Hypertension最新文献

{"title":"Explaining Variance in Pulse Wave Velocity in Youth: The Youth Vascular Consortium.","authors":"Vimarsha Kodithuwakku, Monique Breslin, Yanina Zocalo, Daniel Bia, Peter M Nilsson, Giacomo Pucci, Gaetano Vaudo, Marco D'abbondanza, Francesca Battista, Andrea Kelly, Manish Sinha, Piotr Skrzypczyk, Michał Szyszka, Christopher J A Pugh, Barry J McDonnell, Vikas Dharnidharka, Nazia Kulsum-Mecci, Iván Cavero-Redondo, Celia Alvarez-Bueno, Pierre Boutouyrie, Rosa-Maria Bruno, Elaine M Urbina, Seana Gall, Rachel E Climie","doi":"10.1161/HYPERTENSIONAHA.126.26866","DOIUrl":"10.1161/HYPERTENSIONAHA.126.26866","url":null,"abstract":"<p><strong>Background: </strong>Cardiovascular disease is a leading cause of global mortality. Carotid-femoral pulse wave velocity (cfPWV) is the gold-standard noninvasive measure of arterial stiffness and is commonly used to assess early vascular aging, as it predicts future cardiovascular events. Although the influence of cardiovascular risk factors on cfPWV is well studied in adults, evidence in youth is limited. This study aimed to identify common cardiovascular risk factors that best explain variation in cfPWV among young people.</p><p><strong>Methods: </strong>This study included 6763 participants aged 5 to 40 years with cfPWV measured using the SphygmoCor device, drawn from the Youth Vascular Consortium. Analyses were conducted across 5 subsets based on data completeness. Multiple linear regression models, stratified by sex and age (≤19 and >19 years), were developed to identify cardiovascular risk factors explaining cfPWV variation. Model selection was guided by Akaike information criterion and adjusted R².</p><p><strong>Results: </strong>Age and systolic blood pressure were consistent predictors, explaining <40% of cfPWV variance in cfPWV. Heart rate and waist circumference also emerged as key predictors of cfPWV, although lipids contributed modestly only in young adults. Waist circumference was the strongest anthropometric predictor in most groups.</p><p><strong>Conclusions: </strong>Age, systolic blood pressure, and heart rate were the strong contributors among traditional risk factors, yet explained <40% of variance in cfPWV in most groups. These findings highlight the role of hemodynamic load in shaping arterial stiffness even in childhood and adolescence, when structural changes are evolving. A large proportion of variance remains unexplained, suggesting that genetic, prenatal, environmental, and behavioral factors warrant investigation.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"e26866"},"PeriodicalIF":9.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148808425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association Between Follow-Up Mean Blood Pressure and Blood Pressure Control: A Meta-Regression Analysis of 101 Randomized Trials.","authors":"Abdul Salam, Rupasvi Dhurjati, Rashmi Pant, Sasi Kumar Tiruttani, Gautam Satheesh, Krishna Nandakumar, Shwetha Rajaram, Anshika Mittal, Faraidoon Haghdoost, Sonali R Gnanenthiran, Kota Vidyasagar, Esam Hariprasad, Prachi Kaistha, Raju Kanukula, Paul K Whelton, Mark D Huffman, Neil R Poulter, Anthony Rodgers","doi":"10.1161/HYPERTENSIONAHA.125.26580","DOIUrl":"10.1161/HYPERTENSIONAHA.125.26580","url":null,"abstract":"<p><strong>Background: </strong>The relationship between mean blood pressure (BP) and BP control remains uncertain, particularly the mean BP required to achieve BP control (<140/90 mm Hg) in most patients. This review assesses the association between mean BP and BP control using data from randomized clinical trials (RCTs).</p><p><strong>Methods: </strong>Electronic literature databases were searched to identify individual RCTs (iRCTs) and cluster RCTs (cRCTs) that randomized adults to BP-lowering interventions and reported both mean BP at the final follow-up visit (mean BP) and the proportion of participants achieving BP control at the final follow-up visit (BP control).</p><p><strong>Results: </strong>A linear regression model was used to evaluate the association between mean BP and BP control. A total of 101 RCTs (65 iRCTs [57 201 participants] and 36 cRCTs [28 154 participants]) were included. Overall, mean systolic BP (SBP) of 120, 125, 130, and 135 mm Hg corresponded to BP control in 85%, 75%, 65% and 55% of the participants in iRCTs and 91%, 80%, 68%, 56% in cRCTs. Each 1 mm Hg reduction in mean SBP was associated with approximately a 2% increase in BP control (Pseudo-<i>R</i>²=78% for iRCTs; 76% for cRCTs). This association was consistent across BP-lowering drug classes, baseline SBP categories, and pretrial treatment status in iRCTs, and across country income levels and baseline SBP categories in cRCTs. A similar association was seen for DBP.