Hypertension最新文献

Background: Postprandial hypotension (PPH) may contribute to falls among older adults, particularly those taking antihypertensive medication. However, evidence on this association in community-dwelling populations is limited. Since ambulatory blood pressure (BP) monitoring captures BP during daily activities, it may provide accurate assessments of PPH outside the clinic setting.

Methods: This prospective cohort study examined the association between PPH and fall risk among community-dwelling adults aged ≥65 years taking antihypertensive medication. At baseline, participants underwent 24-hour ambulatory BP monitoring; subsequently, they completed monthly fall calendars during a 12-month follow-up. PPH by systolic BP (SBP; systolic PPH) was defined as a postprandial SBP decline, mean SBP during the hour before the meal minus the minimum SBP during the 2 hours after the meal, following any meal of ≥20 mm Hg, or a decrease to SBP ≤90 mm Hg when preprandial SBP was ≥100 mm Hg.

Results: Among 626 participants (mean±SD age, 74.6±6.2 years; 56.1% women), 442 (70.6%) experienced systolic PPH. The mean±SD number of meals was 2.6±0.8 during the ambulatory BP monitoring period. During the 12-month follow-up, falls occurred in 169 of 442 (38.2%) participants with systolic PPH and 70 of 184 (38.0%) participants without systolic PPH. Systolic PPH was not associated with fall risk (adjusted hazard ratio, 0.93 [95% CI, 0.69-1.26]). A restricted cubic spline analysis demonstrated no evidence of an association between the largest postprandial SBP decline across all meals and fall risk.

Conclusions: In this cohort study, PPH identified by ambulatory BP monitoring was common but not associated with risk of falls.

Background: Home blood pressure (BP) monitoring (HBPM) is increasingly used as an alternative to office BP. However, factors influencing agreement between office and home BP among very old adults remain unclear.

Methods: During ARIC (Atherosclerosis Risk in Communities) visit 10, participants underwent 3 automated office BP (AOBP) measurements using an Omron HEM-907XL and performed HBPM twice daily for 8 days using an Omron BP7450. Discordance was defined as a systolic BP difference of ±10 mm Hg between mean AOBP and HBPM. Multivariable regression models evaluated demographic, anthropometric, and clinical factors associated with discordance.

Results: Among 792 participants (58% female; mean age, 84±3.7 years), mean systolic BP was 130.6 mm Hg (AOBP) and 129.6 mm Hg (HBPM). Despite a minimal average difference (1.0±15.7 mm Hg), 49% had ≥10 mm Hg systolic BP discordance. Higher AOBP was associated with greater discordance. Compared with females, males had lower AOBP relative to HBPM (-4.69 mm Hg [95% CI, -6.86 to -2.51]). Smaller arm circumference was associated with higher discordance (β=14.4 mm Hg [95% CI, 4.78-24.04]). Frail adults had lower AOBP relative to HBPM (β, -5.1 mm Hg [95% CI, -11.0 to 0.9]). Baseline AOBP systolic BP ≥140 mm Hg strongly predicted discordance ≥+10 mm Hg (odds ratio, 8.27 [95% CI, 5.52-12.40]). Participants aged 91 to 100 years had lower AOBP than those aged 78 to 80 years (β, -5.0 mm Hg [95% CI, -10.06 to 0.001]).

Conclusions: Among very old adults, substantial BP discordance between AOBP and HBPM was common and influenced by higher BP, age, male sex, arm circumference, and frailty.

Background: Ambulatory blood pressure monitoring is indispensable for diagnosing nocturnal hypertension (NH) among patients with chronic kidney disease, but it is costly and time-consuming. Screening tools for predicting high-risk NH are urgently needed.

Methods: A large cohort of 5769 patients with nondialysis chronic kidney disease were enrolled (hospital A: 4565; hospital B: 1204). Patients from hospital A were split 8:2 into training/internal test sets; hospital B served as the external test set. A total of 1006 patients with at least 2 valid ambulatory blood pressure monitoring recordings were used for secondary validation. We proposed a table-value diffusion model by incorporating generative modeling concepts to map distributions between clinical variables and predict NH. The predicted probabilities for NH were stratified and validated according to patients' true adverse renal/cardiovascular prognoses.

