Pub Date : 2025-03-01eCollection Date: 2025-01-01DOI: 10.5646/ch.2025.31.e8
Jinho Shin, Dong Hoon Cha, Woo-Hyung Bae, In Hyun Jung, Seung-Pyo Hong, Sang-Hyun Kim, Jun-Young Do, Won Min Hwang, Young Youp Koh, Giuseppe Mancia, Athanasios J Manolis, MinYoung Lee
Background: This subanalysis of BENEFIT-KOREA cohort assessed the impact of baseline pulse rate (PR) and posttreatment PR reduction on the blood pressure (BP)-lowering efficacy of nebivolol in patients with hypertension.
Methods: South Korean patients with hypertension were enrolled in the BENEFIT-KOREA study; 3,011 patients received nebivolol as monotherapy/add-on therapy. Time-averaged BP, calculated by sum of the product of BPs at weeks 12 and 24 corrected for number of participants at these timepoints, was evaluated with/without adjustment for baseline BP. Change in BP in baseline PR groups of < 70, 70-79, and ≥ 80 beats/min and posttreatment PR reduction groups of < 1, 1-9, and ≥ 10 beats/min at 24 weeks were evaluated.
Results: The unadjusted time-averaged systolic BP (SBP) at 24 weeks was not significantly different within baseline PR groups or posttreatment PR reduction groups, but the unadjusted time-averaged diastolic BP (DBP) was significantly different within both baseline PR (P < 0.001) and posttreatment PR reduction groups (P < 0.001). Significant differences were observed in adjusted time-averaged SBP (≥ 10 beats/min group: β, -3.4148; P = 0.006) and time-averaged DBP (≥ 10 beats/min: β, -4.5781; P < 0.001) only within the posttreatment PR reduction groups. The majority of adverse events reported with nebivolol were mild.
Conclusions: The efficacy of nebivolol for BP reduction seems to be indicated not by baseline PR but by posttreatment PR reduction. These findings suggest the presence of other mechanisms in addition to sympathetic inhibition which potentially weaken the relationship between baseline PR and BP reduction.
{"title":"Posttreatment pulse rate reduction and not baseline pulse rate as an indicator of blood pressure response to nebivolol: a subanalysis from the real-world BENEFIT-KOREA study.","authors":"Jinho Shin, Dong Hoon Cha, Woo-Hyung Bae, In Hyun Jung, Seung-Pyo Hong, Sang-Hyun Kim, Jun-Young Do, Won Min Hwang, Young Youp Koh, Giuseppe Mancia, Athanasios J Manolis, MinYoung Lee","doi":"10.5646/ch.2025.31.e8","DOIUrl":"10.5646/ch.2025.31.e8","url":null,"abstract":"<p><strong>Background: </strong>This subanalysis of BENEFIT-KOREA cohort assessed the impact of baseline pulse rate (PR) and posttreatment PR reduction on the blood pressure (BP)-lowering efficacy of nebivolol in patients with hypertension.</p><p><strong>Methods: </strong>South Korean patients with hypertension were enrolled in the BENEFIT-KOREA study; 3,011 patients received nebivolol as monotherapy/add-on therapy. Time-averaged BP, calculated by sum of the product of BPs at weeks 12 and 24 corrected for number of participants at these timepoints, was evaluated with/without adjustment for baseline BP. Change in BP in baseline PR groups of < 70, 70-79, and ≥ 80 beats/min and posttreatment PR reduction groups of < 1, 1-9, and ≥ 10 beats/min at 24 weeks were evaluated.</p><p><strong>Results: </strong>The unadjusted time-averaged systolic BP (SBP) at 24 weeks was not significantly different within baseline PR groups or posttreatment PR reduction groups, but the unadjusted time-averaged diastolic BP (DBP) was significantly different within both baseline PR (<i>P</i> < 0.001) and posttreatment PR reduction groups (<i>P</i> < 0.001). Significant differences were observed in adjusted time-averaged SBP (≥ 10 beats/min group: β, -3.4148; <i>P</i> = 0.006) and time-averaged DBP (≥ 10 beats/min: β, -4.5781; <i>P</i> < 0.001) only within the posttreatment PR reduction groups. The majority of adverse events reported with nebivolol were mild.</p><p><strong>Conclusions: </strong>The efficacy of nebivolol for BP reduction seems to be indicated not by baseline PR but by posttreatment PR reduction. These findings suggest the presence of other mechanisms in addition to sympathetic inhibition which potentially weaken the relationship between baseline PR and BP reduction.</p><p><strong>Trial registration: </strong>ClinicalTrials.gov Identifier: NCT03847350.</p>","PeriodicalId":10480,"journal":{"name":"Clinical Hypertension","volume":"31 ","pages":"e8"},"PeriodicalIF":2.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11903211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: The correlation between serum uric acid/creatinine (SUA/Cr) ratio and hypertension risk has not been well studied. This study aims to examine whether the SUA/Cr ratio is a predictor of hypertension.
Methods: This cohort study comprised 171 men aged 64 ± 11 (mean ± standard deviation) years and 266 women aged 65 ± 10 years recruited for a survey at the community-based annual medical check-up. The main outcome was the presence of hypertension (antihypertensive medication) and having systolic blood pressure (SBP) ≥ 140 mmHg and diastolic blood pressure (DBP) ≥ 90 mmHg.