</p><p><strong>Conclusions: </strong>An SBP below 125 mm Hg was associated with achieving BP control in ≈80% of patients. These findings can inform guideline recommendations, guide clinical management and shape hypertension control programs.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"e26580"},"PeriodicalIF":9.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148766459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipid Infusion Enhances Sympathetic Transduction via Redox-Sensitive Pathways.","authors":"Colten G Miller, Jack C Kovarik, Megan E Gangwish, Davina A Clonch, Leonidas E Bantis, John P Thyfault, John M Miles, Seth W Holwerda","doi":"10.1161/HYPERTENSIONAHA.126.27191","DOIUrl":"10.1161/HYPERTENSIONAHA.126.27191","url":null,"abstract":"<p><strong>Background: </strong>Elevated circulating lipids increase oxidative stress and impair vascular function, but their effects on sympathetic-vascular control in humans are not well understood. We tested the hypothesis that intravenous lipid infusion enhances sympathetic-vascular transduction and beat-to-beat arterial pressure variability in humans, and that these effects are mediated, in part, by oxidative stress.</p><p><strong>Methods: </strong>In a randomized, double-blind, placebo-controlled crossover study, healthy adults underwent 2 hours of intravenous lipid infusion (20% Intralipid) with coinfusion of ascorbic acid or saline control. Endothelial function was assessed by brachial artery flow-mediated dilation, and muscle sympathetic nerve activity (MSNA) was recorded using microneurography. Sympathetic-vascular transduction was quantified by signal-averaging beat-to-beat mean arterial pressure (MAP) and brachial vascular conductance responses after spontaneous MSNA bursts.</p><p><strong>Results: </strong>Plasma malondialdehyde increased during lipid+saline (peak: 48±12 versus BL: 42±11 ng/mL; <i>P</i><0.01) and decreased with lipid+ascorbic acid (nadir: 34±12 versus baseline: 45±14 ng/mL; <i>P</i><0.01). Lipid+saline reduced flow-mediated dilation (4.1±2.7 versus baseline: 6.8±3.2%; <i>P</i><0.01), increased beat-to-beat MAP variability (1.7±0.5 versus baseline: 1.5±0.4 mm Hg; <i>P</i>=0.01), and augmented responses to large MSNA bursts for MAP (4.7±2.0 versus baseline: 3.4±1.4%; <i>P</i>=0.03) and vascular conductance (-9.3±3.4 versus BL: -6.7±3.7%; <i>P</i>=0.01). Despite lipid-mediated increases in MSNA burst amplitude, coinfusion of ascorbic acid was not associated with an increase in beat-to-beat MAP variability (1.6±0.4 versus baseline: 1.5±0.4 mm Hg; <i>P</i>=0.23) and MAP (4.4±0.9 versus baseline: 4.1±0.8%; <i>P</i>=0.37) and vascular conductance (-6.8±4.6 versus baseline: -9.4±5.5%; <i>P</i><0.01) responses to large MSNA bursts, although reductions in flow-mediated dilation were observed (5.0±3.0 versus baseline: 8.1±3.8%; <i>P</i><0.01).</p><p><strong>Conclusions: </strong>Lipid infusion enhances sympathetic-vascular transduction and arterial pressure variability, consistent with a redox-sensitive mechanism, while impairing endothelial function via pathways that ascorbic acid does not fully reverse.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier: NCT04832009.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"e27191"},"PeriodicalIF":9.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13492495/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148792384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Isolated Diastolic Hypertension and Cardiovascular Disease Risk in Young Adults.","authors":"Rui Tang, Jaejin An, Andrew E Moran, Daichi Shimbo, Norrina B Allen, Vanessa Xanthakis, Kristi Reynolds, Yiyi Zhang","doi":"10.1161/HYPERTENSIONAHA.126.27333","DOIUrl":"10.1161/HYPERTENSIONAHA.126.27333","url":null,"abstract":"<p><strong>Background: </strong>Whether isolated diastolic hypertension (IDH) in young adults represents a benign, age-specific phenotype or confers increased cardiovascular disease risk remains uncertain. We assessed the associations between hypertension subtypes, IDH, isolated systolic hypertension, and systolic-diastolic hypertension, with atherosclerotic cardiovascular disease and heart failure. We also characterized longitudinal transitions in hypertension subtypes from young adulthood into later life.