathogenesis. Studies have revealed specific biomarkers linked to ACS and provided novel tools for risk evaluation and early diagnosis. Genomic breakthroughs have enabled exploration of genetic factors contributing to ACS. Transcriptomics has facilitated the analysis of gene expression alterations in patients with ACS. Proteomics has identified potential therapeutic targets by pinpointing biomarkers, paving the way for new drug development. Advances in metabolomics have enabled monitoring of changes in metabolic pathways, offering valuable information for early diagnosis and disease prognosis. In summary, multiomics research has shed light on the critical aspects of ACS clinical strategies, facilitating advancements in early diagnosis, risk assessment, and personalized therapy, and will increasingly assume a pivotal role in future clinical practice.

Our previous study has found that miPEP31, which is encoded by pri-miRNA-31, inhibits the transcription of pri-miRNA-31 and alleviates angiotensin (Ang) II-induced hypertension. miR-31 is involved in proliferation of primary vascular smooth muscle cells (VSMCs), the key functional cells involved in hypertensive vascular remodeling. However, the role and mechanism of miPEP31 in the proliferation of VSMCs remain unclear. The aim of this study is to investigate whether miPEP31 plays an important role in VSMC proliferation and contributes to vascular remodeling. We found that the administration of synthetic miPEP31 mitigated but miPEP31 deficiency aggravated the Ang II-induced aortic thickness of intima plus media and fibrotic area. miPEP31 is endogenously expressed and penetrates into nuclei in VSMCs. miPEP31 inhibits PDGF-BB-induced VSMC proliferation in a dose-dependent manner and decreases the Ang Ⅱ-induced aortic α-SMA staining area. Mechanistically, we demonstrated that miPEP31 acts as a transcriptional repressor and inhibits miR-31 expression by cooperating with Trps1, a GATA family zinc finger transcription factor. In summary, our study suggests that miPEP31 protects against vascular remodeling in Ang II-infused mice via cooperation with transcription factor Trps1 to inhibit miR-31 expression and, subsequently, VSMC proliferation. This finding highlights the therapeutic effect and role of miPEP31 on hypertensive target organs and functional cells.

Objective: To evaluate the clinical utility of non-invasive hemodynamic indicators in assessing cardiovascular risk among hypertensive patients with coronary atherosclerotic heart disease (CAD), and to explore their correlation with lipid metabolism disorders.

Methods: A cross-sectional study was conducted on 598 hypertensive patients (312 hypertension-only vs. 286 hypertension-CAD). Participants underwent non-invasive hemodynamic monitoring (BioZ-Standard device) and lipid profiling. Group comparisons were performed using t-tests, and Pearson correlation was used to analyze associations between hemodynamics, lipids, and CAD. Receiver operating characteristic (ROC) curve analysis was used to assess diagnostic utility.

Results: The combined group demonstrated significantly impaired hemodynamic function compared to the hypertension-only group, with a lower CO (3.41 ± 0.45 vs 4.38 ± 0.51 L/min), SV (44.09 ± 4.38 vs 50.91 ± 4.63 mL), and CI (1.94 ± 0.25 vs 2.49 ± 0.29 L min^-1 m^-2) (all p < 0.001). Lipid profiles were markedly worse in patients with CAD, showing higher TC (4.76 ± 0.34 vs 4.35 ± 0.31 mmol/L) and LDL-C (3.32 ± 0.39 vs 2.89 ± 0.42 mmol/L) and lower HDL-C (1.09 ± 0.21 vs 1.23 ± 0.19 mmol/L) (all p < 0.001). Strong negative correlations were detected between the hemodynamic parameters and CAD status (CO: r = -0.672, p < 0.001; SV: r = -0.589, p < 0.001), and positive correlations were detected between dyslipidemia and CAD (LDL-C: r = 0.458, p < 0.001; HDL-C: r = -0.381, p < 0.001).

Conclusion: Non-invasive hemodynamic monitoring, particularly the measurement of CO and SV, combined with lipid profiling, offers quantitative markers for risk stratification in hypertensive patients. The significant correlations and diagnostic potential indicated by ROC analysis (AUC > 0.75 for key parameters) suggest that these measures can aid in the early detection and management of CAD in this high-risk population.

This retrospective cohort study assessed the predictive value of routine clinical indicators for diabetic nephropathy (DN) in elderly patients (≥60 years) with type 2 diabetes mellitus (T2DM) and hypertension. A total of 102 hospitalized patients (January 2022-December 2023) were divided into DN and non-DN groups. Fasting blood glucose (FBG), 2-h postprandial glucose (2hPG), HbA1c, systolic blood pressure (SBP), urinary microalbumin (UMA), and urinary albumin-to-creatinine ratio (UACR) were analyzed using univariate and multivariate logistic regression to identify independent predictors. A nomogram based on these indicators was developed and evaluated by receiver operating characteristic (ROC) analysis. All six factors independently predicted DN (p < 0.05), with 2hPG showing the strongest association (OR = 8.922). The combined model achieved high predictive accuracy (AUC = 0.906), outperforming any single indicator. This model offers a practical tool for early DN risk stratification in elderly T2DM patients with hypertension, supporting individualized prevention and intervention.

Objective: This study investigated the association between several dietary quality scores-including the healthy eating index-2015(HEI-2015), dietary inflammatory index (DII), and dietary approaches to stop hypertension (DASH)-and the risk of cardiovascular disease(CVD) mortality in hypertension treatment group.