Results: The baseline SUA/Cr ratio was significantly correlated only with DBP at 3 years in men (r = 0.217, P = 0.004) and women (r = 0.126, P = 0.040), and with both SBP (r = 0.103, P = 0.031) and DBP (r = 0.15, P = 0.001) in the overall participants of men and women. A plausible prognostic cut-off of SUA/Cr ratio (≥ 7.41) was found and was the same in women and in all participants. Multivariable logistic regressions showed that SUA/Cr ratio was significantly linked with hypertension (as a categorical variable, SUA/Cr ratio-2 vs. SUA/Cr ratio-1: odds ratio [OR], 1.68; 95% confidence interval [CI], 0.66-4.30; P = 0.275, SUA/Cr ratio-3 vs. SUA/Cr ratio-1: OR, 2.86; 95% CI, 1.08-7.60; P = 0.035, SUA/Cr ratio-4 vs. SUA/Cr ratio ratio-1: OR, 4.05; 95% CI, 1.32-12.5; P = 0.031, and SUA/Cr ratio ≥ 7.41 vs. SUA/Cr ratio < 7.41: OR, 2.25; 95% CI, 1.32-3.84; P = 0.003). Significant ORs were found for age < 65 years, women, and BMI <25 kg/m2, but no interactions were identified within each group.
Conclusions: These results suggest that the baseline SUA/Cr ratio could be an important predictor for the incidence of hypertension in Japanese community-dwelling persons.
背景:血清尿酸/肌酐(SUA/Cr)比值与高血压风险的相关性尚未得到很好的研究。本研究旨在探讨SUA/Cr比值是否为高血压的预测因子。方法:本队列研究招募了171名男性(64±11岁)和266名女性(65±10岁),在社区年度体检中进行调查。主要结局是存在高血压(抗高血压药物),收缩压(SBP)≥140 mmHg,舒张压(DBP)≥90 mmHg。结果:基线SUA/Cr比值仅与3年时男性(r = 0.217, P = 0.004)和女性(r = 0.126, P = 0.040)的舒张压(r = 0.103, P = 0.031)和舒张压(r = 0.15, P = 0.001)显著相关。SUA/Cr比值的预后临界值(≥7.41)在女性和所有参与者中都是相同的。多变量logistic回归显示,SUA/Cr比值与高血压显著相关(作为分类变量,SUA/Cr比值为2 vs. SUA/Cr比值为1:比值比[OR], 1.68;95%置信区间[CI], 0.66-4.30;P = 0.275, SUA/Cr ratio-3 vs. SUA/Cr ratio-1 OR为2.86;95% ci, 1.08-7.60;P = 0.035, SUA/Cr比值为4 vs. SUA/Cr比值为1:OR为4.05;95% ci, 1.32-12.5;P = 0.031, SUA/Cr比值≥7.41 vs. SUA/Cr比值< 7.41:OR, 2.25;95% ci, 1.32-3.84;P = 0.003)。在年龄< 65岁、女性和BMI 2中发现了显著的or,但在每组中没有发现相互作用。结论:这些结果表明基线SUA/Cr比值可能是日本社区居民高血压发病率的重要预测指标。
{"title":"High serum uric acid/creatinine ratio is a useful predictor of hypertension among Japanese community-dwelling persons.","authors":"Ryuichi Kawamoto, Kikuchi Asuka, Daisuke Ninomiya, Teru Kumagi, Masanori Abe","doi":"10.5646/ch.2025.31.e9","DOIUrl":"10.5646/ch.2025.31.e9","url":null,"abstract":"<p><strong>Background: </strong>The correlation between serum uric acid/creatinine (SUA/Cr) ratio and hypertension risk has not been well studied. This study aims to examine whether the SUA/Cr ratio is a predictor of hypertension.</p><p><strong>Methods: </strong>This cohort study comprised 171 men aged 64 ± 11 (mean ± standard deviation) years and 266 women aged 65 ± 10 years recruited for a survey at the community-based annual medical check-up. The main outcome was the presence of hypertension (antihypertensive medication) and having systolic blood pressure (SBP) ≥ 140 mmHg and diastolic blood pressure (DBP) ≥ 90 mmHg.</p><p><strong>Results: </strong>The baseline SUA/Cr ratio was significantly correlated only with DBP at 3 years in men (<i>r</i> = 0.217, <i>P</i> = 0.004) and women (<i>r</i> = 0.126, <i>P</i> = 0.040), and with both SBP (<i>r</i> = 0.103, <i>P</i> = 0.031) and DBP (<i>r</i> = 0.15, <i>P</i> = 0.001) in the overall participants of men and women. A plausible prognostic cut-off of SUA/Cr ratio (≥ 7.41) was found and was the same in women and in all participants. Multivariable logistic regressions showed that SUA/Cr ratio was significantly linked with hypertension (as a categorical variable, SUA/Cr ratio-2 vs. SUA/Cr ratio-1: odds ratio [OR], 1.68; 95% confidence interval [CI], 0.66-4.30; <i>P</i> = 0.275, SUA/Cr ratio-3 vs. SUA/Cr ratio-1: OR, 2.86; 95% CI, 1.08-7.60; <i>P</i> = 0.035, SUA/Cr ratio-4 vs. SUA/Cr ratio ratio-1: OR, 4.05; 95% CI, 1.32-12.5; <i>P</i> = 0.031, and SUA/Cr ratio ≥ 7.41 vs. SUA/Cr ratio < 7.41: OR, 2.25; 95% CI, 1.32-3.84; <i>P</i> = 0.003). Significant ORs were found for age < 65 years, women, and BMI <25 kg/m<sup>2</sup>, but no interactions were identified within each group.</p><p><strong>Conclusions: </strong>These results suggest that the baseline SUA/Cr ratio could be an important predictor for the incidence of hypertension in Japanese community-dwelling persons.</p>","PeriodicalId":10480,"journal":{"name":"Clinical Hypertension","volume":"31 ","pages":"e9"},"PeriodicalIF":2.6,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11903210/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143623860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: This cross-sectional study investigated the multi-stage and phenotype-specific association between urine-estimated salt intake and hypertension (HTN) in the Tehran Lipid and Glucose Study.
