Hypertension最新文献

Background: The latest updated 2025 and 2017 American College of Cardiology and the American Heart Association guidelines lowered the diagnostic threshold for hypertension to 130/80 mm Hg. Whether the new classification for hypertension has implications for reproductive outcomes remains uncertain.

Methods: This retrospective cohort study was conducted at the Reproductive Medicine Center of Shandong University in China. Women who underwent the initial embryo transfer of their first in vitro fertilization cycle were categorized into the normal blood pressure (BP), elevated BP, stage 1 hypertension, and stage 2 hypertension groups based on BP levels measured just before in vitro fertilization treatment. We examined associations of prepregnancy BP and reproductive outcomes.

Results: This study included 43 629 women who received in vitro fertilization treatment. The rate of live birth was lower in women with stage 1 and stage 2 hypertensions (46.1% and 41.4%, respectively) compared with women with normal BP (49.2%), with the adjusted relative ratios of 0.97 (95% CI, 0.937-0.996; P=0.027) and 0.91 (95% CI, 0.85-0.98; P=0.009), respectively. Compared with normal BP, both stage 1 and stage 2 hypertension were associated with higher risks of pregnancy loss, preeclampsia, and preterm delivery. Elevated BP was associated with a higher risk of gestational hypertension. Optimal BP cutoffs for adverse reproductive outcomes were consistent with the diagnostic threshold for stage 1 hypertension.

Conclusions: Compared with normal BP, prepregnancy stage 1 and stage 2 hypertension were associated with a lower rate of live birth after in vitro fertilization treatment and increased risks of pregnancy complications.

Blood pressure (BP) instability is a hallmark of disrupted autonomic cardiovascular control after spinal cord injury (SCI). Individuals frequently experience hypertensive surges during autonomic dysreflexia and hypotensive drops during orthostatic hypotension, yet the commonly used thresholds for defining these events are derived from expert consensus rather than outcome-based evidence. Similarly, arterial stiffness, typically assessed by pulse wave velocity, is consistently elevated in SCI, but no validated cut points exist to guide clinical intervention. This lack of outcome-anchored thresholds limits risk stratification and leaves clinicians without tools to evaluate the cumulative cardiovascular burden imposed by chronic hemodynamic instability. Accumulating data indicate that individuals with SCI demonstrate profound BP variability, particularly those with cervical or high thoracic injuries, and exhibit higher rates of ischemic heart disease, stroke, and sudden cardiac death compared with the general population. Pulse wave velocity values are also markedly increased across multiple cohorts, indicating the presence of accelerated vascular aging. However, the long-term consequences of BP instability and increased pulse wave velocity remain unquantified. A comprehensive, multicenter prospective framework is urgently needed to link BP fluctuations and pulse wave velocity changes to hard cardiovascular end points. Advances in registry-based longitudinal cohorts now make this achievable. Establishing outcome-validated thresholds, whether based on absolute BP levels, frequency of BP excursions, or degree of arterial stiffness, would enable the development of SCI-specific cardiovascular risk calculators and shift clinical practice from reactive management to proactive prevention. Closing this evidence gap is essential to reducing the disproportionate cardiovascular burden faced by individuals living with SCI.

Background: Heart failure with preserved ejection fraction (HFpEF) accounts for ≈50% of heart failure, and hypertension often coexists. Although strain imaging detects subclinical dysfunction, the relative diagnostic value of left atrial (LA) versus left ventricular (LV) strain for identifying hypertensive HFpEF remains uncertain. We compared LA and LV strain using cardiac MR feature tracking to determine optimal markers for HFpEF detection.

Methods: A single-center, retrospective study included 191 participants: 71 with HFpEF and hypertension (HFpEF-HTN), 60 with essential hypertension, and 60 controls who underwent cardiac MR. Cardiac MR feature tracking quantified LV global strains and strain rates, and LA reservoir (εs), conduit (εe), and booster pump (εa) strain with corresponding strain rates. One-way ANOVA compared groups, logistic regression identified HFpEF-HTN predictors, and receiver operating characteristic analysis with area under the curve assessed diagnostic accuracy.

