American Journal of Hypertension最新文献

{"title":"Sucrose induces Cardiac Hypertrophy and Renal Perivascular Fibrosis in a Novel Mouse Model of Hypertension.","authors":"Yuka Terada, Yuki Nakayama, Youjie Zhang, Busra Cetinkaya-Un, Katherine J Elliott, Tomoki Hashimoto, Adebowale Adebiyi, Patrick Osei-Owusu, Satoru Eguchi","doi":"10.1093/ajh/hpag122","DOIUrl":"https://doi.org/10.1093/ajh/hpag122","url":null,"abstract":"<p><strong>Background: </strong>Excess sugar consumption increases the risk for hypertension. We previously reported pilot data demonstrating that male mice drinking 2% sucrose water develop hypertension. However, the sucrose effects on left ventricular hypertrophy, kidney fibrosis, or sex difference in hypertension remain unclear. In the present study, we characterized the cardiac and renal pathology in a larger cohort including female mice to establish a novel sucrose-induced mouse model of hypertension associated with cardiovascular remodeling.</p><p><strong>Methods: </strong>Eight- to nine- week-old C57BL6 mice were given drinking water containing 2% sucrose or regular water for 4 weeks. Blood pressure was monitored using a tail-cuff system. Echocardiography was performed to evaluate cardiac remodeling. Sirius red staining was performed to evaluate heart and kidney fibrosis.</p><p><strong>Results: </strong>Male mice drinking the sucrose water developed hypertension (systolic blood pressure 122.0±1.3mmHGvs 162.2±4.3 mmHG at day 28). Sucrose treatment increased left ventricular wall thickness and induced perivascular fibrosis of the heart and kidney compared to control mice. Cardiac functions were preserved. In female mice, sucrose treatment induced milder hypertension than male mice (126.9±2.4 mmHg vs 143.7±3.2 mmHg at day 28). However, sucrose treatment caused similar degree of left ventricular hypertrophy in female mice.</p><p><strong>Conclusion: </strong>Sucrose water induced hypertension, cardiac hypertrophy, and fibrosis of the heart and kidney in male mice. Female mice were partially protected from hypertension but not from cardiac hypertrophy. This mouse model represents a useful tool to investigate molecular mechanisms by which hypertension and end organ damage develop with excess sugar consumption.</p>","PeriodicalId":7578,"journal":{"name":"American Journal of Hypertension","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149226939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amlodipine and Nifedipine Associations with B-Type Natriuretic Peptide in Women with Hypertension and Heart Failure with Preserved Ejection Fraction.","authors":"Eisaku Harada, Toshihiro Yamada, Yuji Mizuno, Yuichiro Arima, Makoto Muta, Koichi Kikuta, Hirofumi Yasue","doi":"10.1093/ajh/hpag123","DOIUrl":"https://doi.org/10.1093/ajh/hpag123","url":null,"abstract":"<p><strong>Background: </strong>Calcium channel blockers (CCBs) are frequently prescribed to manage hypertension in patients with heart failure with preserved ejection fraction (HFpEF). However, whether individual dihydropyridine agents exert uniform class effects on myocardial wall stress remains unclear.</p><p><strong>Methods: </strong>This retrospective, single-center observational study analyzed 465 consecutive patients with hypertension and HFpEF (354 women and 111 men) evaluated at Kumamoto Kinoh Hospital between May 2012 and July 2018. Multivariable linear regression models assessed associations between individual dihydropyridine CCBs (amlodipine vs. nifedipine) and plasma log-transformed B-type natriuretic peptide (lnBNP) levels.</p><p><strong>Results: </strong>In multiple imputation models among women, adjusted differences in lnBNP relative to no-CCB were 0.236 (95% CI, 0.031 to 0.441) for nifedipine and -0.118 (95% CI, -0.273 to 0.037) for amlodipine. Direct linear contrasts in women confirmed lower lnBNP levels with amlodipine than with nifedipine (adjusted difference, -0.355; 95% CI, -0.562 to - 0.147). In men, the corresponding amlodipine-versus-nifedipine difference was -0.051 (95% CI, -0.697 to 0.595; P=0.876). The formal sex-by-drug interaction contrast in complete-case analysis yielded an adjusted difference of - 0.424 (95% CI, -1.055 to 0.208; P = 0.188), with male precision constrained by sample size (7 male nifedipine users).