Methods: Adult participants (n = 1,782, mean age of 43.0 ± 13.7 years and 46.0% were men) were recruited (2015-2017) for 24-hour urine (24hU)-estimated salt intake and blood pressure (BP) measurements. Multivariable-adjusted multinomial logistic regression was used to estimate the association between 24hU-estimated salt intake (quintile categories and per each 1 g increment over recommended level) and HTN stages (Pre-HTN, stage 1 [S1-HTN], and stage 2 [S2-HTN]) and HTN phenotypes (isolated systolic HTN [ISH], isolated diastolic HTN [IDH], and systolic-diastolic HTN [SDH]).
Results: The prevalence of Pre-HTN, S1- and S2-HTN was 5.7%, 29.3%, and 9.1%, respectively. The prevalence of ISH, IDH, and SDH was 2.5%, 27.9%, and 8.0%, respectively. 24hU-estimated salt intake > 10.9 vs. < 6.7 g/day was associated with an elevated probability of Pre-HTN and S1-HTN, IDH, and SDH by 2.50, 1.65, 1.74, and 2.03-fold, respectively. Every 1 g-increment of salt intake over 5 g/day was associated with an increased chance of having Pre-HTN, S1-HTN, and IDH by 15%, 8%, and 8%, respectively.
Conclusions: The contribution of high salt intake to the development of HTN might be more pronounced during the initial stages of BP elevation, potentially impacting diastolic BP to a greater extent than systolic BP.
{"title":"The association between urine-estimated salt intake and hypertension: findings of a population-based study.","authors":"Zahra Bahadoran, Parvin Mirmiran, Asghar Ghasemi, Fereidoun Azizi","doi":"10.5646/ch.2025.31.e4","DOIUrl":"10.5646/ch.2025.31.e4","url":null,"abstract":"<p><strong>Background: </strong>This cross-sectional study investigated the multi-stage and phenotype-specific association between urine-estimated salt intake and hypertension (HTN) in the Tehran Lipid and Glucose Study.</p><p><strong>Methods: </strong>Adult participants (<i>n</i> = 1,782, mean age of 43.0 ± 13.7 years and 46.0% were men) were recruited (2015-2017) for 24-hour urine (24hU)-estimated salt intake and blood pressure (BP) measurements. Multivariable-adjusted multinomial logistic regression was used to estimate the association between 24hU-estimated salt intake (quintile categories and per each 1 g increment over recommended level) and HTN stages (Pre-HTN, stage 1 [S<sub>1</sub>-HTN], and stage 2 [S<sub>2</sub>-HTN]) and HTN phenotypes (isolated systolic HTN [ISH], isolated diastolic HTN [IDH], and systolic-diastolic HTN [SDH]).</p><p><strong>Results: </strong>The prevalence of Pre-HTN, S<sub>1</sub>- and S<sub>2</sub>-HTN was 5.7%, 29.3%, and 9.1%, respectively. The prevalence of ISH, IDH, and SDH was 2.5%, 27.9%, and 8.0%, respectively. 24hU-estimated salt intake > 10.9 vs. < 6.7 g/day was associated with an elevated probability of Pre-HTN and S<sub>1</sub>-HTN, IDH, and SDH by 2.50, 1.65, 1.74, and 2.03-fold, respectively. Every 1 g-increment of salt intake over 5 g/day was associated with an increased chance of having Pre-HTN, S<sub>1</sub>-HTN, and IDH by 15%, 8%, and 8%, respectively.</p><p><strong>Conclusions: </strong>The contribution of high salt intake to the development of HTN might be more pronounced during the initial stages of BP elevation, potentially impacting diastolic BP to a greater extent than systolic BP.</p>","PeriodicalId":10480,"journal":{"name":"Clinical Hypertension","volume":"31 ","pages":"e4"},"PeriodicalIF":2.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11800285/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143406137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: The aim of this study was to determine the association between low density lipoprotein cholesterol (LDL-C) and risks of stroke and mortality in the hypertensive patients with high risk of atherosclerotic cardiovascular disease (ASCVD).
Methods: A total of 19,507 hypertensive patients with high risk of ASCVD from the Kailuan cohort study were included in the present study. Patients were categorized into 5 groups by the levels of LDL-C: < 1.40 mmol/L (55 mg/dL), 1.40-1.79 mmol/L (55-69 mg/dL), 1.80-2.59 mmol/L (70-99 mg/dL), 2.60-3.39 mmol/L (100-130 mg/dL), and ≥ 3.40 mmol/L (131 mg/dL). The primary outcomes of this study included hemorrhagic stroke (HS), ischemic stroke (IS), and all-cause mortality. Cox proportional hazard models were used to calculate the hazard ratios (HRs) and 95% confidence intervals (CIs) of incident HS, IS, and all-cause mortality among hypertensive patients with high risk of ASCVD across LDL-C groups.
Results: During a median follow-up of 15.81 years, 3,055 cases of stroke (including 500 cases of HS and 2,555 cases of IS) and 5,340 cases of all-cause mortality were documented. Patients with LDL-C < 1.40 mmol/L had the highest incidences of HS and all-cause mortality among the 5 LDL-C groups. After adjusting for potential confounders, the HRs of HS, IS, and all-cause mortality were 1.34 (95% CI, 1.01-1.80), 1.08 (95% CI, 0.94-1.24), and 1.10 (95% CI, 1.01-1.21) for patients with LDL-C < 1.40 mmol/L compared with those with LDL-C 1.80-2.59 mmol/L. Similar results were generated across LDL-C groups with several sensitivity analyses.