Results: All LA strain parameters showed stepwise impairment from controls to hypertension to HFpEF-HTN (all P<0.05). LV global strains decreased in HFpEF-HTN versus controls, while hypertension exhibited only reduced global longitudinal strain (all P<0.05). LA parameters demonstrated superior discriminatory performance over LV parameters. εs best distinguished HFpEF-HTN from hypertension (area under the curve, 0.802 [95% CI, 0.724-0.867]), while εe best discriminated hypertension from controls (area under the curve, 0.892 [95% CI, 0.823-0.942]).

Conclusions: LA strain parameters, particularly εs, provided superior diagnostic performance over LV strain in distinguishing HFpEF-HTN from hypertension. These findings support the potential role of LA strain as a sensitive imaging biomarker for detecting HFpEF-HTN. Prospective validation is needed before clinical implementation.

Background: Chronic anxiety increases the risk of incident hypertension, yet mechanisms remain equivocal. Recent evidence documents that trait anxiety is positively associated with muscle sympathetic nerve activity (MSNA), a known contributor to hypertension risk. The purpose of this study was to address the hypothesis that the association between trait anxiety, MSNA, and elevated blood pressure would be moderated by cardiac vagal activity estimated via heart rate variability (HRV).

Methods: Resting blood pressure, MSNA (microneurography), and heart rate (ECG) were collected at rest in 130 adults (71 men, 59 women; age, 25±8 years; body mass index, 25±4 kg/m²). Moderation analyses were used to investigate the moderating role of HRV on the association between trait anxiety, MSNA, and blood pressure.

Results: The association between trait anxiety and MSNA was significantly moderated by resting HRV such that the relationship between anxiety and MSNA was stronger (B=0.322, P=0.005) in those with lower HRV (-1 SD) compared with those with average (B=0.146, P=0.067) or higher (+1 SD) HRV (B=-0.031, P=0.785). Conversely, HRV did not moderate the positive association between trait anxiety and blood pressure.

Conclusions: The present findings demonstrate that elevated trait anxiety is associated with elevated sympathetic neural activity and blood pressure. The association between trait anxiety and elevated sympathetic nerve activity is particularly prominent in those with low HRV, suggesting a potential utility of HRV as a cardiovascular risk biomarker in individuals with heightened anxiety.

Background: Although low-dose triple single-pill combination therapies show promising efficacy and safety, studies comparing them to standard-dose monotherapies remain limited. This phase III, randomized, double-blind trial evaluated the efficacy and safety of a low-dose single-pill combination of telmisartan, amlodipine, and chlorthalidone versus standard-dose telmisartan monotherapy in patients with essential hypertension.

Methods: After a 4-week placebo run-in period, 314 eligible subjects were randomized to either receive telmisartan/amlodipine/chlorthalidone 20/2.5/6.25 mg or telmisartan 40 mg for 8 weeks. The primary efficacy end point was the change in mean sitting systolic blood pressure from baseline to week 8, with noninferiority assessed in the per-protocol set (PPS), followed by superiority testing in the full analysis set using a gatekeeping approach to control for type I error.

Results: At week 8, the combination group demonstrated significant mean sitting systolic blood pressure reduction compared with monotherapy in the per-protocol set analysis (least squares mean difference, -3.8 mm Hg [95% CI: -6.7 to -0.9]; P=0.01), establishing its noninferiority. Furthermore, the superiority of the combination therapy was confirmed in the full analysis set (LS mean difference, -4.0 mm Hg [95% CI, -6.8 to -1.3]; P<0.01). Mean sitting diastolic BP, BP normalization rates, and response rates also favored the combination group at weeks 4 and 8 (all P<0.01). Subgroup analyses showed consistent efficacy across clinical strata, including age and prior antihypertensive treatment. The incidence of adverse events was comparable between groups, with no serious drug-related events reported.

Conclusions: Low-dose triple single-pill combination of telmisartan/amlodipine/chlorthalidone demonstrated superior BP-lowering efficacy with well-tolerated and comparable safety to standard-dose telmisartan monotherapy.

Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT06348576.

Background: The impact of intensive blood pressure (BP) control on cognitive function in East Asian populations remains uncertain. We aimed to assess the effect of a lower systolic BP target on global cognitive function in Chinese hypertensive adults.

