Pub Date : 2026-01-21DOI: 10.1161/hypertensionaha.125.25906
Lance N Benson,Kelly A Hyndman,David M Pollock,Jennifer S Pollock
{"title":"Time of Day Drives Angiotensin II-Dependent Hypertension.","authors":"Lance N Benson,Kelly A Hyndman,David M Pollock,Jennifer S Pollock","doi":"10.1161/hypertensionaha.125.25906","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.25906","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"277 1","pages":"e25906"},"PeriodicalIF":8.3,"publicationDate":"2026-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146015106","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}
Pub Date : 2026-01-21DOI: 10.1161/hypertensionaha.125.26437
Samuel S Gidding,Raymond R Townsend
{"title":"One Way Children With Elevated Blood Pressure Become Adults With Hypertension.","authors":"Samuel S Gidding,Raymond R Townsend","doi":"10.1161/hypertensionaha.125.26437","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.26437","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"31 1","pages":"e26437"},"PeriodicalIF":8.3,"publicationDate":"2026-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146015116","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}
Pub Date : 2026-01-19DOI: 10.1161/hypertensionaha.125.26077
Tapan A Patel,Hong Zheng,Kaushik P Patel
BACKGROUNDCongestive heart failure (CHF) is characterized by the activation of neurohumoral drive concomitant with avid fluid retention. Renal denervation alleviates this fluid retention. SGLT2 (sodium-glucose cotransporter 2) inhibitors have shown remarkable improvement in patients with cardiovascular diseases. We have recently demonstrated a relationship between enhanced renal sympathetic nerve activity and SGLT2 expression as well as function during CHF; however, the precise molecular mechanisms involved in the expression and translocation of SGLT2 and associated scaffolding proteins to the luminal membrane remain to be examined.METHODSCHF was induced by coronary artery ligation followed by bilateral renal denervation 4 weeks later, in rats. Western blot analysis and immunohistochemistry were performed to evaluate changes in the expression of SGLT2, MAP17 (membrane-associated protein 17), PDZK1 (PDZ domain containing 1), and activation of ERK (extracellular signal-regulated kinase)/NF-KB (nuclear factor κB) in renal cortex. Human adult proximal tubular cells were used to determine the direct effect of norepinephrine on the expression of SGLT2-MAP17-PDZK1 and activation of the ERK/NF-KB pathway.RESULTSRats with CHF exhibited significantly enhanced expression of SGLT2, MAP17, and PDZK1 with a concomitant significant activation of ERK and NF-KB in the renal cortex. In rats with CHF, renal denervation mitigated enhanced expression of SGLT2-MAP17-PDZK1 as well as activation of ERK and NF-KB. Direct action of norepinephrine on human adult proximal tubular cells cells triggered enhanced expression of SGLT2-MAP17-PDZK1 by the activation of the ERK/NF-KB pathway.CONCLUSIONSEnhanced basal renal sympathetic nerve activity in CHF activates the ERK/NF-KB pathway, which in turn facilitates the enhanced expression and translocation of the SGLT2-MAP17-PDZK1 scaffolding protein complex to the luminal membrane, augmenting sodium reabsorption in CHF.