Conclusions: LDL-C < 1.40 mmol/L was associated with increased risk of HS and all-cause mortality in hypertensive patients with high-risk of ASCVD.
{"title":"Association of LDL-C with stroke and all-cause mortality in hypertensive patients with high risk of ASCVD.","authors":"Shuang Guo, Chi Wang, Taoyu Hu, Lihua Lan, Zhen Ge, Jianxiang Huang, Shuohua Chen, Shouling Wu, Hao Xue","doi":"10.5646/ch.2025.31.e7","DOIUrl":"10.5646/ch.2025.31.e7","url":null,"abstract":"<p><strong>Background: </strong>The aim of this study was to determine the association between low density lipoprotein cholesterol (LDL-C) and risks of stroke and mortality in the hypertensive patients with high risk of atherosclerotic cardiovascular disease (ASCVD).</p><p><strong>Methods: </strong>A total of 19,507 hypertensive patients with high risk of ASCVD from the Kailuan cohort study were included in the present study. Patients were categorized into 5 groups by the levels of LDL-C: < 1.40 mmol/L (55 mg/dL), 1.40-1.79 mmol/L (55-69 mg/dL), 1.80-2.59 mmol/L (70-99 mg/dL), 2.60-3.39 mmol/L (100-130 mg/dL), and ≥ 3.40 mmol/L (131 mg/dL). The primary outcomes of this study included hemorrhagic stroke (HS), ischemic stroke (IS), and all-cause mortality. Cox proportional hazard models were used to calculate the hazard ratios (HRs) and 95% confidence intervals (CIs) of incident HS, IS, and all-cause mortality among hypertensive patients with high risk of ASCVD across LDL-C groups.</p><p><strong>Results: </strong>During a median follow-up of 15.81 years, 3,055 cases of stroke (including 500 cases of HS and 2,555 cases of IS) and 5,340 cases of all-cause mortality were documented. Patients with LDL-C < 1.40 mmol/L had the highest incidences of HS and all-cause mortality among the 5 LDL-C groups. After adjusting for potential confounders, the HRs of HS, IS, and all-cause mortality were 1.34 (95% CI, 1.01-1.80), 1.08 (95% CI, 0.94-1.24), and 1.10 (95% CI, 1.01-1.21) for patients with LDL-C < 1.40 mmol/L compared with those with LDL-C 1.80-2.59 mmol/L. Similar results were generated across LDL-C groups with several sensitivity analyses.</p><p><strong>Conclusions: </strong>LDL-C < 1.40 mmol/L was associated with increased risk of HS and all-cause mortality in hypertensive patients with high-risk of ASCVD.</p>","PeriodicalId":10480,"journal":{"name":"Clinical Hypertension","volume":"31 ","pages":"e7"},"PeriodicalIF":2.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11800280/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143406144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Although the association between C-reactive protein (CRP) and hypertension has been acknowledged, the associations between parental high-sensitive CRP (hs-CRP) levels and offspring hypertension remain unexplored. To investigate the relationship between parental and offspring hs-CRP levels, as well as the association between parental hs-CRP levels and offspring hypertension.
Methods: We included 6,848 father-offspring and 1,588 mother-offspring pairs from the Kailuan study. Time-weighted average hs-CRP (TWA-CRP) was calculated by cumulative hs-CRP/Timestart-end. Hypertension were defined as systolic blood pressure (BP) ≥ 140 mmHg and/or diastolic BP ≥ 90 mmHg. The generalized estimating equation model was used to explored the relationship between parental TWA-CRP and offspring TWA-CRP, and the association between parental TWA-CRP and offspring hypertension. The Cox proportional hazard model was applied to examine the relationship between offspring TWA-CRP and hypertension risk.
Results: The regression coefficient and 95% confidence intervals (CIs) for offspring TWA-CRP were 0.50 (0.38-0.62) in father-offspring pairs and 0.53 (0.29-0.76) in mother-offspring pairs with high parental TWA-CRP. The odds ratios (ORs) and 95% CIs for offspring hypertension were 1.30 (1.11-1.52) in father-offspring pairs and 1.32 (0.95-1.84) in mother-offspring pairs with high parental TWA-CRP. When both parent and offspring had a high TWA-CRP, the ORs (95% CIs) for offspring hypertension were 1.92 (1.43-2.56) in father-offspring pairs and 2.44 (1.35-4.35) in mother-offspring pairs. The hazard ratios and 95% CIs for offspring hypertension were 1.43 (1.15-1.76) in father-offspring pairs and 2.48 (1.18-5.22) in mother-offspring pairs with high offspring TWA-CRP.
Conclusions: Parental high TWA-CRP may increase the risk of offspring hypertension.
Trial registration: Chinese Clinical Trial Registry Identifier: ChiCTR2000029767.