</p><p><strong>Conclusion: </strong>In women with hypertension and heart failure with preserved ejection fraction, amlodipine use was associated with lower adjusted ln(BNP) levels than nifedipine use. These observational findings challenge the assumption of an interchangeable dihydropyridine class effect on myocardial wall stress, suggesting that individual pharmacological profiles-rather than uniform class-level equivalence-warrant attention in clinical evaluations.</p>","PeriodicalId":7578,"journal":{"name":"American Journal of Hypertension","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149219819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Telmisartan-Chlorthalidone Fixed-Dose Combination at Two Chlorthalidone Dose Levels versus Telmisartan in Uncontrolled Hypertension: A Phase III Trial.","authors":"Seung-Whan Lee, Jin-Man Cho, Soon Jun Hong, Seung Hwan Han, Gyu Chul Oh, Seong Hwan Kim, Jung-Hoon Sung, Sang-Rok Lee, Gyung-Min Park, Hyun-Jae Kang, Jun-Hee Lee, Ji-Yong Choi, Kyung Hee Lim, Cheol Ung Choi, Byeong-Keuk Kim, Sang-Hyun Kim, In-Ho Chae","doi":"10.1093/ajh/hpag081","DOIUrl":"https://doi.org/10.1093/ajh/hpag081","url":null,"abstract":"<p><strong>Background: </strong>Evidence comparing different diuretic doses within fixed-dose combinations (FDCs) remains limited. We evaluated telmisartan/chlorthalidone FDCs according to chlorthalidone dose in patients with blood pressure (BP) inadequately controlled on telmisartan monotherapy.</p><p><strong>Methods: </strong>In this randomized, double-blind trial, 254 patients with uncontrolled BP [sitting systolic blood pressure (SBP) ≥140 and <180 mmHg; sitting diastolic blood pressure (DBP) <110 mmHg] after a telmisartan run-in period were randomized (1:1:1) to receive either telmisartan/chlorthalidone FDCs (40/12.5 or 40/6.25 mg), or telmisartan 40 mg for 8 weeks. The primary endpoint was the change in sitting SBP from baseline to Week 8.</p><p><strong>Results: </strong>At Week 8, telmisartan/chlorthalidone FDCs demonstrated greater reductions in sitting SBP compared with telmisartan monotherapy: least-squares mean differences were -9.5 mmHg [95% CI, -13.5 to - 5.6] for the 40/12.5 mg and -6.1 mmHg [95% CI, -10.4 to - 1.9] for the 40/6.25 mg. BP control rates (target BP: SBP/DBP <140/90 mmHg, or < 130/80 mmHg in patients with albuminuric chronic kidney disease or established cardiovascular disease) at Week 8 also favored telmisartan/chlorthalidone FDCs over telmisartan monotherapy (53.2% for the 40/12.5 mg and 43.0% for the 40/6.25 mg versus 32.9% for telmisartan 40 mg). Safety profiles were comparable among treatment groups.</p><p><strong>Conclusions: </strong>In patients inadequately controlled on telmisartan alone, FDCs of telmisartan with two different doses of chlorthalidone provided greater BP reduction than telmisartan monotherapy without increased safety risk, supporting its role as an effective and well-tolerated treatment option.</p>","PeriodicalId":7578,"journal":{"name":"American Journal of Hypertension","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149134876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond Cuff Availability: From Extra-Large Cuff Access to Accurate Home Blood Pressure Measurement.","authors":"Y Song, G Lei, Y Lin","doi":"10.1093/ajh/hpag121","DOIUrl":"https://doi.org/10.1093/ajh/hpag121","url":null,"abstract":"","PeriodicalId":7578,"journal":{"name":"American Journal of Hypertension","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149134928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond Inflammation: The NLRP3 Inflammasome as a Cellular and Mechanical Hub of Vascular Remodeling in Hypertension.","authors":"Palida Abulaiti, Shajidan Abudureyimu, Dilare Adi, Zhang Yu, Hui Li, Maolin Lü, Zhenqin Dai, Ying Gao","doi":"10.1093/ajh/hpag116","DOIUrl":"https://doi.org/10.1093/ajh/hpag116","url":null,"abstract":"<p><p>Hypertension is sustained not only by abnormal vascular tone but also by structural and mechanical remodeling of resistance and conduit arteries. Although innate immune activation is recognized in hypertension, how inflammatory sensing becomes a stable vascular phenotype remains unclear. The NLR family pyrin domain-containing 3 (NLRP3) inflammasome responds to neurohumoral, ionic, metabolic, mitochondrial and mechanical stress signals and may provide this missing link. This review develops a cell-resolved model in which NLRP3 activation in endothelial cells, vascular smooth muscle cells, myeloid cells, adventitial fibroblasts and perivascular adipose tissue coordinates endothelial dysfunction, smooth-muscle