{"title":"Neural Upregulation of SGLT2-MAP17-PDZK1 Complex in Kidneys of Rats With Heart Failure.","authors":"Tapan A Patel,Hong Zheng,Kaushik P Patel","doi":"10.1161/hypertensionaha.125.26077","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.26077","url":null,"abstract":"BACKGROUNDCongestive heart failure (CHF) is characterized by the activation of neurohumoral drive concomitant with avid fluid retention. Renal denervation alleviates this fluid retention. SGLT2 (sodium-glucose cotransporter 2) inhibitors have shown remarkable improvement in patients with cardiovascular diseases. We have recently demonstrated a relationship between enhanced renal sympathetic nerve activity and SGLT2 expression as well as function during CHF; however, the precise molecular mechanisms involved in the expression and translocation of SGLT2 and associated scaffolding proteins to the luminal membrane remain to be examined.METHODSCHF was induced by coronary artery ligation followed by bilateral renal denervation 4 weeks later, in rats. Western blot analysis and immunohistochemistry were performed to evaluate changes in the expression of SGLT2, MAP17 (membrane-associated protein 17), PDZK1 (PDZ domain containing 1), and activation of ERK (extracellular signal-regulated kinase)/NF-KB (nuclear factor κB) in renal cortex. Human adult proximal tubular cells were used to determine the direct effect of norepinephrine on the expression of SGLT2-MAP17-PDZK1 and activation of the ERK/NF-KB pathway.RESULTSRats with CHF exhibited significantly enhanced expression of SGLT2, MAP17, and PDZK1 with a concomitant significant activation of ERK and NF-KB in the renal cortex. In rats with CHF, renal denervation mitigated enhanced expression of SGLT2-MAP17-PDZK1 as well as activation of ERK and NF-KB. Direct action of norepinephrine on human adult proximal tubular cells cells triggered enhanced expression of SGLT2-MAP17-PDZK1 by the activation of the ERK/NF-KB pathway.CONCLUSIONSEnhanced basal renal sympathetic nerve activity in CHF activates the ERK/NF-KB pathway, which in turn facilitates the enhanced expression and translocation of the SGLT2-MAP17-PDZK1 scaffolding protein complex to the luminal membrane, augmenting sodium reabsorption in CHF.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"15 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145994872","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}
Pub Date : 2026-01-19DOI: 10.1161/hypertensionaha.125.26125
Lucas Ferreira de Almeida,Ulrich Wenzel,A H Jan Danser,Giuseppe Lembo,Maria Luisa S Sequeira-Lopez,R Ariel Gomez
{"title":"Balancing Blood Pressure Targets and Kidney Health: The Potential Risk of Kidney Disease Due to Concentric Arterial and Arteriolar Hypertrophy From Renin-Angiotensin-Aldosterone Inhibitors.","authors":"Lucas Ferreira de Almeida,Ulrich Wenzel,A H Jan Danser,Giuseppe Lembo,Maria Luisa S Sequeira-Lopez,R Ariel Gomez","doi":"10.1161/hypertensionaha.125.26125","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.26125","url":null,"abstract":"","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"49 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145994827","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}
Pub Date : 2026-01-14DOI: 10.1161/hypertensionaha.125.26399
So Mi Jemma Cho,Yunfeng Ruan,Hyeok-Hee Lee,Satoshi Koyama,Stephen P Juraschek,Norrina B Allen,Eugene Yang,John W McEvoy,Eric Secemsky,Michael C Honigberg,Akl C Fahed,Aniruddh Patel,Whitney E Hornsby,Pradeep Natarajan
BACKGROUNDSuboptimal blood pressure (BP) control remains a major cardiovascular disease risk factor. Whether genetically predicted BP independently predicts long-term BP control is unknown. We examined the associations of BP polygenic scores (PGSs) with long-term BP control and treatment-resistant hypertension.METHODSWe identified 22 456 Mass General Brigham Biobank participants with hypertension. Longitudinal BP control was defined as the percentage of time above-target systolic BP (SBP) ≥130 mm Hg or diastolic BP (DBP) ≥80 mm Hg over 5 years. Using multivariable regression, we assessed the associations of BP PGS with duration above-target BP and lifetime treatment-resistant hypertension incidence. Incremental prognostic utility of BP PGSs was assessed based on the discrimination C-index, Brier score, and net reclassification index. Validation was performed in the population-based UK Biobank cohort using the SBP/DBP ≥140/90 mm Hg threshold.RESULTSAmong 10 853 (48.3%) were female, the mean SBP/DBP (SD) at index date was 132 (18)/75 (11) mm Hg, and 4126 (18.4%) developed treatment-resistant hypertension over lifetime. In reference to the low (<20th percentile) PGS group, the high (≥80th percentile) BP PGS was associated with 8.01 (95% CI, 6.68%-9.34%) longer duration with above-target SBP and 6.19 (95% CI, 5.05%-7.33%) with high DBP. Each high SBP and DBP PGS conferred 2.36 (95% CI, 2.07-2.68) and 1.75 (95% CI, 1.55-1.99)-fold higher odds of treatment-resistant hypertension. Adding BP PGSs to traditional risk factors improved treatment-resistant hypertension prediction from C-index (95% CI), 0.74 (0.73-0.75) to 0.78 (0.77-0.79). BP PGSs consistently predicted longitudinal BP management to a comparable extent in the UK Biobank.CONCLUSIONSHarnessing BP PGSs may inform anticipated trends in BP control to warrant vigilant monitoring and augment prioritization of intensive therapy.