</p><p><strong>Methods: </strong>Adults aged ≥18 years without cardiovascular disease were included from 4 US cohorts. Hypertension subtypes were defined using blood pressure thresholds of ≥130/80 mm Hg. Cox proportional hazards models were used to estimate the associations of hypertension subtypes with atherosclerotic cardiovascular disease and heart failure.</p><p><strong>Results: </strong>Among 23 957 participants (mean age, 44.5 years, 42.5% were young adults aged 18-39 years, 45.1% were male), 2320 atherosclerotic cardiovascular disease and 1243 heart failure events occurred over a median follow-up of 17.2 years. Among young adults, the adjusted hazard ratios (95% CI) for atherosclerotic cardiovascular disease were 1.36 (95% CI, 1.11-1.68) for IDH, 1.54 (95% CI, 1.02-2.32) for isolated systolic hypertension, and 1.84 (95% CI, 1.46-2.32) for systolic-diastolic hypertension, compared with normotension. Corresponding hazard ratios for heart failure were 1.69 (95% CI, 1.24-2.31) for IDH, 1.92 (95% CI, 1.09-3.40) for isolated systolic hypertension, and 1.69 (95% CI, 1.17-2.43) for systolic-diastolic hypertension. Associations were consistent among adults aged ≥40 years. Among young adults with IDH, 29.8% remained with IDH, whereas 36.5% progressed to systolic-diastolic hypertension later in life.</p><p><strong>Conclusions: </strong>IDH in young adulthood represents an early marker of increased cardiovascular disease risk and a precursor to more adverse hypertension subtypes. These findings underscore the importance of early recognition, ongoing blood pressure monitoring, and guideline-concordant pharmacological treatment, when indicated, among young adults with IDH to reduce long-term cardiovascular disease risk.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"e27333"},"PeriodicalIF":9.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13483358/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148759171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"2024 Donald Seldin Lecture: New Insights Into Soluble (Pro)Renin Receptor in Hypertension and Kidney Disease.","authors":"Tianxin Yang","doi":"10.1161/HYPERTENSIONAHA.126.25708","DOIUrl":"10.1161/HYPERTENSIONAHA.126.25708","url":null,"abstract":"<p><p>Also known as ATP6AP2, the PRR ([pro]renin receptor) was originally cloned over 2 decades ago as a component of the renin-angiotensin system due to its property of nonproteolytic activation of prorenin. After heated debates, this concept has been confirmed and expanded with advances in sPRR (soluble PRR) research. sPRR is a 28-kDa protein that is derived from the extracellular domain of PRR and is primarily released by site-1 protease. Circulating sPRR is elevated in patients with multiple diseases, including diabetes, hypertension, preeclampsia, and kidney disease. A decade ago, sPRR was found to have an antidiuretic function that occurs through the modulation of vasopressin signaling in the collecting duct. This finding signified the beginning of a new chapter in understanding the biological function of sPRR in multiple organ systems, particularly the kidney, and blood pressure regulation. In the past few years, numerous groundbreaking discoveries in this field have shed new light on the complex biology of sPRR, including its heterogeneity due to proteolysis and the multifaceted interaction between sPRR and the intrarenal renin-angiotensin system. The goal of this review is to summarize new advances in this emerging field of sPRR research.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"e25708"},"PeriodicalIF":9.