Methods: Data were obtained from 11,310 participants in the the U.S. Centers for Disease Control and Prevention's National Health and Nutrition Examination Survey (1999-2016). Diet quality scores were calculated based on the type and quantity of food and beverages consumed by participants in the past 24 h. CVD mortality was defined as deaths from heart or cerebrovascular disease (ICD-10). We used cox proportional hazards regression to assess the association between diet quality scores and CVD mortality.

Results: During an average follow-up period of 109 months, 1324 deaths from CVD were confirmed. HEI-2015 and DII showed statistically significant negative association (HR, 0.9404 (95% CI = 0.8846, 0.9998), p = 0.0491) and positive correlation (HR, 1.0514 (95% CI = 1.0055, 1.0995), p = 0.0278) with CVD mortality. DASH showed no statistically significant negative correlation with CVD mortality (HR, 0.9639 (95% CI = 0.9215, 1.0083), p = 0.1096). However, trend tests for all three diet quality scores were significant (p < 0.05).

Conclusion: The HEI-2015 and DASH dietary patterns reduce the risk of CVD mortality in the hypertension treatment group. In contrast, the DII dietary pattern increases the risk of CVD mortality in such patients.

Objective: Gestational hypertension, pre-eclampsia, and eclampsia pose significant risks to maternal and fetal health, yet their underlying causes remain unclear. This study investigates the associations between 233 metabolites and these conditions.

Methods: We analyzed data from the Genome-Wide Association Studies (GWAS) database for gestational hypertension, pre-eclampsia, and eclampsia. The bidirectional two-sample MR analysis examined causal relationships using inverse variance weighting as the primary method, supplemented by MR-Egger, weighted median, simple mode, and weighted mode. Sensitivity analyses assessed robustness, heterogeneity, and horizontal pleiotropy.

Results: In the forward Mendelian randomization analysis, a reduction in citrate levels (OR = 0.906, 95% CI = 0.829-0.990, p = .029) is associated with an increased risk of gestational hypertension. The ratio of conjugated linoleic acid to total fatty acids (OR = 1.172, 95% CI = 1.026-1.339, p = .019) is associated with an increased risk of gestational hypertension. The ratio of conjugated linoleic acid to total fatty acids (OR = 1.288, 95% CI = 1.064-1.560, p = .009) is associated with an increased risk of preeclampsia and eclampsia. The phospholipids to total lipids ratio in large HDL (OR = 1.227, 95% CI = 1.120-1.344, p = 9.91 × 10^-6) is associated with an increased risk of preeclampsia and eclampsia. The total cholesterol to total lipids ratio in chylomicrons and extremely large VLDL (OR = 0.884, 95% CI = 0.789-0.990, p = .033) is associated with an increased risk of preeclampsia and eclampsia. In the reverse Mendelian randomization analysis, the occurrence of gestational hypertension is associated with a reduction in Cholesteryl esters to total lipids ratio in very large VLDL (OR = 0.987, 95% CI = 0.975-0.999, p = .044). The occurrence of preeclampsia and eclampsia is associated with a reduction in total choline levels (OR = 0.989, 95% CI = 0.979-0.998, p = .029), and with a reduction in total phosphoglycerides levels (OR = 0.988, 95% CI = 0.978-0.997, p = .012). Sensitivity analysis did not detect significant heterogeneity or pleiotropy.

Conclusion: This research elucidates the causal links between specific metabolites and gestational hypertension, pre-eclampsia, and eclampsia, potentially informing new clinical approaches for diagnosis and treatment.

Objectives: To evaluate the efficacy and safety of intensive blood pressure control in patients over 60 years.

Methods: Databases including PubMed, Embase and Cochrane library were searched from inception through February 1, 2024. Randomized controlled trials evaluating the efficacy or safety of intensive blood pressure control in patients over 60 years were included in the meta-analysis.

Results: Intensive blood pressure control in individuals with mild hypertension has been shown to reduce the risk of heart failure, stroke, myocardial infarction, major cardiovascular events, cardiovascular mortality, and all-cause mortality. The benefits of intensive blood pressure control in patients with moderate to severe hypertension are comparable to those observed in individuals with mild hypertension, with the exception of a reduced impact on all-cause mortality and cardiovascular mortality. Compared with maintaining systolic blood pressure (SBP) above 140 mmHg, SBP below 140 mmHg is associated with a decreased risk of major cardiovascular events in patients aged over 70, as well as a reduced risk of stroke in patients aged 60-69. Furthermore, compared to maintaining SBP above 130 mmHg, SBP below 130 mmHg is linked to a lower risk of major cardiovascular events, heart failure and myocardial infarction in patients over 60, a reduced risk of stroke and cardiovascular mortality in patients aged 60-69, and a decreased risk of all-cause mortality in patients over 70. However, a lower baseline blood pressure or more aggressive blood pressure control may be associated with an increased risk of hypotension.

Conclusions: Patients with hypertension aged over 60 years can derive benefits from intensive blood pressure management without experiencing significant adverse events, aside from hypotension.

Amlodipine has been used as a front-line anti-hypertensive therapy for decades by virtue of blocking voltage-operated calcium channels with high affinity and specificity. Recently, the safety of amlodipine has been questioned, as it was reported to activate Ca²⁺ release-activated Ca²⁺ (CRAC) channels and increase the risk of heart failure. Here we show, using a variety of approaches, that amlodipine does not activate CRAC channels at therapeutic concentrations. Combined with our previous meta-analysis, our study should reassure physicians that amlodipine should continue to be prescribed for treating hypertension.