背景：亚理想血压（BP）控制仍然是心血管疾病的主要危险因素。基因预测的血压是否能独立预测长期的血压控制尚不清楚。我们研究了血压多基因评分（pgs）与长期血压控制和治疗难治性高血压的关系。方法：选取22456名麻省总医院布里格姆生物样本库高血压患者。纵向血压控制定义为5年内收缩压(SBP)≥130 mm Hg或舒张压(DBP)≥80 mm Hg高于目标时间的百分比。使用多变量回归，我们评估了BP PGS与持续时间高于目标血压和终生治疗抵抗性高血压发病率的关系。基于判别c指数、Brier评分和净再分类指数评估BP pgs的增量预后效用。在以人群为基础的UK Biobank队列中，使用收缩压/舒张压≥140/90 mm Hg阈值进行验证。结果10853例（48.3%）患者为女性，指标日平均收缩压/舒张压（SD）为132 (18)/75 (11)mm Hg， 4126例（18.4%）患者出现难治性高血压。在低（<20百分位）PGS组中，高（≥80百分位）BP PGS与高于目标收缩压的时间延长8.01 （95% CI, 6.68%-9.34%）和高DBP的时间延长6.19 （95% CI, 5.05%-7.33%）相关。每一次高收缩压和舒张压PGS分别使难治性高血压的发生几率增加2.36倍（95% CI, 2.07-2.68）和1.75倍（95% CI, 1.55-1.99）。在传统危险因素中加入BP pgs可提高对治疗抵抗性高血压的预测，其c指数（95% CI）从0.74（0.73-0.75）提高到0.78（0.77-0.79）。在英国生物银行中，BP pgs一致地预测了纵向BP管理。结论：监测BP pgs可以预测BP控制的趋势，以保证警惕监测和加强强化治疗的优先级。
{"title":"Blood Pressure Polygenic Score Predicts Long-Term Blood Pressure Control and Treatment-Resistant Hypertension.","authors":"So Mi Jemma Cho,Yunfeng Ruan,Hyeok-Hee Lee,Satoshi Koyama,Stephen P Juraschek,Norrina B Allen,Eugene Yang,John W McEvoy,Eric Secemsky,Michael C Honigberg,Akl C Fahed,Aniruddh Patel,Whitney E Hornsby,Pradeep Natarajan","doi":"10.1161/hypertensionaha.125.26399","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.26399","url":null,"abstract":"BACKGROUNDSuboptimal blood pressure (BP) control remains a major cardiovascular disease risk factor. Whether genetically predicted BP independently predicts long-term BP control is unknown. We examined the associations of BP polygenic scores (PGSs) with long-term BP control and treatment-resistant hypertension.METHODSWe identified 22 456 Mass General Brigham Biobank participants with hypertension. Longitudinal BP control was defined as the percentage of time above-target systolic BP (SBP) ≥130 mm Hg or diastolic BP (DBP) ≥80 mm Hg over 5 years. Using multivariable regression, we assessed the associations of BP PGS with duration above-target BP and lifetime treatment-resistant hypertension incidence. Incremental prognostic utility of BP PGSs was assessed based on the discrimination C-index, Brier score, and net reclassification index. Validation was performed in the population-based UK Biobank cohort using the SBP/DBP ≥140/90 mm Hg threshold.RESULTSAmong 10 853 (48.3%) were female, the mean SBP/DBP (SD) at index date was 132 (18)/75 (11) mm Hg, and 4126 (18.4%) developed treatment-resistant hypertension over lifetime. In reference to the low (<20th percentile) PGS group, the high (≥80th percentile) BP PGS was associated with 8.01 (95% CI, 6.68%-9.34%) longer duration with above-target SBP and 6.19 (95% CI, 5.05%-7.33%) with high DBP. Each high SBP and DBP PGS conferred 2.36 (95% CI, 2.07-2.68) and 1.75 (95% CI, 1.55-1.99)-fold higher odds of treatment-resistant hypertension. Adding BP PGSs to traditional risk factors improved treatment-resistant hypertension prediction from C-index (95% CI), 0.74 (0.73-0.75) to 0.78 (0.77-0.79). BP PGSs consistently predicted longitudinal BP management to a comparable extent in the UK Biobank.CONCLUSIONSHarnessing BP PGSs may inform anticipated trends in BP control to warrant vigilant monitoring and augment prioritization of intensive therapy.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"259 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145961449","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}
Pub Date : 2026-01-14DOI: 10.1161/hypertensionaha.125.25490
Katie Williams,Benjamin Grobman,Fredrick Larbi Kwapong,Hannah Col,Ruth-Alma N Turkson-Ocran,Long H Ngo,Mingyu Zhang,Natalie R Daya,Elizabeth Selvin,Pamela L Lutsey,Josef Coresh,Beverly Gwen Windham,Lynne Wagenknecht,Stephen P Juraschek