{"title":"Association between parental high-sensitive C-reactive protein and hypertension in offspring: an intergenerational study.","authors":"Xuemei Yang, Feipeng Cui, Shuohua Chen, Guodong Wang, Shouling Wu, Liufu Cui","doi":"10.5646/ch.2025.31.e6","DOIUrl":"10.5646/ch.2025.31.e6","url":null,"abstract":"<p><strong>Background: </strong>Although the association between C-reactive protein (CRP) and hypertension has been acknowledged, the associations between parental high-sensitive CRP (hs-CRP) levels and offspring hypertension remain unexplored. To investigate the relationship between parental and offspring hs-CRP levels, as well as the association between parental hs-CRP levels and offspring hypertension.</p><p><strong>Methods: </strong>We included 6,848 father-offspring and 1,588 mother-offspring pairs from the Kailuan study. Time-weighted average hs-CRP (TWA-CRP) was calculated by cumulative hs-CRP/Time<sub>start-end</sub>. Hypertension were defined as systolic blood pressure (BP) ≥ 140 mmHg and/or diastolic BP ≥ 90 mmHg. The generalized estimating equation model was used to explored the relationship between parental TWA-CRP and offspring TWA-CRP, and the association between parental TWA-CRP and offspring hypertension. The Cox proportional hazard model was applied to examine the relationship between offspring TWA-CRP and hypertension risk.</p><p><strong>Results: </strong>The regression coefficient and 95% confidence intervals (CIs) for offspring TWA-CRP were 0.50 (0.38-0.62) in father-offspring pairs and 0.53 (0.29-0.76) in mother-offspring pairs with high parental TWA-CRP. The odds ratios (ORs) and 95% CIs for offspring hypertension were 1.30 (1.11-1.52) in father-offspring pairs and 1.32 (0.95-1.84) in mother-offspring pairs with high parental TWA-CRP. When both parent and offspring had a high TWA-CRP, the ORs (95% CIs) for offspring hypertension were 1.92 (1.43-2.56) in father-offspring pairs and 2.44 (1.35-4.35) in mother-offspring pairs. The hazard ratios and 95% CIs for offspring hypertension were 1.43 (1.15-1.76) in father-offspring pairs and 2.48 (1.18-5.22) in mother-offspring pairs with high offspring TWA-CRP.</p><p><strong>Conclusions: </strong>Parental high TWA-CRP may increase the risk of offspring hypertension.</p><p><strong>Trial registration: </strong>Chinese Clinical Trial Registry Identifier: ChiCTR2000029767.</p>","PeriodicalId":10480,"journal":{"name":"Clinical Hypertension","volume":"31 ","pages":"e6"},"PeriodicalIF":2.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11800284/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143406141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-02eCollection Date: 2025-01-01DOI: 10.5646/ch.2025.31.e3
Jaehyun Kong, Seokjun Kim, Yejun Son, Soeun Kim, Wonwoo Jang, Yesol Yim, Hyeon Jin Kim, Hyesu Jo, Jaeyu Park, Kyeongmin Lee, Hayeon Lee, Damiano Pizzol, Jiseung Kang, Selin Woo, Jiyoung Hwang, Dong Keon Yon
Background: Hypertension, a significant risk factor for global public health, is well-known to be preventable and manageable through physical activity (PA). However, many studies suggest that excessive PA may not provide additional benefits. Thus, we aimed to conduct a quantitative analysis of the relationship between hypertension and PA levels.
Methods: This study analyzed the association between PA and hypertension using data from 2,429,588 South Korean adults aged 30 years and older from the Korean Community Health Survey conducted from 2009 to 2022. We used weighted binary logistic regression and generalized additive models to examine the relationship, adjusting for various sociodemographic factors. PA was categorized into moderate-intensity PA (MPA) and vigorous-intensity PA (VPA) based on World Health Organization guidelines to study the association between hypertension and PA intensity.
Results: The greatest reduction in hypertension risk was associated with 1,090 metabolic equivalent of task (MET) minutes per week, with no additional reduction beyond this point. Additionally, MPA (odds ratio [OR], 0.92; 95% confidence interval [CI], 0.90-0.93) had a stronger association with reducing hypertension risk compared to VPA (OR, 0.95; 95% CI, 0.94-0.97) at higher levels of PA (> 1,800 MET minutes per week). Subgroup analyses showed that older age, lower education level, and lower income were associated with greater reductions in hypertension risk at the same PA levels.
Conclusions: Moderate amounts of PA are associated with a lower risk of hypertension, but additional activity beyond this may not provide further benefits. With a high amount of PA, MPA is more effective than VPA in reducing hypertension risk. Since the effectiveness of PA in preventing hypertension varies across different sociodemographic factors, appropriate policies tailored to specific groups are necessary.
{"title":"Dose-response association between physical activity and diagnosed hypertension in 2.4 million Korean population: Korea Community Health Survey 2009-2022.","authors":"Jaehyun Kong, Seokjun Kim, Yejun Son, Soeun Kim, Wonwoo Jang, Yesol Yim, Hyeon Jin Kim, Hyesu Jo, Jaeyu Park, Kyeongmin Lee, Hayeon Lee, Damiano Pizzol, Jiseung Kang, Selin Woo, Jiyoung Hwang, Dong Keon Yon","doi":"10.5646/ch.2025.31.e3","DOIUrl":"10.5646/ch.2025.31.e3","url":null,"abstract":"<p><strong>Background: </strong>Hypertension, a significant risk factor for global public health, is well-known to be preventable and manageable through physical activity (PA). However, many studies suggest that excessive PA may not provide additional benefits. Thus, we aimed to conduct a quantitative analysis of the relationship between hypertension and PA levels.</p><p><strong>Methods: </strong>This study analyzed the association between PA and hypertension using data from 2,429,588 South Korean adults aged 30 years and older from the Korean Community Health Survey conducted from 2009 to 2022. We used weighted binary logistic regression and generalized additive models to examine the relationship, adjusting for various sociodemographic factors. PA was categorized into moderate-intensity PA (MPA) and vigorous-intensity PA (VPA) based on World Health Organization guidelines to study the association between hypertension and PA intensity.</p><p><strong>Results: </strong>The greatest reduction in hypertension risk was associated with 1,090 metabolic equivalent of task (MET) minutes per week, with no additional reduction beyond this point. Additionally, MPA (odds ratio [OR], 0.92; 95% confidence interval [CI], 0.90-0.93) had a stronger association with reducing hypertension risk compared to VPA (OR, 0.95; 95% CI, 0.94-0.97) at higher levels of PA (> 1,800 MET minutes per week). Subgroup analyses showed that older age, lower education level, and lower income were associated with greater reductions in hypertension risk at the same PA levels.</p><p><strong>Conclusions: </strong>Moderate amounts of PA are associated with a lower risk of hypertension, but additional activity beyond this may not provide further benefits. With a high amount of PA, MPA is more effective than VPA in reducing hypertension risk. Since the effectiveness of PA in preventing hypertension varies across different sociodemographic factors, appropriate policies tailored to specific groups are necessary.</p>","PeriodicalId":10480,"journal":{"name":"Clinical Hypertension","volume":"31 ","pages":"e3"},"PeriodicalIF":2.6,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11800283/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143406158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-02eCollection Date: 2025-01-01DOI: 10.5646/ch.2025.31.e1
Ja-Yeon Lee, Sun Hwa Lee
Hypertensive disorders of pregnancy (HDPs) are the leading cause of global maternal mortality and morbidity. Moreover, HDP is associated with an increased risk of cardiovascular disease later in the lives of affected women. The prevalence of hypertension during pregnancy is expected to increase as women's age at first pregnancy rises, as does the prevalence of cardiovascular comorbidities such as obesity, maternal diabetes, and hypertension. Due to a lack of data, there has been controversy over the optimal treatment for HDP. The purpose of this review is to address the management of HDP in pregnant women before, during, and after pregnancy as well as its definition and pathophysiology, including recent trials and updated guidelines.
