Hypertension is one component of metabolic syndrome (MetS). Here, the study evaluated hypertension-associated metabolites in relation to other MetS components. Fasting plasma samples were collected from 22 hypertensive and 63 normotensive subjects for non-targeted metabolomics. Compared with normotensive subjects, hypertensive patients were more diabetic (6.3% vs. 36.4%) and had dyslipidemia (27.0% vs. 63.6%) (both p < .05). By non-targeted metabolomics, 758 metabolites in 22 classes were identified and 56 were differentially regulated between hypertensive and normotensive groups. Amongst these 56 metabolites, receiver operating characteristic analysis showed that 14 had an area under the curve above 0.6. Multivariate-adjusted logistic regression analysis demonstrated that per one-fold increase of L-glutmatic acid, L-cystine, (9S,10E,12Z,15Z)-9-Hydroxy-10,12,15-octadecatrienoic acid, deoxyribose 5-phosphate, and falcarinolone, the odds ratios were 3.64, 4.61, 0.26, 0.26, and 0.37 for having the risk of hypertension, respectively. Of five metabolites, by Spearman's correlation analysis, only L-glutmatic acid and L-cystine levels were positively associated with systolic and diastolic blood pressure (all p < .05). Spearman's correlation analysis further revealed that L-glutmatic acid levels were positively correlated with to body mass index (BMI), fasting blood glucose, and serum triglyceride but negatively associated with HDL-c (all p < .05) whereas L-cystine levels were not related to any of these components (p ≥ .13). Multivariate-adjusted linear regression analysis confirmed the positive correlation between L-cystine levels and systolic or diastolic blood pressure (β = 2.66 for SBP; β = 2.50 for DBP; both p < .05). In conclusion, L-cystine could be a potent metabolite for increased risk of hypertension.
{"title":"Blood L-cystine levels positively related to increased risk of hypertension.","authors":"Haijun Chen, Yalan Deng, Hailing Zhou, Wenzhong Wu, Jinhua Bao, Deyou Cao, Yuze Li, Yingmei Feng","doi":"10.1111/jch.14902","DOIUrl":"https://doi.org/10.1111/jch.14902","url":null,"abstract":"<p><p>Hypertension is one component of metabolic syndrome (MetS). Here, the study evaluated hypertension-associated metabolites in relation to other MetS components. Fasting plasma samples were collected from 22 hypertensive and 63 normotensive subjects for non-targeted metabolomics. Compared with normotensive subjects, hypertensive patients were more diabetic (6.3% vs. 36.4%) and had dyslipidemia (27.0% vs. 63.6%) (both p < .05). By non-targeted metabolomics, 758 metabolites in 22 classes were identified and 56 were differentially regulated between hypertensive and normotensive groups. Amongst these 56 metabolites, receiver operating characteristic analysis showed that 14 had an area under the curve above 0.6. Multivariate-adjusted logistic regression analysis demonstrated that per one-fold increase of L-glutmatic acid, L-cystine, (9S,10E,12Z,15Z)-9-Hydroxy-10,12,15-octadecatrienoic acid, deoxyribose 5-phosphate, and falcarinolone, the odds ratios were 3.64, 4.61, 0.26, 0.26, and 0.37 for having the risk of hypertension, respectively. Of five metabolites, by Spearman's correlation analysis, only L-glutmatic acid and L-cystine levels were positively associated with systolic and diastolic blood pressure (all p < .05). Spearman's correlation analysis further revealed that L-glutmatic acid levels were positively correlated with to body mass index (BMI), fasting blood glucose, and serum triglyceride but negatively associated with HDL-c (all p < .05) whereas L-cystine levels were not related to any of these components (p ≥ .13). Multivariate-adjusted linear regression analysis confirmed the positive correlation between L-cystine levels and systolic or diastolic blood pressure (β = 2.66 for SBP; β = 2.50 for DBP; both p < .05). In conclusion, L-cystine could be a potent metabolite for increased risk of hypertension.</p>","PeriodicalId":50237,"journal":{"name":"Journal of Clinical Hypertension","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142479537","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}
Taotao Wei, Xin Lin, Jie Ma, Luosha Wang, Jing Su, Jing Yu