BACKGROUNDHigher relative risk for cardiovascular disease (CVD) events at lower blood pressure (BP) thresholds in female versus male adults suggest that hypertension thresholds should be sex-specific.METHODSWe used the ARIC study (Atherosclerosis Risk in Communities) visit 1 (1987-1989) to compare the BP distribution, estimated risk (via the 10-year Predicting Risk of Cardiovascular Disease Events score), absolute risk, and relative risk of CVD according to BP thresholds, stratified by sex and hypertension treatment status, in participants without prior CVD.RESULTSOf 13 418 participants (56% women, mean age [54±5.7 years]), 25% were treated for hypertension. Males had higher average 10-year CVD risk scores regardless of treatment. The distribution of BP and prevalence of CVD risk factors was similar for male and female adults. Incidence rates (per 10 000 person-years) comparing a systolic BP threshold of ≥140 versus <140 mm Hg for coronary heart disease were 30.9 and 12.0 among untreated male and female adults (P=0.07) and 27.4 versus 16.5 among treated male and female adults (P=0.63). HRs comparing a systolic BP threshold of ≥140 versus <140 mm Hg for coronary heart disease were 1.49 and 1.72 among untreated male and female adults (P=0.16) and 1.30 versus 1.40 among treated male and female adults (P=0.93).CONCLUSIONSIn this middle-aged population, there were no consistent differences in BP distribution, risk factor burden, absolute risk, or relative risk of CVD between male and female adults. These findings do not support a sex-specific threshold for hypertension.
背景：与男性相比，女性在较低血压阈值时发生心血管疾病（CVD）事件的相对风险更高，这表明高血压阈值应该是性别特异性的。方法：我们使用ARIC研究（社区动脉粥样硬化风险）访问1(1987-1989)，根据BP阈值，按性别和高血压治疗状况分层，比较无CVD的参与者的BP分布、估计风险（通过10年心血管疾病事件预测风险评分）、CVD绝对风险和相对风险。结果在13418名参与者中（56%为女性，平均年龄[54±5.7岁]），25%接受高血压治疗。无论接受何种治疗，男性的平均10年心血管疾病风险评分都较高。男性和女性成年人的血压分布和心血管疾病危险因素患病率相似。冠心病收缩压阈值≥140与<140 mm Hg的发病率（每10000人年）在未治疗的男性和女性成人中分别为30.9和12.0 (P=0.07)，在接受治疗的男性和女性成人中分别为27.4和16.5 （P=0.63）。冠心病收缩压阈值≥140与<140 mm Hg的男性和女性成人的hr比较，未治疗的男性和女性成人的hr分别为1.49和1.72 (P=0.16)，治疗的男性和女性成人的hr分别为1.30和1.40 （P=0.93）。结论：在这一中年人群中，男性和女性成人在血压分布、危险因素负担、心血管疾病绝对风险或相对风险方面没有一致的差异。这些发现不支持高血压的性别特异性阈值。
{"title":"Sex-Specific Blood Pressure Thresholds in Middle-Aged Adults.","authors":"Katie Williams,Benjamin Grobman,Fredrick Larbi Kwapong,Hannah Col,Ruth-Alma N Turkson-Ocran,Long H Ngo,Mingyu Zhang,Natalie R Daya,Elizabeth Selvin,Pamela L Lutsey,Josef Coresh,Beverly Gwen Windham,Lynne Wagenknecht,Stephen P Juraschek","doi":"10.1161/hypertensionaha.125.25490","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.25490","url":null,"abstract":"BACKGROUNDHigher relative risk for cardiovascular disease (CVD) events at lower blood pressure (BP) thresholds in female versus male adults suggest that hypertension thresholds should be sex-specific.METHODSWe used the ARIC study (Atherosclerosis Risk in Communities) visit 1 (1987-1989) to compare the BP distribution, estimated risk (via the 10-year Predicting Risk of Cardiovascular Disease Events score), absolute risk, and relative risk of CVD according to BP thresholds, stratified by sex and hypertension treatment status, in participants without prior CVD.RESULTSOf 13 418 participants (56% women, mean age [54±5.7 years]), 25% were treated for hypertension. Males had higher average 10-year CVD risk scores regardless of treatment. The distribution of BP and prevalence of CVD risk factors was similar for male and female adults. Incidence rates (per 10 000 person-years) comparing a systolic BP threshold of ≥140 versus <140 mm Hg for coronary heart disease were 30.9 and 12.0 among untreated male and female adults (P=0.07) and 27.4 versus 16.5 among treated male and female adults (P=0.63). HRs comparing a systolic BP threshold of ≥140 versus <140 mm Hg for coronary heart disease were 1.49 and 1.72 among untreated male and female adults (P=0.16) and 1.30 versus 1.40 among treated male and female adults (P=0.93).CONCLUSIONSIn this middle-aged population, there were no consistent differences in BP distribution, risk factor burden, absolute risk, or relative risk of CVD between male and female adults. These findings do not support a sex-specific threshold for hypertension.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"52 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145961450","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}