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148764841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selective Cell Death of Adrenocortical Cells by Pharmacological Activation of Mutant KCNJ5.","authors":"Sanas Mir-Bashiri, Stefan Rakete, Jia Wei, Mirko Peitzsch, Stefanie Hahner, Martin Reincke, Tracy Ann Williams","doi":"10.1161/HYPERTENSIONAHA.126.27181","DOIUrl":"10.1161/HYPERTENSIONAHA.126.27181","url":null,"abstract":"<p><strong>Background: </strong>Primary aldosteronism is frequently caused by mutations in the <i>KCNJ5</i> (potassium inwardly rectifying channel subfamily J member 5) gene, encoding a G-protein inwardly rectifying potassium channel. These mutations disrupt the channel's selectivity filter, permitting abnormal sodium influx. We aimed to identify compounds that selectively activate mutant KCNJ5 channels. By further increasing sodium conductance, such compounds could induce lethal sodium influx in mutant adrenal cells, providing a targeted therapeutic strategy for primary aldosteronism caused by <i>KCNJ5</i> mutations.</p><p><strong>Methods: </strong>Six small molecules identified in our prior work as potential KCNJ5 agonists were evaluated. Their effects on cell viability, sodium influx, membrane potential, and steroidogenesis were assessed in 2-dimensional and 3-dimensional human adrenocortical cells, clone 15.</p><p><strong>Results: </strong>Candidate agonists were tested for their ability to enhance adrenal cell death induced by overexpression of mutant KCNJ5. Compound 105 (C105; 2'-amino-6-chloro-1'-[2,4-difluorophenyl]-7-methyl-2,5'-dioxo-1,2,5',6',7',8'-hexahydro-1'H-spiro[indole-3,4'-quinoline]-3'-carbonitrile) increased mutant KCNJ5-induced cell death by 40% without affecting cells expressing wild-type KCNJ5. The toxic effect of C105 was abolished under low-sodium conditions. Inductively coupled plasma tandem mass spectrometry demonstrated a 25% increase in intracellular sodium after C105 treatment without significantly affecting potassium concentrations. Molecular docking indicated binding of C105 to the G-protein-binding site of KCNJ5, a key region involved in channel activation. These findings suggest that C105 promotes adrenal cell death through activation of mutant KCNJ5 and increased sodium conductance.</p><p><strong>Conclusions: </strong>C105 acts as a first-in-class mutant KCNJ5 agonist candidate and may enable pharmacological ablation of mutant cells in a subset of aldosterone-producing adenomas and familial hyperaldosteronism type III. These findings provide proof of concept for mutation-selective targeting of KCNJ5-driven primary aldosteronism.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":"e27181"},"PeriodicalIF":9.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148759525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"American Heart Association's Strategic Approach to Promoting Blood Pressure Control: A Science Advisory From the American Heart Association.","authors":"Yvonne Commodore-Mensah, Brandon K Bellows, Alison P Smith, Joseph T Flynn, Alyssa D Pressley, Sally Honeycutt, Eduardo Sanchez, Marwah Abdalla, Shawna Nesbitt","doi":"10.1161/HYP.0000000000000266","DOIUrl":"https://doi.org/10.1161/HYP.0000000000000266","url":null,"abstract":"<p><p>Hypertension, which affects ≈122.4 million American adults and contributes substantially to preventable deaths and economic burden, represents a major public health challenge. Despite the availability of effective therapeutic interventions, only 20.7% of individuals diagnosed with hypertension achieve optimal blood pressure control, defined as readings <130/80 mm Hg. Disparities persist across racial, ethnic, socioeconomic, and geographic groups, prompting urgent calls to improve hypertension management strategies. In response to these challenges, the American Heart Association has established equitable blood pressure control as a cornerstone priority and adopted a comprehensive socioecologic framework to address barriers to care. This science advisory presents the American Heart Association Blood Pressure Control Logic Model, a visual framework that maps how program resources and activities can lead to desired outcomes and effects through collaborative multisector strategies across health care and community settings. The model delineates how organizational inputs-including staff expertise, data systems, funding resources, and strategic partnerships-are channeled through 4 fundamental intervention strategies to achieve measurable outcomes and population-level effects. These strategies encompass transforming health care environments through research initiatives and policy reform, delivering culturally appropriate educational programs, implementing improvements in clinical care quality, and actively engaging community organizations and workplace environments in health promotion activities. The simultaneous implementation of these strategies aims to achieve equitable health outcomes with reduced risk of cardiovascular events, advancing the American Heart Association's mission to promote longer, healthier lives. This adaptable model provides a framework that can be implemented by other organizations. This science advisory emphasizes the importance of rigorous evaluation and sustained multisector collaboration to effectively manage hypertension and promote cardiovascular health.