Results: Through a rigorous selection process combining univariate ranking and clinical expertise, we selected 7 core predictors: age, body mass index, clinic systolic/diastolic blood pressure, estimated glomerular filtration rate, hypertension history, and use of non-renin-angiotensin-aldosterone system antihypertensive agents. In the test sets, the 7-variable diffusion model achieved a significantly higher area under the curve than the 7-variable logistic model (internal: 0.870 versus 0.807, P<0.001; external: 0.854 versus 0.792, P<0.001). Secondary validation confirmed the 7-variable diffusion model's stability (area under the curve=0.869, Cohen kappa index=0.560). Risk stratification was established (high-risk >0.692, intermediate-risk 0.692-0.515, and low-risk <0.515). Patients in the high-risk group had a higher incidence of adverse renal/cardiovascular events than those in the low-risk group.

Conclusions: We developed a concise 7-variable diffusion model for NH using a table-value diffusion model, supporting targeted ambulatory blood pressure monitoring screening in patients with chronic kidney disease.

Background: Sympathetic overactivity is associated with hepatic steatosis. Renal denervation (RDN) is an approved treatment for uncontrolled hypertension through sympathetic modulation; however, its hepatic effects are unknown. This study aimed to assess the effects of RDN on noninvasive tests for hepatic steatosis.

Methods: This single-center study included patients with uncontrolled hypertension and cardiometabolic comorbidities undergoing RDN (n=32) or a sham procedure (n=10). Noninvasive tests for hepatic steatosis, including the hepatic steatosis index (HSI) and fatty liver index (FLI), were calculated at baseline and follow-up visits. An external cohort from the UK Biobank was used to validate the correlation between proton density fat fraction magnetic resonance imaging scans of the liver and these surrogates.

Results: Compared with the control group, RDN significantly reduced HSI at 3 months (0.4±0.5 versus -1.3±0.3; P=0.009), 6 months (0.0±0.9 versus -2.6±0.5; P=0.027), and 12 months (0.0±0.6 versus -2.1±0.5; P=0.013), as well as FLI at 3 months (2.6±2.2 versus -3.8±1.2; P=0.021), 6 months (4.1±2.4 versus -5.7±1.2; P=0.002), and 12 months (2.0±2.7 versus -6.2±1.3; P=0.018). No significant differences were found in HSI (-1.9±0.7 versus -2.2±0.7; P=0.77) and FLI (-7.1±1.8 versus -5.3±1.7; P=0.49) between subjects in the intervention group whose office blood pressure decreased above or below the median of 19.5 mm Hg after 12 months. In the UK Biobank, correlation analysis showed a significant relationship between proton density fat fraction magnetic resonance imaging and HSI (r=0.40; P<0.0001) and FLI (r=0.27; P<0.0001).

Conclusions: RDN significantly reduced HSI and FLI in patients with uncontrolled hypertension and cardiometabolic comorbidities, suggesting a potential role of sympathetic modulation in metabolic disorders.

Background: The placenta is known to be critical in the etiology of preeclampsia. However, there is a subset of preeclampsia cases without identifiable placental pathology. We evaluated which clinical preeclampsia classification system best distinguishes preeclampsia with placental pathology from preeclampsia without placental pathology.

Methods: We evaluated 5 placental pathological features in 197 placentas from patients with preeclampsia grouped by 3 clinical preeclampsia subclasses: (1) preeclampsia with calculated infant birthweight <10th percentile for gestational age (small for gestational age [SGA] preeclampsia) versus preeclampsia with birthweight ≥10th percentile for gestational age (not SGA preeclampsia); (2) preeclampsia with delivery before 34 weeks of gestation (early delivery preeclampsia) versus preeclampsia with delivery at or after 34 weeks of gestation (late delivery preeclampsia); and (3) preeclampsia with severe features versus preeclampsia without severe features. Clinical, histological and molecular findings in patients with preeclampsia were compared with normotensive patients, with and without SGA infants (N=1078 total).

Results: The SGA versus not small for gestational age preeclampsia classification system performed best (likelihood ratios [95% CI] for ≥3 of 5 placental pathological findings: 15.7 [6.5-38.1] in SGA preeclampsia versus not small for gestational age preeclampsia; 6.8 [4.3-10.8] in early delivery preeclampsia versus late delivery preeclampsia; and 5.2 [1.95-14.1] in preeclampsia with severe features versus preeclampsia without severe features; all P<0.0001). SGA preeclampsia and SGA normotensive placentas were abnormal and shared alterations in hypoxia, TNFα (tumor necrosis factor alpha), glycolysis, unfolded protein response, estrogen response, ultraviolet response, p53, TGFβ (transforming growth factor beta), and mTORC1 (mammalian target of rapamycin complex 1) signaling pathways.

Conclusions: Classifying preeclampsia based on birthweight percentile for gestational age is the most useful system for consistently identifying preeclampsia associated with placental pathology.