BACKGROUNDSpironolactone is recommended as first-line therapy for patients with idiopathic primary aldosteronism. The aim of this study is to evaluate the impact of low and high doses of spironolactone on arterial blood pressure control, potassium levels, and the incidence of drug-related adverse effects.METHODSWe retrospectively included 394 patients with primary aldosteronism receiving spironolactone. Patients were divided into 2 groups, according to the median prescribed dose in our population (50 mg, 25-75): subjects treated with doses ≤50 mg versus >50 mg.RESULTSThe median follow-up after the introduction of spironolactone was 12 months, and 128 patients experienced adverse effects, with a proportion higher in men than in women (44.70% versus 15.70%). The most frequently reported adverse effect was gynecomastia, followed by sexual dysfunction. Subjects receiving a dose >50 mg of spironolactone displayed a higher prevalence of adverse effects (39.1%) compared to the ≤50 mg group (29.3%); this effect was significantly different only in men (P=0.002). Patients in the low-dose group were treated with a higher number of antihypertensive drugs, especially diuretics. No significant differences were seen between the 2 subgroups in blood pressure control, potassium and renin levels, and occurrence of cardiovascular events at follow-up.CONCLUSIONSTreatment with low doses of spironolactone, in association with other antihypertensive drugs, is effective in achieving an appropriate blood pressure control in primary aldosteronism, while it improves adherence with lower adverse effects. These findings could help the clinician choose the best therapeutic option for each patient.
{"title":"Efficacy and Safety of Treatment With Low Doses of Spironolactone in Patients With Primary Aldosteronism: A Retrospective Observational Study in a Tertiary Center.","authors":"Elisa Sconfienza,Julien Riancho,Nicole Gebara,Diana Ferrão,Jacopo Burrello,Jean-Baptiste de Freminville,Elisa Deflorenne,Aurélien Lorthioir,Michel Azizi,Laurence Amar","doi":"10.1161/hypertensionaha.125.24881","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.24881","url":null,"abstract":"BACKGROUNDSpironolactone is recommended as first-line therapy for patients with idiopathic primary aldosteronism. The aim of this study is to evaluate the impact of low and high doses of spironolactone on arterial blood pressure control, potassium levels, and the incidence of drug-related adverse effects.METHODSWe retrospectively included 394 patients with primary aldosteronism receiving spironolactone. Patients were divided into 2 groups, according to the median prescribed dose in our population (50 mg, 25-75): subjects treated with doses ≤50 mg versus >50 mg.RESULTSThe median follow-up after the introduction of spironolactone was 12 months, and 128 patients experienced adverse effects, with a proportion higher in men than in women (44.70% versus 15.70%). The most frequently reported adverse effect was gynecomastia, followed by sexual dysfunction. Subjects receiving a dose >50 mg of spironolactone displayed a higher prevalence of adverse effects (39.1%) compared to the ≤50 mg group (29.3%); this effect was significantly different only in men (P=0.002). Patients in the low-dose group were treated with a higher number of antihypertensive drugs, especially diuretics. No significant differences were seen between the 2 subgroups in blood pressure control, potassium and renin levels, and occurrence of cardiovascular events at follow-up.CONCLUSIONSTreatment with low doses of spironolactone, in association with other antihypertensive drugs, is effective in achieving an appropriate blood pressure control in primary aldosteronism, while it improves adherence with lower adverse effects. These findings could help the clinician choose the best therapeutic option for each patient.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"6 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145949716","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}
Pub Date : 2026-01-12DOI: 10.1161/hypertensionaha.125.26346
Sanna Darvish,Kevin O Murray,Sophia A Mahoney,Nicholas S VanDongen,Melanie C Zigler,Charlie Ambrose,Martinique A Flickinger,Julie A Reisz,Angelo D'Alessandro,Kristen L Nowak,Zachary S Clayton,Kerrie L Moreau,Douglas R Seals,Matthew J Rossman
