Journal of Hypertension最新文献

Objective: Pregnancy-induced hypertension (PIH) is a significant health concern affecting both maternal and fetal well-being, with limited effective interventions currently available. The objective of this study is to examine the relationship between stable blood pressure and changes in gut microbiota in pregnancy-induced hypertension (PIH) rats following treatment with probiotic-fermented buffalo milk (PBM).

Methods: Twenty-four Sprague-Dawley pregnant rats were allocated into four groups: the normal control (NC) group, model control (MC) group, fermented buffalo milk (FBM) group, and labetalol positive control (LPC) group. Rats in the FBM and LPC groups received oral gavage with PBM at a dose of 20 mg/kg/day and labetalol hydrochloride (LH) at 4 mg/kg/day, respectively, from the first day of pregnancy until day 21. Rats in the NC and MC groups were administered an equivalent volume of saline (10 ml). Pregnancy-induced hypertension was established by subcutaneous injection of l -nitro-arginine methyl ester daily from day 15 to day 21 of pregnancy. Blood pressure was monitored regularly across all groups, and differences in gut microbiota composition and functional activity were analyzed using high-throughput 16S rRNA sequencing and metabolomic profiling.

Results: PBM demonstrated a superior ability to stabilize blood pressure in pregnant rats compared to LH. PBM modulated the gut microbiota by increasing the relative abundance of propionate-producing bacteria, including Fusobacterium , Lachnospira , and Roseburia . Additionally, PBM reduced phenylalanine metabolism, thereby inhibiting the production of phenylacetylglycine, a metabolite associated with hypertension.

Conclusion: The blood pressure-lowering effect of PBM in PIH rats may be associated with the regulation of propionate-producing bacteria and their metabolic functions.

Purpose: Hypertension-induced alterations in cerebral blood flow (CBF) precede overt cerebrovascular structural damage. This study classified SBP control into four threshold ranges based on clinical staging criteria for hypertension, with particular focus on elucidating the differential effects of long-term SBP management on CBF dynamics.

Methods: Randomized controlled trials (RCTs) were collected. Data were retrieved from four databases, spanning their inception until 3 October 2024. Independent data extraction was conducted, and the risk of bias was assessed. First, an overall assessment of the impact of SBP control on CBF was carried out. Second, studies were assigned into four subgroups: 120-129, 130-139, 140-159, and at least 160 mmHg. And then, subgroup was analyzed to explore effects of different SBP control on CBF. The effects of CBF were compared between intensive (120-129 mmHg) and standard SBP control (130-139 mmHg).

Results: The meta-analysis included 12 RCTs with 1100 participants. Four long-term trials (33.33%) were identified as high risk with attrition bias due to dropout rates exceeding 20%. Overall, SBP control, both acute and long-term, improved CBF [standardized mean difference (SMD), 0.17; 95% confidence interval (CI) 0.02-0.31; P  = 0.02, I2  = 39%] with moderate robustness. Specially, long-term SBP control improved CBF (SMD, 0.15; 95% CI 0.01-0.29; P  = 0.04, I2  = 37%) with low robustness, due to the change of P value when removing a large-sample trial. Intensive SBP control, maintaining 120-129 mmHg, significantly increased long-term CBF (SMD, 0.21; 95% CI 0.07-0.34; P  = 0.003, I2  = 0%) with low heterogeneity and high robustness. In contrast, long-term SBP control above 130 mmHg did not lead to significant change in CBF. Although intensive SBP control showed a nonsignificant improvement in CBF compared with standard SBP control, it demonstrated a promising effect size (SMD 2.17; P  = 0.07).

Conclusion: This review suggests that intensive SBP control might provide a potential advantage on CBF improvement and deceleration of cerebral small vessel disease (CSVD) development, and might affect cognitive function but requires further verification in the hypertensive population.

Target trial emulation (TTE) is a demanding framework for causal inference using observational data, yet its use in hypertension research is limited. This scoping review maps current TTE applications, highlights methodological strengths and gaps, and suggests future directions. Following Joanna Briggs Institute (JBI) and Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) guidelines, we screened multiple databases and included 14 of 1352 articles. Common methods for confounding adjustment included inverse probability weighting (50%) and the g-formula (21.5%), often alongside regression models. Time-varying confounders were inconsistently addressed, and loss to follow-up was typically handled via simple censoring. Residual confounding remained a concern; although unobserved confounders were noted, only five studies (36%) used negative controls or e-values. Subgroup analyses were frequent, but causal machine learning for heterogeneous treatment effect (HTE) estimation was not reported. Although still in its early stages, TTE in hypertension research shows promise for addressing key challenges, including HTE, long-term outcomes, and dynamic treatment strategies.