Background: Proteomic signatures may enhance the prediction of cardiometabolic diseases for targeted prevention. We evaluated whether a proteomic risk score (ProtRS) improves the prediction of incident hypertension.

Methods: Within the UK Biobank Proteomics data set, participants at risk for incident hypertension were randomly split into derivation (n=25 158) and test (n=10 781) sets. A ProtRS was trained in the derivation cohort using least absolute shrinkage and selection operator penalized Cox regression and evaluated in the test set with sequential adjustment for demographics, clinical risk factors, and a polygenic risk score (PRS). External replication was performed in the Asklepios study (n=793).

Results: In UK Biobank Proteomics (2312 events), each 1-SD higher ProtRS was associated with incident hypertension after covariate adjustment (hazard ratio, 1.68 [95% CI, 1.59-1.78]; P<0.001). Adding the protein score to demographics, clinical variables, and PRS improved model fit (global χ² from 1733 to 2048, P<0.001), discrimination (C-index, 0.745-0.765), net reclassification improvement (19.0% [95% CI, 15.9-22.0]), and integrated discrimination improvement (2.9% [95% CI, 2.4-3.8]). In Asklepios (221 events), the ProtRS was associated with an increased risk of hypertension (hazard ratio, 1.32 [95% CI, 1.13-1.55]; P<0.001) after covariate adjustment, and improved global χ² (from 120.4 to 132.4; P<0.001), C-index (from 0.723 to 0.736) and discrimination (net reclassification improvement, 13.1% [95% CI, 1.2%-24.1%]). Pathway analysis highlighted neutrophil degranulation, insulin-like growth factor, PI3K signaling, and extracellular matrix remodeling.

Conclusions: A ProtRS improves prediction of incident hypertension beyond demographics, clinical, and genetic information in UK Biobank Proteomics, with supportive external replication. Proteomic information may enhance individualized hypertension risk stratification and provide biologic insights into disease development.

Background: Altered gut microbiota composition has been implicated in the development of hypertension. Evidence suggests bacterial products and metabolites can enter circulation, act on peripheral tissues, and modulate blood pressure (BP). We identified extracellular vesicles (EVs) of bacterial origin (bacterial extracellular vesicles [bEVs]) in the circulation of spontaneously hypertensive stroke-prone rats (SHRSP). We hypothesized that bEVs mediate communication between microbiota and the host, and that bEVs from SHRSP microbiota contain unique cargo that promotes hypertension.

Methods: EVs were isolated from plasma and cecal content of SHRSP and Wistar-Kyoto (WKY) rats. Multiomics analysis, including 16S rRNA sequencing, small RNA sequencing, lipidomics, and proteomics were performed to assess the cargo of bEVs. BEVs from WKY and SHRSP were transplanted by oral gavage to WKY and SHRSP recipients, and the effects on BP and sympathetic activity were monitored. The potential role of bEVs on BP was also evaluated in Dahl salt sensitive (S) and obstructive sleep apnea models of hypertension.

Results: Significant differences were observed in WKY and SHRSP bEV cargo, including small RNAs, proteins, and PAMPs (pathogen-associated molecular patterns). Transplantation of SHRSP bEVs to WKY rats increased renal sympathetic nerve activity and elevated BP. Moreover, we showed that bEVs influence BP regulation in Dahl S and obstructive sleep apnea-induced hypertension.

Conclusions: Our findings position bEVs as critical mediators of microbiota-host communication in BP regulation and demonstrate that bEVs from the altered SHRSP microbiota promote hypertension. Our findings shed new light on the role of bEVs in hypertension pathogenesis and offer new perspectives for diagnostics and therapeutic interventions.

Background: Endothelial dysfunction is a key feature of pulmonary arterial hypertension (PAH). Previously, we demonstrated decreased Wnt7a transcript levels, causing reduced angiogenesis in PAH. Wnt7a expression correlates with tip formation via ROR2 (receptor tyrosine kinase-like orphan receptor 2), a tyrosine kinase receptor. We hypothesized that ROR2 activation in pulmonary microvascular endothelial cells (PMVECs) promotes angiogenesis, particularly endothelial barrier establishment, and its loss causes PAH.

Methods: Endothelial-specific ROR2 knockout (ROR2 ECKO) and wild-type mice were studied under normoxia and chronic hypoxia using echocardiography, hemodynamics, and lung morphometry. PMVECs from healthy and PAH lungs were transfected with ROR2 siRNA/constructs for functional and molecular studies. Focal adhesion activation and force generation were assessed via Förster resonance energy transfer-based methods. Bulk and single-cell transcriptomic analyses were performed on siROR2 (ROR2 siRNA) PMVECs and ROR2 ECKO lungs.