BACKGROUNDA later age at menopause (≥55 years) is associated with lower cardiovascular disease risk compared with a normal age at menopause (45-54 years) in postmenopausal women (PMW). Aortic stiffening increases cardiovascular disease risk, but the impact of late-onset menopause on aortic stiffness is unknown.METHODSTotal aortic stiffness (carotid-femoral pulse wave velocity [PWVCF]) was measured in 40 late-onset and 86 normal-onset PMW. Structural- and load/blood pressure-dependent PWVCF were calculated with exponential models; the percent of total PWVCF attributable to each was determined. Elastic modulus was assessed in aortic rings from female C57BL/6 N mice (3-6 months) exposed to 5% PMW serum. Lipidomics and triglyceride-related metabolite exposure of aortas with/without the mitochondrial antioxidant MitoQ identified lipid drivers of mitochondrial reactive oxygen species-related stiffness.RESULTSPWVCF was 128 cm/s lower in late-onset (835±24 cm/s) versus normal-onset (963±24 cm/s) PMW. The difference in PWVCF remained >100 cm/s in multivariable models adjusted for age and education, cardiovascular disease risk factors, and medication use. Systolic and diastolic blood pressure were 10 and 6 mm Hg lower in late-onset PMW. Some (<20%) of the attenuated PWVCF in late-onset PMW was related to lower load-dependent PWVCF. However, the majority (≈85%) was attributable to lower structural-dependent PWVCF. Elastic modulus was 35% lower in aortas exposed to serum from late- versus normal-onset PMW because of less mitochondrial reactive oxygen species-dependent stiffness. Triglyceride (16:0) was a driver of the effects of serum.CONCLUSIONSOur findings suggest attenuated aortic stiffening via lower structural-dependent factors may be 1 mechanism by which late-onset menopause lowers cardiovascular disease risk.
{"title":"Late-Onset Menopause and Attenuated Aortic Stiffness.","authors":"Sanna Darvish,Kevin O Murray,Sophia A Mahoney,Nicholas S VanDongen,Melanie C Zigler,Charlie Ambrose,Martinique A Flickinger,Julie A Reisz,Angelo D'Alessandro,Kristen L Nowak,Zachary S Clayton,Kerrie L Moreau,Douglas R Seals,Matthew J Rossman","doi":"10.1161/hypertensionaha.125.26346","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.26346","url":null,"abstract":"BACKGROUNDA later age at menopause (≥55 years) is associated with lower cardiovascular disease risk compared with a normal age at menopause (45-54 years) in postmenopausal women (PMW). Aortic stiffening increases cardiovascular disease risk, but the impact of late-onset menopause on aortic stiffness is unknown.METHODSTotal aortic stiffness (carotid-femoral pulse wave velocity [PWVCF]) was measured in 40 late-onset and 86 normal-onset PMW. Structural- and load/blood pressure-dependent PWVCF were calculated with exponential models; the percent of total PWVCF attributable to each was determined. Elastic modulus was assessed in aortic rings from female C57BL/6 N mice (3-6 months) exposed to 5% PMW serum. Lipidomics and triglyceride-related metabolite exposure of aortas with/without the mitochondrial antioxidant MitoQ identified lipid drivers of mitochondrial reactive oxygen species-related stiffness.RESULTSPWVCF was 128 cm/s lower in late-onset (835±24 cm/s) versus normal-onset (963±24 cm/s) PMW. The difference in PWVCF remained >100 cm/s in multivariable models adjusted for age and education, cardiovascular disease risk factors, and medication use. Systolic and diastolic blood pressure were 10 and 6 mm Hg lower in late-onset PMW. Some (<20%) of the attenuated PWVCF in late-onset PMW was related to lower load-dependent PWVCF. However, the majority (≈85%) was attributable to lower structural-dependent PWVCF. Elastic modulus was 35% lower in aortas exposed to serum from late- versus normal-onset PMW because of less mitochondrial reactive oxygen species-dependent stiffness. Triglyceride (16:0) was a driver of the effects of serum.CONCLUSIONSOur findings suggest attenuated aortic stiffening via lower structural-dependent factors may be 1 mechanism by which late-onset menopause lowers cardiovascular disease risk.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"3 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145949711","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}