The weight-adjusted-waist index (WWI) is an innovative measure of obesity that appears to surpass body mass index (BMI) in assessing lean body mass and fat mass. This study aimed to evaluate the relationship between WWI and AS in hypertensive adults in the United States. The study included 9753 adults diagnosed with hypertension from the National Health and Nutrition Examination Survey (NHANES), which spanned the years 2007-2016. WWI was calculated by dividing waist circumference (in cm) by the square root of body weight (in kg), and arterial stiffness (represented by estimated pulse wave velocity [ePWV]) was analyzed as the outcome. Weighted multiple linear regression and smooth curve fitting were used to test for linear and nonlinear associations. Threshold effects were determined using a two-part linear regression model. Additionally, subgroup analyses and interaction tests were conducted to gain a more in-depth understanding of the observed associations. The mean WWI of the participants was 11.32 ± 0.76. After multivariable adjustment, WWI showed a significant nonlinear association with ePWV, with a U-shaped association observed between the two. Specifically, WWI below the threshold of 10.23 was negatively associated with arterial stiffness (β = -0.39, 95% CI: -0.54 to -0.25), while WWI above the threshold of 10.23 was positively associated with arterial stiffness (β = 0.04, 95% CI: 0.01-0.07). To conclude, the present findings imply that maintaining WWI within an optimal range could reduce AS in hypertensive individuals and potentially decrease cardiovascular risk. However, this observation needs to be confirmed in large clinical trials.
{"title":"U-shaped Association Between Weight-Adjusted-Waist Index and Arterial Stiffness Among Adult Hypertensive Patients: A Population-Based Study in the United States.","authors":"Taotao Wei, Xin Lin, Jie Ma, Luosha Wang, Jing Su, Jing Yu","doi":"10.1111/jch.14914","DOIUrl":"https://doi.org/10.1111/jch.14914","url":null,"abstract":"<p><p>The weight-adjusted-waist index (WWI) is an innovative measure of obesity that appears to surpass body mass index (BMI) in assessing lean body mass and fat mass. This study aimed to evaluate the relationship between WWI and AS in hypertensive adults in the United States. The study included 9753 adults diagnosed with hypertension from the National Health and Nutrition Examination Survey (NHANES), which spanned the years 2007-2016. WWI was calculated by dividing waist circumference (in cm) by the square root of body weight (in kg), and arterial stiffness (represented by estimated pulse wave velocity [ePWV]) was analyzed as the outcome. Weighted multiple linear regression and smooth curve fitting were used to test for linear and nonlinear associations. Threshold effects were determined using a two-part linear regression model. Additionally, subgroup analyses and interaction tests were conducted to gain a more in-depth understanding of the observed associations. The mean WWI of the participants was 11.32 ± 0.76. After multivariable adjustment, WWI showed a significant nonlinear association with ePWV, with a U-shaped association observed between the two. Specifically, WWI below the threshold of 10.23 was negatively associated with arterial stiffness (β = -0.39, 95% CI: -0.54 to -0.25), while WWI above the threshold of 10.23 was positively associated with arterial stiffness (β = 0.04, 95% CI: 0.01-0.07). To conclude, the present findings imply that maintaining WWI within an optimal range could reduce AS in hypertensive individuals and potentially decrease cardiovascular risk. However, this observation needs to be confirmed in large clinical trials.</p>","PeriodicalId":50237,"journal":{"name":"Journal of Clinical Hypertension","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142479539","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}
This study aimed to examine the association between the triglyceride-glucose (TyG) index and chronic kidney disease (CKD) in normotensive adults with hypertension and further investigate potential effect modifiers of this association. A total of 7975 normoweight hypertensive participants were enrolled from the Chinese H-type hypertension registry (CHHRS) cohort. The TyG index was calculated using the formula: ln (fasting triglyceride [mg/dL] × fasting plasma glucose [mg/dL])/2. CKD was defined as an estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m2 of body surface area. Multivariate logistic regression analysis revealed a 50% increased risk of CKD (OR: 1.50, 95% CI: 1.26-1.79) for each unit increase in the TyG index. A linear dose-response relationship between the TyG index and CKD risk was observed using restricted cubic spline analysis. Compared to the first quartile of the TyG index, the fourth quartile showed a significantly higher risk of CKD (OR: 1.88; 95% CI: 1.41-2.50). Subgroup analysis identified a stronger association between the TyG index and CKD risk in males and individuals with a history of alcohol consumption (all p values for interaction < 0.05). In conclusions, the TyG index was significantly associated with an increased risk of CKD in normoweight adults with hypertension, particularly in males and those with a history of alcohol consumption.