Results: ROR2 ECKO mice exacerbated pulmonary hypertension and vascular remodeling in hypoxia. Single-cell RNA-sequencing of lung endothelial cells revealed dysregulated barrier formation and angiogenesis. Evans blue dye extravasation confirmed reduced endothelial barrier integrity in ROR2 ECKO mice. ROR2-deficient PAH PMVECs displayed increased adhesion, permeability, and focal adhesion numbers, with reduced VE-cadherin at cell junctions. Confocal imaging and foster resonance energy transfer revealed ROR2 localization in focal adhesions, interacting with ITGB1 (integrin β1) which remained in an active, adhesion-promoting state in ROR2-deficient cells. Restoring ROR2 in PAH PMVECs normalized adhesion, barrier function, and focal adhesion abundance. Transcriptomic analysis revealed Rab12 mediated ROR2-ITGB1 crosstalk, whose knockdown mimicked ROR2 deficiency in PMVECs.

Conclusions: ROR2 regulates pulmonary angiogenesis by maintaining endothelial barrier integrity and facilitating integrin recycling. ROR2 restoration could be a potential therapeutic approach for PAH.

Hypertension remains the most prevalent modifiable risk factor for cardiovascular morbidity and mortality worldwide, yet rates of effective blood pressure control remain persistently suboptimal despite the availability of multiple therapeutic options. This gap reflects fundamental limitations of current care models, which rely on episodic measurements, population-based treatment algorithms, and incomplete representation of the biological, behavioral, and social complexity underlying blood pressure regulation. Artificial intelligence (AI) offers a transformative framework to address these challenges by enabling the integration of longitudinal, multimodal data and modeling nonlinear, dynamic relationships that are difficult to capture with conventional approaches. This systematic review synthesizes emerging evidence on the application of AI across the hypertension care continuum, including risk prediction, phenotyping, blood pressure measurement, wearable-based monitoring, clinical trial analysis, population health modeling, detection of secondary hypertension, behavioral and adherence interventions, and multi-omics-driven precision medicine. We highlight the methodological foundations required for clinically meaningful AI, emphasizing robust ground-truth definitions, external and temporal validation, interpretability, workflow integration, and equity-aware design. The review also examines the promise and limitations of natural language processing, cuffless blood pressure technologies, and AI-guided decision support systems, alongside ethical, regulatory, and implementation challenges. Collectively, current evidence suggests that AI has the potential to shift hypertension management from a reactive, threshold-based paradigm toward a more predictive, personalized, and patient-centered model. Realizing this potential will depend on rigorous validation, thoughtful implementation, and sustained alignment with clinical, ethical, and equity principles.

Background: Bilateral macronodular adrenocortical disease is often linked to autonomous cortisol secretion, but may also present with primary aldosteronism (PA).

Methods: This international (Europe, United States, Asia) retrospective cohort study included adults with radiological evidence of bilateral macronodular adrenocortical disease and biochemically confirmed PA. The primary end points was major adverse cardiovascular events; secondary end points included cardiometabolic comorbidities and surgical outcomes per PA surgical outcome criteria.

Results: Two hundred forty-nine patients from 41 centers in 12 countries were included (median age, 55 years; 62% male). Median hypertension duration at PA diagnosis was 9.9 years. Among 178 tested, 52% had cortisol cosecretion and 47% isolated PA. At baseline, 56% had metabolic comorbidities, and 16% had ≥1 major adverse cardiovascular event. Patients with major adverse cardiovascular events were older, more often male, had longer hypertension duration, and higher diabetes rates. Eighty-nine patients underwent adrenalectomy: 50 without MRA (mineralocorticoid receptor antagonists), 38 with MRA, and 1 with steroidogenesis inhibitors. One hundred twenty-four patients received continued MRA without adrenalectomy or steroidogenesis inhibitors. Adrenal venous sampling showed lateralized PA in 89% of surgical versus 19% of MRA-treated patients (P<0.001). Over a median follow-up of 36 (MRA) and 18 months (surgery; P=0.2), major adverse cardiovascular events occurred in 8% and 6%, respectively (P=1.0). Blood pressure and organ damage were similar, but more MRA-treated patients needed ≥3 antihypertensives (MRA: 48% versus adrenalectomy: 14%; P<0.001). Among operated patients, complete clinical and biochemical success was 26% and 71%, respectively.

Conclusions: Bilateral macronodular adrenocortical disease with PA carries a high cardiometabolic burden. Early detection and precise subtyping are key to optimizing management and preventing target organ damage.