BACKGROUNDPreeclampsia is a hypertensive disorder affecting 2% to 8% of pregnancies. Women with a history of preeclampsia have an increased risk of cardiovascular disease. The long noncoding RNA MALAT1 is shown to regulate inflammatory responses linked to cardiovascular disease. MALAT1 is decreased in preeclampsia placentas and may have a cis-regulatory function on neighboring RNAs.METHODSExpression of MALAT1, NEAT1, mascRNA, SCYL1, and FRMD8 was assessed in peripheral blood mononuclear cells, and MALAT1 in plasma and extracellular vesicles, at 22 to 24 and 36 to 38 weeks of gestation in healthy (n=214) and preeclampsia (n=37) women from the STORK cohort study and at 5-year follow-up in women with and without history of preeclampsia (n=29; n=271). We investigated their associations with established markers of disease activity and later cardiometabolic risk. MALAT1 was silenced in lipopolysaccharide-stimulated THP-1 differentiated macrophages in vitro.RESULTSMALAT1, NEAT1, mascRNA, and FRMD8 are decreased in peripheral blood mononuclear cells during preeclampsia development. At follow-up in women with a previous preeclampsia diagnosis, MALAT1 and NEAT1 are decreased in peripheral blood mononuclear cells and show associations with cardiometabolic markers. Silencing MALAT1 in macrophages increased secretion of IL (interleukin)-6 and reduced MMP9 (matrix metalloproteinase-9) and VEGF (vascular endothelial growth factor) A levels.CONCLUSIONSGiven the association of MALAT1 and neighboring RNAs with preeclampsia during pregnancy and at follow-up, as well as with cardiometabolic markers and results from silencing experiments, these transcripts may be potential targets for preeclampsia development and cardiometabolic risk in women with previous preeclampsia.
{"title":"Circulating MALAT1 in Preeclampsia and Association With Cardiometabolic Risk.","authors":"Tove Lekva,Monica Frøystad,Annika E Michelsen,Yusuf Khan,Pål Aukrust,Bente Halvorsen,Marie Cecilie Paasche Roland,Thor Ueland","doi":"10.1161/hypertensionaha.125.26379","DOIUrl":"https://doi.org/10.1161/hypertensionaha.125.26379","url":null,"abstract":"BACKGROUNDPreeclampsia is a hypertensive disorder affecting 2% to 8% of pregnancies. Women with a history of preeclampsia have an increased risk of cardiovascular disease. The long noncoding RNA MALAT1 is shown to regulate inflammatory responses linked to cardiovascular disease. MALAT1 is decreased in preeclampsia placentas and may have a cis-regulatory function on neighboring RNAs.METHODSExpression of MALAT1, NEAT1, mascRNA, SCYL1, and FRMD8 was assessed in peripheral blood mononuclear cells, and MALAT1 in plasma and extracellular vesicles, at 22 to 24 and 36 to 38 weeks of gestation in healthy (n=214) and preeclampsia (n=37) women from the STORK cohort study and at 5-year follow-up in women with and without history of preeclampsia (n=29; n=271). We investigated their associations with established markers of disease activity and later cardiometabolic risk. MALAT1 was silenced in lipopolysaccharide-stimulated THP-1 differentiated macrophages in vitro.RESULTSMALAT1, NEAT1, mascRNA, and FRMD8 are decreased in peripheral blood mononuclear cells during preeclampsia development. At follow-up in women with a previous preeclampsia diagnosis, MALAT1 and NEAT1 are decreased in peripheral blood mononuclear cells and show associations with cardiometabolic markers. Silencing MALAT1 in macrophages increased secretion of IL (interleukin)-6 and reduced MMP9 (matrix metalloproteinase-9) and VEGF (vascular endothelial growth factor) A levels.CONCLUSIONSGiven the association of MALAT1 and neighboring RNAs with preeclampsia during pregnancy and at follow-up, as well as with cardiometabolic markers and results from silencing experiments, these transcripts may be potential targets for preeclampsia development and cardiometabolic risk in women with previous preeclampsia.","PeriodicalId":13042,"journal":{"name":"Hypertension","volume":"23 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145907750","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}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：