phenotypic switching, immune amplification and extracellular-matrix remodeling. In experimental systems, these responses collectively contribute to inward remodeling of resistance arteries, fibrosis, rarefaction and conduit-artery stiffening, which in turn generate mechanical stress, mitochondrial injury, damage-associated molecular patterns and cellular senescence that sustain inflammasome activity. We propose vascular aging as a temporal amplifier of the NLRP3-remodeling feed-forward loop rather than merely a parallel comorbidity. Genetic and pharmacological studies provide causal evidence in selected angiotensin II- and salt/mineralocorticoid-driven experimental models. By contrast, human evidence remains largely associative, and no trial has shown that selective NLRP3 inhibition lowers blood pressure or reverses vascular remodeling in primary hypertension. Early clinical studies demonstrate target engagement. Future trials should enrich for inflammation-active, salt-sensitive, metabolic or early-vascular-aging phenotypes and incorporate arterial stiffness, microvascular structure and target-engagement biomarkers alongside ambulatory blood pressure. This approach may determine whether NLRP3 is a modifiable driver of hypertensive vascular disease or primarily a marker of established injury.</p>","PeriodicalId":7578,"journal":{"name":"American Journal of Hypertension","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149102998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Methodological and Statistical Considerations for Circulating miR-23b-3p in Hypertensive Nephropathy.","authors":"Serdar Hıra","doi":"10.1093/ajh/hpag120","DOIUrl":"https://doi.org/10.1093/ajh/hpag120","url":null,"abstract":"","PeriodicalId":7578,"journal":{"name":"American Journal of Hypertension","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149102964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The challenge of introducing aldosterone synthase inhibitors into multidisciplinary practice.","authors":"Lauren E Heath, Sunil V Badve, Jun Yang, Brendon L Neuen","doi":"10.1093/ajh/hpag074","DOIUrl":"https://doi.org/10.1093/ajh/hpag074","url":null,"abstract":"<p><p>Novel therapeutic agents are required to improve hypertension control globally, which remains one of the leading modifiable risk factors for premature cardiovascular mortality. Aldosterone synthase inhibitors (ASIs) are a novel class of agents that suppress aldosterone production and have demonstrated clinically meaningful blood pressure reductions in phase 2 and phase 3 trials in patients with uncontrolled and resistant hypertension. As these therapies approach clinical adoption, important questions remain regarding effects on cardiovascular and kidney outcomes, safety profile, and optimal positioning within existing treatment algorithms. This review synthesizes the current clinical evidence for ASIs, highlights key knowledge gaps, and examines practical considerations for their real-world implementation, including persistent pharmacodynamic effects after treatment withdrawal, short-term changes in glomerular filtration rate, the risk of hyperkalemia, and the potential role of multidisciplinary care models to support safe and effective adoption.</p>","PeriodicalId":7578,"journal":{"name":"American Journal of Hypertension","volume":"39 Supplement_1","pages":"S97-S105"},"PeriodicalIF":2.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149134570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Entering a new era of hypertension treatment.","authors":"Luke J Laffin","doi":"10.1093/ajh/hpag075","DOIUrl":"https://doi.org/10.1093/ajh/hpag075","url":null,"abstract":"","PeriodicalId":7578,"journal":{"name":"American Journal of Hypertension","volume":"39 Supplement_1","pages":"S1-S2"},"PeriodicalIF":2.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149134562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optimizing multidisciplinary and interprofessional collaboration in the management of patients with difficult-to-control and resistant hypertension.","authors":"John M Giacona, Wanpen Vongpatanasin","doi":"10.1093/ajh/hpag076","DOIUrl":"https://doi.org/10.1093/ajh/hpag076","url":null,"abstract":"<p><strong>Background: </strong>Hypertension remains one of the leading causes of cardiovascular morbidity and mortality worldwide, yet blood pressure (BP) control rates remain suboptimal despite available therapeutic options. Patients with difficult-to-control or resistant hypertension face elevated cardiovascular risk and require intensive, coordinated management that addresses measurement accuracy, medication adherence, and treatment intensification. Multidisciplinary collaboration has emerged as a highly effective approach, with systematic reviews demonstrating significant BP reductions and increases in control rate vs usual care.