Elevated blood pressure (BP) is the most significant modifiable risk factor for cardiovascular morbidity and mortality. However, the optimal systolic BP target in hypertensive patients remains unclear. We conducted a meta-analysis of randomized controlled trials (RCTs) comparing intensive (≤120 mmHg) versus standard (≤140 mmHg) systolic BP control. A systematic search of three databases identified six RCTs including 39 811 patients (mean age 64.8 years). Intensive BP control significantly reduced the risk of stroke [risk ratio (RR) 0.81; 95% confidence interval (CI) 0.74-0.90], myocardial infarction (RR 0.83; 95% CI 0.73-0.95), cardiovascular death (RR 0.73; 95% CI 0.58-0.91), and all-cause mortality (RR 0.87; 95% CI 0.76-0.99). No significant differences were observed in bradycardia (RR 1.12; 95% CI 0.70-1.77) or symptomatic hypotension (RR 2.25; 95% CI 0.61-8.24), though syncope occurred more frequently with intensive control (RR 1.54; 95% CI 1.23-1.92). Intensive systolic BP control may offer substantial cardiovascular benefits with minimal adverse effects and should be considered in clinical practice.

Background: The increasing accessibility of high altitudes due to modern lifts has led to rise in individuals reaching high elevations without acclimatization or medical screening. Acute exposure to hypobaric hypoxia induces hemodynamic and metabolic stress, increasing blood pressure (BP) and heart rate while reducing oxygen saturation. These effects are particularly concerning for individuals with preexisting cardiovascular diseases.

Methods: We conducted an observational cross-sectional study at the base station (1300 m) of the Skyway Monte Bianco cable car, evaluating the demographic and clinical characteristics of unselected participants before ascent. Data were collected via a biometric multiparametric recording system (Keito K9), measuring SpO 2 , heart rate, BP, body composition, and medical history.

Results: A total of 1930 individuals (56% men) participated but anamnestic data were available in 1174 volunteers. Among them, 18% had history of cardiovascular disease, predominantly hypertension (16%). SBP at least 135 mmHg was found in 11.1% of participants, with 4.3% presenting values at least 150 mmHg. The prevalence of individuals with hypertension above the reference limits was higher in cardiac patients. Cardiovascular patients were older, heavier, and had higher BP compared to healthy individuals. Interestingly, no differences in altitude exposure frequency were observed between groups.

Conclusion: Our findings indicate that a significant proportion of individuals, including those with cardiovascular disease, reach low altitudes with BP above the reference limits. Given the potential risks associated with hypoxia-induced sympathetic activation, improved screening and preventive strategies should be considered for high-altitude tourism. Further research is needed to assess acute BP variations at different altitudes and their implications for cardiovascular risk.

Introduction: High blood pressure remains the leading risk factor for cardiovascular and all-cause deaths in Australia. Higher sodium and lower potassium intake are well established risk factors for elevated blood pressure and increased cardiovascular disease risk. Despite decades of global public health efforts, progress in reducing sodium and increasing potassium intake has been limited. The WHO recommends potassium-enriched salt as an effective, affordable, and scalable strategy to lower blood pressure by simultaneously reducing sodium and increasing potassium intake. This position statement was developed to support implementation and address this public health priority.

Main recommendations: For patients with hypertension, core dietary recommendations should include reducing sodium by limiting the regular salt added when cooking and at the table, choosing low-salt foods and increasing potassium intake through fruit and vegetable intake. When these changes are challenging, switching regular salt with potassium-enriched salt offers a practical alternative. We recommend including this switch as an additional dietary recommendation in clinical hypertension guidelines. Suggested wording: 'If patients add salt to their food, they should make a 1 : 1 switch from regular salt to potassium-enriched salt with a composition of approximately 75% sodium chloride and 25% potassium chloride, unless they are at risk of hyperkalaemia because of kidney disease, use of a potassium supplement, use of a potassium sparing diuretic or for another reason." Routine kidney health checks are recommended to support safe implementation.