{"title":"Hypertensive disorders of pregnancy: advances in understanding and management.","authors":"Ja-Yeon Lee, Sun Hwa Lee","doi":"10.5646/ch.2025.31.e1","DOIUrl":"10.5646/ch.2025.31.e1","url":null,"abstract":"<p><p>Hypertensive disorders of pregnancy (HDPs) are the leading cause of global maternal mortality and morbidity. Moreover, HDP is associated with an increased risk of cardiovascular disease later in the lives of affected women. The prevalence of hypertension during pregnancy is expected to increase as women's age at first pregnancy rises, as does the prevalence of cardiovascular comorbidities such as obesity, maternal diabetes, and hypertension. Due to a lack of data, there has been controversy over the optimal treatment for HDP. The purpose of this review is to address the management of HDP in pregnant women before, during, and after pregnancy as well as its definition and pathophysiology, including recent trials and updated guidelines.</p>","PeriodicalId":10480,"journal":{"name":"Clinical Hypertension","volume":"31 ","pages":"e1"},"PeriodicalIF":2.6,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11800281/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143406117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-02eCollection Date: 2025-01-01DOI: 10.5646/ch.2025.31.e5
Yoonsun Won, Jina Yeo, Youngwoo Jang, Joohan Kim, Taeil Yang, Jihye Yoon, Kyung-Jin Ahn, Minsu Kim, Wook-Jin Chung
Background: This study aimed to evaluate the progress of treatment with intensive targeted therapy in high-risk pulmonary arterial hypertension (PAH) patients and focused on setting an appropriate hemodynamic target of pulmonary vascular resistance (PVR) ≤4 Wood units (WU) and mean pulmonary arterial pressure (mPAP) ≤ 40 mmHg.
Methods: We retrospectively evaluated high-risk PAH patients who were administered treprostinil at a single tertiary pulmonary hypertension center between January 2020 and December 2022. Echocardiography, right heart catheterization, 6-minute walk distance (6MWD), and blood tests were obtained 6 and 12 months after the initiation of parenteral treprostinil administration.
Results: Twelve patients (1 male and 11 female; median age, 47.0 years [interquartile range, 33.8-49.8 years]) were included. Five of the 12 patients had 6- and 12-month follow-up data. The median PVR decreased by 22.9% at 6 months and 50.6% at 12 months compared to baseline. The median mPAP decreased by 24.6% at 6 months and 29.8% at 12 months. Importantly, the 6MWD showed a significant improvement of 55.7%, and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels demonstrated a notable decrease of 16.0%, reflecting substantial enhancements in patients' functional status and heart health. Three of these 5 patients reached the hemodynamic target by 12 months and successfully transitioned from parenteral treprostinil to oral selexipag.
Conclusions: This study showed that 3 of 5 patients (60.0%) with high-risk PAH reached PVR ≤ 4 WU and/or mPAP ≤ 40 mmHg by receiving intensive parenteral treprostinil therapy with significant improvements in 6MWD and NT-proBNP levels, and successfully transitioned to oral selexipag. We proposed that transition strategies from parenteral treprostinil to selexipag aiming at hemodynamic targets.