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":""},"PeriodicalIF":9.8,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149074524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Blood Pressure Tunes the Functional Coupling of Cerebrovascular Ca_V1.2 Channels.","authors":"Galina Yu Mironova, Miguel Martín-Aragón Baudel, Chryso Lambride, Sanjay R Kharche, David A Steven, Jonathan Lau, Keith W MacDougall, Melfort Boulton, Franca Schmid, Manuel F Navedo, Donald G Welsh","doi":"10.1161/HYPERTENSIONAHA.126.27574","DOIUrl":"https://doi.org/10.1161/HYPERTENSIONAHA.126.27574","url":null,"abstract":"<p><strong>Background: </strong>The myogenic response is the key autoregulatory mechanism that sets cerebral blood flow, and its mechanistic foundation is intimately tied to depolarization and the voltage gating of L-type Ca²⁺ channels (Ca_V1.2). Although critical, this study argues for an additional mechanism. We hypothesize that increased intravascular pressure enhances Ca_V1.2 channel activity by promoting functional coupling and perimembrane trafficking, thereby increasing pressure-induced myogenic constriction.</p><p><strong>Methods: </strong>These novel insights were pursued at the cell level using patch-clamp electrophysiology and advanced microscopy, and then functionally in pressurized arteries through measures of tone and intracellular [Ca²⁺]_i.</p><p><strong>Results: </strong>Cellular and vessel-level studies identified functional coupling of Ca_V1.2 channels as the mechanism that aligns Ca²⁺ influx with wall stress to maintain arterial tone. A mouse model with disrupted coupling showed a loss of myogenic responsiveness within the autoregulatory range, despite intact voltage control, indicating a selective defect in pressure sensing. This mechanism was supported by Ca_V1.2 cluster dynamics and biophysical analyses; key findings were validated in human cerebral arteries. From cerebral blood flow simulations of semirealistic microvascular networks, we predict that loss of this alternative mechanism leads to maldistribution of brain blood flow and potentially a diminishment of cognitive function.</p><p><strong>Conclusions: </strong>These findings identify pressure-induced functional coupling and perimembrane trafficking of Ca_V1.2 channels as a previously unrecognized mechanism that links intravascular pressure to Ca²⁺ influx and myogenic tone in cerebral arteries. This mechanism is conserved in human vessels and viewed as essential for maintaining cerebral blood flow distribution.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":""},"PeriodicalIF":9.8,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149074547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Safety, Acceptability and Efficacy of Noninvasive Transcutaneous-Autonomic Neuromodulation in Uncontrolled Hypertension.","authors":"Ajay Gupta, David Collier, James Steckelmacher, Jane Field, George Collett, Olivier Zongo, Mital Patel, Manish Saxena, Annastazia Learoyd, Amrita Ahluwalia, Peter Sever","doi":"10.1161/HYPERTENSIONAHA.126.27847","DOIUrl":"https://doi.org/10.1161/HYPERTENSIONAHA.126.27847","url":null,"abstract":"<p><strong>Background: </strong>Despite antihypertensive medications, ≈40% of patients with hypertension fail to achieve recommended blood pressure (BP) targets. Alternative device-based strategies are often expensive or invasive. We evaluated the safety, acceptability, and potential efficacy of a noninvasive transcutaneous autonomic neuromodulation (tAN) device.