</p><p><strong>Methods: </strong>This review discusses evidence supporting collaborative care models, including advanced practice provider-physician partnerships, physician-pharmacist collaborative management, nurse-led interventions, and community health worker programs. Key implementation strategies include standardized treatment protocols, home BP monitoring with clinical support, and health information technology integration.</p><p><strong>Results: </strong>Despite demonstrated cost-effectiveness, significant barriers to collaborative care persist, including inadequate reimbursement, organizational inertia, and workforce limitations. The advanced practice provider-physician model shows promise, with advanced practice providers managing routine and complex hypertension, allowing physicians to focus on more challenging cases. Specialized centers, including American Heart Association Certified Comprehensive Hypertension Centers, provide multidisciplinary expertise for difficult-to-control hypertension.</p><p><strong>Conclusions: </strong>Future directions include sustainable payment models and leveraging technology to enhance team communication and patient engagement. Optimizing interprofessional collaboration represents an evidence-based strategy to close the gap between evidence-based management and real-world BP control.</p>","PeriodicalId":7578,"journal":{"name":"American Journal of Hypertension","volume":"39 Supplement_1","pages":"S88-S96"},"PeriodicalIF":2.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149134629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From low renin to the primary aldosteronism spectrum: aldosterone synthase inhibitors and the endocrine management of hypertension.","authors":"Gregory A Kline","doi":"10.1093/ajh/hpag078","DOIUrl":"https://doi.org/10.1093/ajh/hpag078","url":null,"abstract":"<p><strong>Background: </strong>Hypertension remains a major contributor to global cardiovascular morbidity despite decades of available therapy.</p><p><strong>Aim: </strong>This review advances an endocrinological framework in which chronic hypertension, including resistant hypertension, is understood as a consequence of dysregulated hormonal control of renal sodium handling, mediated by excess renin-angiotensin II activity, inappropriate aldosterone excess, or both.</p><p><strong>Results: </strong>Within this framework, the traditional binary distinction between \"essential\" and \"secondary\" hypertension gives way to a mechanistic continuum characterized by biochemical phenotyping using renin and aldosterone. Primary aldosteronism (PA) is now recognized as existing across a spectrum of severity that is broader than classical diagnostic thresholds suggest, and aldosterone dysregulation, even at subclinical levels, confers adverse cardiorenal outcomes exceeding those of renin-dependent hypertension. Mineralocorticoid receptor antagonists (MRAs) are effective when aldosterone excess is the dominant mechanism but do not correct the underlying endocrinopathy and may be limited by tolerability at the doses required to achieve full biochemical targets. Highly selective second-generation aldosterone synthase inhibitors (ASIs), including baxdrostat and lorundrostat, directly suppress aldosterone production, mirror the biochemical response seen after surgical adrenalectomy, and may confer disease-modifying effects beyond blood pressure reduction.</p><p><strong>Conclusion: </strong>Integrated into a mechanism-first clinical algorithm driven by renin and aldosterone profiling, ASIs and MRAs offer the potential to transform management of low-renin and PA-spectrum hypertension, moving clinicians from empirical, add-on drug strategies toward individualized, pathophysiology-guided care.</p>","PeriodicalId":7578,"journal":{"name":"American Journal of Hypertension","volume":"39 Supplement_1","pages":"S66-S77"},"PeriodicalIF":2.9,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149134552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}