背景:本研究旨在评价高危肺动脉高压(PAH)患者强化靶向治疗的进展,重点探讨肺动脉阻力(PVR)≤4 Wood units (WU)、平均肺动脉压(mPAP)≤40 mmHg的血流动力学指标。方法:我们回顾性评估了2020年1月至2022年12月在单一三期肺动脉高压中心接受曲前列地尼治疗的高风险PAH患者。超声心动图、右心导管、6分钟步行距离(6MWD)和血液检查在静脉注射曲前列替尼6和12个月后进行。结果:12例患者(男1例,女11例;中位年龄为47.0岁(四分位数间距为33.8-49.8岁)。12例患者中有5例有6个月和12个月的随访数据。与基线相比,中位PVR在6个月时下降22.9%,在12个月时下降50.6%。中位mPAP在6个月时下降24.6%,在12个月时下降29.8%。重要的是,6MWD显著改善55.7%,n端前脑利钠肽(NT-proBNP)水平显著降低16.0%,反映了患者功能状态和心脏健康的显著改善。这5例患者中有3例在12个月时达到血流动力学目标,并成功地从静脉注射曲前列汀过渡到口服selexipag。结论:本研究显示,5例高危PAH患者中有3例(60.0%)接受强化肠外treprostinil治疗后PVR≤4wu和/或mPAP≤40mmhg, 6MWD和NT-proBNP水平均有显著改善,并成功过渡到口服selexipag。我们提出了从静脉注射曲前列司尼到针对血流动力学目标的selexipag的过渡策略。
{"title":"Transition from parenteral treprostinil to selexipag aiming at hemodynamic targets in pulmonary arterial hypertension.","authors":"Yoonsun Won, Jina Yeo, Youngwoo Jang, Joohan Kim, Taeil Yang, Jihye Yoon, Kyung-Jin Ahn, Minsu Kim, Wook-Jin Chung","doi":"10.5646/ch.2025.31.e5","DOIUrl":"10.5646/ch.2025.31.e5","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to evaluate the progress of treatment with intensive targeted therapy in high-risk pulmonary arterial hypertension (PAH) patients and focused on setting an appropriate hemodynamic target of pulmonary vascular resistance (PVR) ≤4 Wood units (WU) and mean pulmonary arterial pressure (mPAP) ≤ 40 mmHg.</p><p><strong>Methods: </strong>We retrospectively evaluated high-risk PAH patients who were administered treprostinil at a single tertiary pulmonary hypertension center between January 2020 and December 2022. Echocardiography, right heart catheterization, 6-minute walk distance (6MWD), and blood tests were obtained 6 and 12 months after the initiation of parenteral treprostinil administration.</p><p><strong>Results: </strong>Twelve patients (1 male and 11 female; median age, 47.0 years [interquartile range, 33.8-49.8 years]) were included. Five of the 12 patients had 6- and 12-month follow-up data. The median PVR decreased by 22.9% at 6 months and 50.6% at 12 months compared to baseline. The median mPAP decreased by 24.6% at 6 months and 29.8% at 12 months. Importantly, the 6MWD showed a significant improvement of 55.7%, and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels demonstrated a notable decrease of 16.0%, reflecting substantial enhancements in patients' functional status and heart health. Three of these 5 patients reached the hemodynamic target by 12 months and successfully transitioned from parenteral treprostinil to oral selexipag.</p><p><strong>Conclusions: </strong>This study showed that 3 of 5 patients (60.0%) with high-risk PAH reached PVR ≤ 4 WU and/or mPAP ≤ 40 mmHg by receiving intensive parenteral treprostinil therapy with significant improvements in 6MWD and NT-proBNP levels, and successfully transitioned to oral selexipag. We proposed that transition strategies from parenteral treprostinil to selexipag aiming at hemodynamic targets.</p>","PeriodicalId":10480,"journal":{"name":"Clinical Hypertension","volume":"31 ","pages":"e5"},"PeriodicalIF":2.6,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11800282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143406162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-02eCollection Date: 2025-01-01DOI: 10.5646/ch.2025.31.e2
Tue T Te, Constance H Fung, Mary Regina Boland
Background: Our study investigates the temporality of factors that modulate the risk for developing hypertension (HTN) among patients with obstructive sleep apnea (OSA) without preexisting HTN at baseline.
Methods: Our cohort consisted of OSA cases (based on International Classification of Diseases, 9th/10th Revision) with 20 common comorbidities selected using a previously validated electronic health record (EHR)-based algorithm. We constructed a survival model to estimate time-to-first HTN diagnosis (among patients with OSA without preexisting HTN). Our survival model included those comorbidities along with sex, body mass index, race, and age. We also performed a validation of the date of diagnosis of OSA and HTN identified from our algorithm by utilizing chart reviews in 400 randomly chosen EHR-defined cases.
Results: Among 53,035 OSA cases diagnosed between 2012 and 2021, 31,741 cases (59.8%) were without preexisting HTN at the date of OSA diagnosis and thus met our inclusion criteria. Within our survival cohort, 15,830 OSA cases (50.1%) did not develop HTN. Cardiovascular conditions (including atrial fibrillation, coronary atherosclerosis, hypercholesterolemia, diabetes), tobacco use, anemia, osteoarthrosis, and gastroesophageal reflux disease were observed to increase risk of incident HTN. Allergic rhinitis, fatigue, joint pain, and vitamin D deficiency did not increase risk of incident HTN. Chart review demonstrated diagnoses of OSA and HTN were documented in notes a median of 38 days and 738 days, respectively, prior to being coded in the EHR.
Conclusions: In a large EHR sample, we identified conditions that are associated with increased risk of incident HTN among patients diagnosed with OSA. These findings may help guide counseling efforts among patients newly diagnosed with OSA regarding factors that may modulate risk for developing HTN.