</p><p><strong>Methods: </strong>SCRATCH-HTN (Sham Controlled Randomized Trial Evaluating the Safety, Acceptability and Efficacy of Autonomic Neuromodulation using Transcutaneous Vagal Sensory Stimulation in Uncontrolled Hypertensive Patients) was a double-blind, sham-controlled, phase 2a trial enrolling patients with uncontrolled hypertension (mean daytime systolic BP [SBP] ≥135 mm Hg and diastolic BP ≥85 mm Hg) on 1 or more medications. Participants self-administered active tAN or sham treatment for 30 minutes daily for 14 days, then 10 weekly sessions. Primary end points were safety and acceptability. The primary efficacy end point was change in daytime ambulatory SBP from baseline to 3 months. Secondary end points included BP, heart rate, and quality of life at 1 and 3 months.</p><p><strong>Results: </strong>Sixty-three patients (mean age 47.2 years, 71.4% male, mean daytime BP 150/95 mm Hg) were randomized 2:1 to tAN or sham. tAN did not differ significantly from sham in daytime ambulatory SBP at 3 months (between-group difference, 2.35 mm Hg [95% CI, -4.37 to 9.07]; <i>P</i>=0.49) or 1 month (-1.01 mm Hg [-6.87 to 4.85]; <i>P</i>=0.73). Pre-specified adjusted analysis identified a significant interaction between treatment and baseline SBP (<i>P</i> interaction 0.003): participants with baseline SBP >160 mm Hg showed a greater response to tAN. No significant differences were observed for other secondary end points. tAN was safe and acceptable.</p><p><strong>Conclusions: </strong>tAN is safe and well-tolerated in patients with hypertension. No significant BP-lowering effect was demonstrated, although a potential benefit in subgroups or a modest effect in a larger cohort cannot be excluded and warrants evaluation.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier: NCT05179343. URL: XXX; Unique identifier: 14509154.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":""},"PeriodicalIF":9.8,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149069583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypertensive Disorders of Pregnancy and Cardiovascular-Kidney-Metabolic Syndrome.","authors":"Daniel Ezzat, Maria A Pabon, Linke Li, Annie Chang, Nore De Moor, Zhi Yu, So Mi Jemma Cho, Pradeep Natarajan, Cassandra N Spracklen, Erin S LeBlanc, Charles B Eaton, Michael J LaMonte, Marcia L Stefanick, JoAnn E Manson, Nisha Parikh, Alexander P Reiner, Jason D Roh, Diana C Soria-Contreras, Rosangela Akemi Hoshi, Samia Mora, Olga V Demler, Camille E Powe, Michael C Honigberg","doi":"10.1161/HYPERTENSIONAHA.126.27750","DOIUrl":"10.1161/HYPERTENSIONAHA.126.27750","url":null,"abstract":"<p><strong>Background: </strong>Hypertensive disorders of pregnancy (HDP) affect over 10% of pregnancies worldwide, but their association with cardiovascular-kidney-metabolic (CKM) syndrome remains unexplored.</p><p><strong>Methods: </strong>The present study included parous UK Biobank participants. The primary exposure was HDP history. CKM syndrome was categorized from stage 0 (no risk factors) to 4 (cardiovascular disease). Logistic regression tested the association of HDP history with CKM stage, adjusted for age, age², race, Townsend Deprivation Index, and smoking status. Cox models evaluated progression to stage 4, in addition, adjusting for baseline CKM stage. Replication analyses were performed in the Women Health Initiative, with CKM stage assessed at 2 study visits.</p><p><strong>Results: </strong>Among 219 639 UK Biobank (mean age, 56.9 years) and 3591 Women Health Initiative participants (61.7 years at baseline, 78.1 years at the follow-up visit), 2836 (1.3%) and 304 (8.4%), respectively, had a history of HDP. In the UK Biobank, HDP history was significantly associated with higher CKM stage (adjusted odds ratio, 3.40 [95% CI, 3.12-3.71]; <i>P</i><0.001) in ordinal logistic regression. Compared with CKM stage 0, HDP history was associated with higher odds of stages 2 to 4 (adjusted odds ratios, 6.34, 11.20, and 7.43, respectively; all <i>P</i><0.001). Over a median follow-up of 13.6 years, prior HDP was associated with progression to stage 4 (adjusted hazard ratio, 1.24 [95% CI, 1.10-1.40]; <i>P</i><0.001). Replication in the Women Health Initiative produced consistent results.</p><p><strong>Conclusions: </strong>HDP history was associated with greater CKM stage and progression to advanced CKM syndrome, supporting its use as an early life predictor of adverse CKM trajectories.</p>","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":" ","pages":""},"PeriodicalIF":9.8,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13595891/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149012185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}