Methods: This secondary analysis of a randomized trial involved hypertensive patients with high cardiovascular risk across 116 sites in China. Participants were assigned to receive intensive treatment (systolic BP target <120 mm Hg) or standard treatment (systolic BP target <140 mm Hg) for a median of 3.4 years. Cognitive function was assessed via MMSE (Mini-Mental State Examination) at baseline and the end of the study. Prespecified outcomes were a change in MMSE score and investigator-reported probable dementia.

Results: Among 11 255 randomized participants, all completed cognitive assessment at baseline and 10 440 (92.8%) at the end of the study. The mean change in MMSE score was not significantly different between arms (difference, 0.05 [95% CI, -0.07 to 0.17]), with a mean change of -0.54 (95% CI, -0.63 to -0.46) in the intensive arm and -0.60 (95% CI, -0.68 to -0.51) in the standard arm. Results were robust across sensitivity analyses and consistent across most subgroups. Exceptions included subgroups of coronary heart disease or antiplatelet treatment. The incidence of probable dementia was too low for meaningful interpretation.

Conclusions: Intensive systolic BP lowering to a target of <120 mm Hg for 3 years did not adversely affect global cognitive function in Chinese hypertensive adults, irrespective of age, sex, BP level, and comorbidities, affirming the cognitive safety of this treatment strategy.

Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT04030234.

Background: Endothelial mechanosensing is essential for controlling vascular tone. LRRC8A (leucine-rich repeat-containing protein 8A) was previously identified as a core subunit of the mechanoresponsive LRRC8 complex, functionally encoding the endothelial volume regulatory anion channel and regulating vascular function. This study aims to identify the molecular identity of the endothelial LRRC8 complex and its function in vascular reactivity and blood pressure control.

Methods: We generated germline epitope-tagged Lrrc8a-3xFlag knock-in mice and endothelium-specific Lrrc8a-3xFlag overexpression mice to permit LRRC8A and LRRC8C immunoprecipitation and define LRRC8 subunit interactions. We combined in vivo and in vitro loss-of-function models, electrophysiology, immunoblotting, and pressure myography of third-order mesenteric arteries to examine the contributions of individual LRRC8A/B/C subunits to vascular function and underlying signaling pathways. The contributions of LRRC8C to blood pressure control in vivo were further assessed using the angiotensin-induced hypertension model in Lrrc8c knockout mice.

Results: Although all LRRC8A-E subunits are expressed in endothelium, co-immunoprecipitation revealed enrichment of LRRC8A/B/C, suggesting the existence of an endothelial LRRC8A/B/C heteromer. Lrrc8a/b/c depletion studies showed codependent expression of LRRC8A/B/C, but not LRRC8D. Only LRRC8A and LRRC8C deficiency impaired AKT and endothelial NO synthase phosphorylation, increased myogenic tone (2.2- and 1.9-fold increase, respectively), and reduced endothelial NO synthase-dependent vasodilation (45% and 61% reduction, respectively). Global Lrrc8c knockout mice phenocopied Lrrc8a knockouts and exhibited exacerbated angiotensin-induced hypertension, as evidenced by 15% increase in mean arterial pressure.

Conclusions: LRRC8A/B/C form the endothelial LRRC8 heteromeric complex. LRRC8C is nonredundant in supporting endothelial AKT-endothelial NO synthase signaling, vascular relaxation, and resistance to hypertension.

Background: This study aims to develop a prediction model to identify individuals at risk of hypertensive disorders of pregnancy (HDPs), including gestational hypertension and preeclampsia, by integrating epigenetic biomarkers and clinical factors in the first trimester of pregnancy.

Methods: A 2-stage nested case-control study, matched by age and body mass index, was conducted with 618 pregnant women in China, with peripheral blood samples collected in the first trimester to evaluate the average methylation levels of differentially methylated regions (DMRs) between controls and HDP cases. In stage 1 (discovery set), 24 controls and 27 cases were used to identify the differential DMRs. In stage 2, 294 controls and 273 cases were used to validate the previously identified DMRs. DMRs selected from the intersectional results of lasso regression, XGBoost, random forest, and Shapley Additive Explanations models were further combined with women's clinical risk factors to construct prediction models using logistic regression.