{"title":"Comorbidities that modulate temporal risk for incident hypertension among patients with obstructive sleep apnea.","authors":"Tue T Te, Constance H Fung, Mary Regina Boland","doi":"10.5646/ch.2025.31.e2","DOIUrl":"10.5646/ch.2025.31.e2","url":null,"abstract":"<p><strong>Background: </strong>Our study investigates the temporality of factors that modulate the risk for developing hypertension (HTN) among patients with obstructive sleep apnea (OSA) without preexisting HTN at baseline.</p><p><strong>Methods: </strong>Our cohort consisted of OSA cases (based on International Classification of Diseases, 9th/10th Revision) with 20 common comorbidities selected using a previously validated electronic health record (EHR)-based algorithm. We constructed a survival model to estimate time-to-first HTN diagnosis (among patients with OSA without preexisting HTN). Our survival model included those comorbidities along with sex, body mass index, race, and age. We also performed a validation of the date of diagnosis of OSA and HTN identified from our algorithm by utilizing chart reviews in 400 randomly chosen EHR-defined cases.</p><p><strong>Results: </strong>Among 53,035 OSA cases diagnosed between 2012 and 2021, 31,741 cases (59.8%) were without preexisting HTN at the date of OSA diagnosis and thus met our inclusion criteria. Within our survival cohort, 15,830 OSA cases (50.1%) did not develop HTN. Cardiovascular conditions (including atrial fibrillation, coronary atherosclerosis, hypercholesterolemia, diabetes), tobacco use, anemia, osteoarthrosis, and gastroesophageal reflux disease were observed to increase risk of incident HTN. Allergic rhinitis, fatigue, joint pain, and vitamin D deficiency did not increase risk of incident HTN. Chart review demonstrated diagnoses of OSA and HTN were documented in notes a median of 38 days and 738 days, respectively, prior to being coded in the EHR.</p><p><strong>Conclusions: </strong>In a large EHR sample, we identified conditions that are associated with increased risk of incident HTN among patients diagnosed with OSA. These findings may help guide counseling efforts among patients newly diagnosed with OSA regarding factors that may modulate risk for developing HTN.</p>","PeriodicalId":10480,"journal":{"name":"Clinical Hypertension","volume":"31 ","pages":"e2"},"PeriodicalIF":2.6,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11800288/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143406148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01DOI: 10.1186/s40885-024-00294-5
Richa Awasthi, Priyanka Thapa Manger, Rajesh Kumar Khare, Roshan Alam
Background: Essential hypertension is a most prevalent global health concern. Despite extensive research, the exact mechanisms contributing to essential hypertension remain unclear. Several factors contribute to the pathogenesis of essential hypertension. Klotho, a membrane-bound and soluble protein, has been found to modulate hypertension through physiological processes like vascular function and sodium balance. This study aimed to determine the association of klotho protein with essential hypertension.
Methods: The study included 164 hypertensive cases and 164 normotensive controls, after imposing certain inclusion and exclusion criteria with written consent from all subjects. Subject's details were obtained using structured proforma to account for potential confounding variables. To estimate klotho protein activity using sandwich enzyme-linked immunosorbent assay, 2 mL blood was collected in a plain vial. All data were tested at a 5% significance level.
Results: The analysis revealed a significant decrease in klotho protein levels in cases compared to controls (1.52 ± 0.87 vs. 2.45 ± 0.90, P < 0.001), suggesting an inverse relationship of klotho protein with risk of essential hypertension. All indices in the structural equation model have suggested that the final model fitted the data reasonably (chi-square to df ratio, 1.153; goodness of fit index, 0.990; adjusted goodness of fit index, 0.945; normed fit index, 0.936; standardized root mean square residual, 0.953; root mean square error of approximation, 0.031). Also, klotho was negatively associated with blood pressure. The area under the receiver operating characteristic curve for klotho and blood pressure was 0.765 (95% confidence interval, 0.716-0.815; P < 0.001).
Conclusions: Klotho levels were significantly reduced in essential hypertension cases compared to controls, Also, klotho had a negative direct association with essential hypertension indicating a potential role for klotho as a prognostic and predictive marker for essential hypertension. This suggests that klotho may have a role in the pathogenesis of essential hypertension. Understanding klotho's role in essential hypertension may lead to the development of novel therapeutic strategies for this disease.
{"title":"Klotho protein: a new insight into the pathogenesis of essential hypertension.","authors":"Richa Awasthi, Priyanka Thapa Manger, Rajesh Kumar Khare, Roshan Alam","doi":"10.1186/s40885-024-00294-5","DOIUrl":"https://doi.org/10.1186/s40885-024-00294-5","url":null,"abstract":"<p><strong>Background: </strong>Essential hypertension is a most prevalent global health concern. Despite extensive research, the exact mechanisms contributing to essential hypertension remain unclear. Several factors contribute to the pathogenesis of essential hypertension. Klotho, a membrane-bound and soluble protein, has been found to modulate hypertension through physiological processes like vascular function and sodium balance. This study aimed to determine the association of klotho protein with essential hypertension.</p><p><strong>Methods: </strong>The study included 164 hypertensive cases and 164 normotensive controls, after imposing certain inclusion and exclusion criteria with written consent from all subjects. Subject's details were obtained using structured proforma to account for potential confounding variables. To estimate klotho protein activity using sandwich enzyme-linked immunosorbent assay, 2 mL blood was collected in a plain vial. All data were tested at a 5% significance level.</p><p><strong>Results: </strong>The analysis revealed a significant decrease in klotho protein levels in cases compared to controls (1.52 ± 0.87 vs. 2.45 ± 0.90, P < 0.001), suggesting an inverse relationship of klotho protein with risk of essential hypertension. All indices in the structural equation model have suggested that the final model fitted the data reasonably (chi-square to df ratio, 1.153; goodness of fit index, 0.990; adjusted goodness of fit index, 0.945; normed fit index, 0.936; standardized root mean square residual, 0.953; root mean square error of approximation, 0.031). Also, klotho was negatively associated with blood pressure. The area under the receiver operating characteristic curve for klotho and blood pressure was 0.765 (95% confidence interval, 0.716-0.815; P < 0.001).</p><p><strong>Conclusions: </strong>Klotho levels were significantly reduced in essential hypertension cases compared to controls, Also, klotho had a negative direct association with essential hypertension indicating a potential role for klotho as a prognostic and predictive marker for essential hypertension. This suggests that klotho may have a role in the pathogenesis of essential hypertension. Understanding klotho's role in essential hypertension may lead to the development of novel therapeutic strategies for this disease.</p>","PeriodicalId":10480,"journal":{"name":"Clinical Hypertension","volume":"30 1","pages":"36"},"PeriodicalIF":2.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11608492/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142766899","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}