Changes in management: We advocate for the inclusion of this recommendation in future hypertension management guidelines. Systematic, nation-wide implementation of potassium-enriched salt as a replacement for regular salt should be prioritized as a scalable public health intervention. We call for further research into the impact of potassium-enriched salt in patients with kidney disease, the general population unscreened for hyperkalaemia risk, and patients using different antihypertensive regimens.

Background: Finerenone, a novel nonsteroidal mineralocorticoid receptor (MR) antagonist, has shown antihypertensive activity and improved cardiac function in clinical studies, but the role and target of finerenone in the prevention and treatment of ventricular remodeling in hypertension remains unclear. In the present study, hypertensive rats were employed to evaluate the beneficial effects of finerenone on ventricular remodeling and cardiac function in hypertension and to identify the related targets.

Method: Hypertensive two-kidney, one-clip (2K1C) Sprague-Dawley rats were randomly divided into three groups: sham-operated, 2K1C model, and finerenone-treated groups (2 mg/kg/day, Bayer Pharmaceuticals, HJ20220057). All groups were treated for 8 weeks. Blood pressure, echocardiographic measurements, biochemical parameters related to cardiovascular remodeling and endoplasmic reticulum (ER) stress markers were evaluated. Cultured H9C2 cells were used to determine the effect of finerenone on cardiomyocytes administered Ang-II.

Result: Compared with the model group, finerenone significantly reduced SBP, DBP, cardiac index, left ventricular mass index, NT-proBNP, and sST2 levels. Left ventricular remodeling and cardiac function were significantly improved after treatment with finerenone for 8 weeks. Finerenone effectively decreased the protein expression of the ER stress marker GRP78 and reduced the protein levels of p-IRE1, XBP1, and TRAF2 in myocardial tissue samples from hypertensive rats, thus decreasing ER stress in the myocardial tissue, as well as the production of the inflammatory factors IL-6 and TNF-α. In addition, finerenone significantly decreased apoptosis in H9C2 cells induced by Ang-II. Furthermore, the modulatory effects of finerenone on ER stress factors in cardiomyocytes were identified.

Conclusion: Finerenone effectively lowers blood pressure and improves ventricular remodeling and cardiac function in hypertensive rats. These effects may be mediated via IRE1-dependent regulation of XBP1 and TRAF2, leading to reduced ER stress, inflammation, and cardiomyocyte apoptosis. Comparisons among the sham, model, and treatment groups confirm the cardioprotective role of finerenone in hypertensive heart disease.

Objective: Guidelines from ACC/AHA, ESC/ESH, and JNC 8 recommend ACE inhibitors (ACEi), ARBs, calcium channel blockers (CCBs), and diuretics for hypertension in patients with cardiometabolic multimorbidity (CMM). Their effectiveness in Asians is underexplored. This study evaluates their association with mortality in Taiwanese patients with hypertension and CMM.

Methods: A population-based cohort study was conducted using Taiwan's administrative health databases (2004-2014). Patients aged ≥20 years with hypertension and ≥8 outpatient blood pressure measurements were included. All-cause mortality was assessed using inverse probability weighted Cox models, evaluating medication classes, adherence, and systolic blood pressure (SBP) control.

Results: Of 80 748 patients (mean age 60 years, 56.3% male), 41.7% had one CMM, and 9.4% had multiple CMMs. ARBs reduced mortality in multimorbid patients [hazard ratio (HR) = 0.80, 95% confidence interval (CI) 0.67-0.95], while diuretics (HR = 1.63, 95% CI 1.33-1.99) and vasodilators (HR = 1.22, 95% CI 1.03-1.45) increased risk. ACEi and CCBs were neutral. Optimal SBP control (120-139 mmHg) benefited multimorbid patients, but intensive control (<120 mmHg) increased risk in those with ≤1 CMM (HR = 1.37, 95% CI 1.20-1.55). High SBP variability (SD >18 mmHg) raised mortality risk (HR = 1.62, 95% CI 1.07-2.44).

Conclusions: Antihypertensive effectiveness varies by CMM burden. ARBs reduce mortality in multimorbid patients, while diuretics and vasodilators may increase risk. Optimal SBP control (120-139 mmHg) benefits multimorbid patients, but intensive control may harm less complex cases. Further research is needed.