Results: In stage 1, 52 differential DMRs were identified with a false-positive rate <0.05. In stage 2, 12 differential DMRs were consistently observed, and 3 DMRs located in the CTSA, HMGB1, and miR1908/FADS2 genes were selected to construct a prediction model for HDPs. After combining the selected DMRs with clinical factors, the model achieved an area under the curve of 0.863 (95% CI, 0.826-0.901) in the training set and 0.757 (95% CI, 0.686-0.828) in the test set.

Conclusion: Findings of this study offer potential opportunities to identify high-risk patients with HDP in early pregnancy through DMRs identified in peripheral blood and provide new insights into the epigenetic cause of HDP.

Background: HIV infection is associated with cardiovascular events in adults. We compared mean blood pressure (BP) obtained at study visits between youth with/without perinatally acquired HIV infection and evaluated whether HIV disease severity was associated with BP.

Methods: BP was compared between participants with/without HIV in the Adolescent Master Protocol of the Pediatric HIV/AIDS Cohort Study. Marginal repeated measures analyses using generalized estimating equations evaluated the association of HIV disease severity with BP index (mean BP/95th percentile BP) and abnormal BP.

Results: 447 youth with HIV and 226 youth without HIV were included. Youth with HIV were more often Black non-Hispanic (66% versus 54%), had greater household income (54% versus 35%), and lower measures of adiposity than those without. Systolic BP was similar between groups, but mean diastolic BP was lower for preadolescents (63.3 mm Hg [95% CI, 59.0-67.0] versus 65.0 [61.5-68.7]) with HIV. Although youth with HIV had lower diastolic BP index (-0.011 [95% CI, -0.021 to -0.001]) and lower prevalence of abnormal BP (odds ratio, 0.78 [95% CI, 0.62-0.97]) at study visits in initial adjusted models, these associations were attenuated after adjustment for body mass index (-0.007 [95% CI, -0.017 to 0.003], odds ratio, 0.94 [95% CI, 0.76, 1.17], respectively). HIV disease severity was not associated with systolic or diastolic BP.

Conclusions: Youth with HIV had lower adiposity and BP than youth without HIV during study visits. Although youth with HIV had a lower risk of abnormal BP, this association did not persist after adjustment for adiposity. Prevention and treatment of other traditional cardiovascular disease risk factors remain important among youth living with HIV.

Background: The mGlide RCT (randomized controlled trial) evaluated whether a pharmacist-led, mobile health technology facilitated care model improves hypertension control in diverse populations.

Methods: We recruited adult English, Spanish, or Hmong-speaking patients with uncontrolled hypertension from a large health care system and smaller community clinics serving low-income patients. Participants were randomized 1:1 to mGlide or usual care. The 6-month intervention included daily blood pressure (BP) self-monitoring using a smartphone and wireless monitor, automated app-based data sharing, and responsive medication adjustment by a pharmacist-led provider-team. Comparison participants received a digital monitor. Outcomes included mean 6-month systolic BP (SBP), 12-month sustained BP control, 24-hour ambulatory BP and patient activation.

Results: A total of 395 participants (mean age, 66.9 years; 46.6% women; mean [SD] SBP, 143.4 [16.5] mm Hg) were randomized to mGlide (n=198) or usual care (n=197). Mean (SD) 6-month SBP (mm Hg) was lower in the mGlide arm (128.1 [13.9] versus 134.0 [16.0]). The adjusted mean difference between groups for the primary outcome of 6-month SBP favored mGlide: -5.8 mm Hg (95% CI, -8.6 to -3.0), sustained at 12 months (-5.7 mm Hg [-8.7 to -2.6]). The mGlide arm also had a 4.8 mm Hg (P=0.014) lower 24-hour average ambulatory SBP. The 6-month intervention effect varied significantly by activation level, with a difference of -12.6 mm Hg (-20.5 to -4.8) SBP among the lowest versus -2.5 mm Hg (-6.5 to 1.6) among the highest activation level participants.

Conclusions: A mobile health-facilitated care model with pharmacist-led medication adjustment was effective in lowering BP in diverse populations. Patients with low activation benefited more from the intervention; activation levels may inform efficient intervention selection.

Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT03612271.