{"title":"Association Between Triglyceride Glucose Index and Chronic Kidney Disease in Normal-Weight Chinese Adults With Hypertension.","authors":"Chao Yu, Wei Zhou, Xinlei Zhou, Lingjuan Zhu, Tao Wang, Huihui Bao, Xiaoshu Cheng","doi":"10.1111/jch.14913","DOIUrl":"https://doi.org/10.1111/jch.14913","url":null,"abstract":"<p><p>This study aimed to examine the association between the triglyceride-glucose (TyG) index and chronic kidney disease (CKD) in normotensive adults with hypertension and further investigate potential effect modifiers of this association. A total of 7975 normoweight hypertensive participants were enrolled from the Chinese H-type hypertension registry (CHHRS) cohort. The TyG index was calculated using the formula: ln (fasting triglyceride [mg/dL] × fasting plasma glucose [mg/dL])/2. CKD was defined as an estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m<sup>2</sup> of body surface area. Multivariate logistic regression analysis revealed a 50% increased risk of CKD (OR: 1.50, 95% CI: 1.26-1.79) for each unit increase in the TyG index. A linear dose-response relationship between the TyG index and CKD risk was observed using restricted cubic spline analysis. Compared to the first quartile of the TyG index, the fourth quartile showed a significantly higher risk of CKD (OR: 1.88; 95% CI: 1.41-2.50). Subgroup analysis identified a stronger association between the TyG index and CKD risk in males and individuals with a history of alcohol consumption (all p values for interaction < 0.05). In conclusions, the TyG index was significantly associated with an increased risk of CKD in normoweight adults with hypertension, particularly in males and those with a history of alcohol consumption.</p>","PeriodicalId":50237,"journal":{"name":"Journal of Clinical Hypertension","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142479604","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}
Although observational studies have linked primary aldosteronism (PA) with cardiovascular diseases (CVDs), the causality remains uncertain. In this study, we aimed to investigate whether PA is causally associated with CVD risk and cardiac magnetic resonance (CMR) parameters using the Mendelian randomization (MR) method. Independent and genome-wide significant single nucleotide polymorphisms for PA were extracted from genome-wide association study (GWAS) summary statistics. Genetic associations with the CVDs and CMR parameters were obtained from recent large-scale GWASs or genetic consortia. Inverse-variance weighted (IVW) method was utilized for the preliminary estimates, and multiple sensitivity analyses (including weighted median, Cochran's Q test, MR-Egger, MR-PRESSO, and leave-one-out analysis) were conducted to verify the robustness of the results. The MR analyses using the IVW method showed that genetically predicated PA was significantly associated with atrial fibrillation (OR = 1.046, 95% CI: 1.029–1.062, padj < 0.001), myocardial infarction (OR = 1.029, 95% CI: 1.005–1.053, padj = 0.027), heart failure (OR = 1.023, 95% CI: 1.004–1.042, padj = 0.027), any stroke (OR = 1.062, 95% CI: 1.031–1.095, padj < 0.001), any ischemic stroke (OR = 1.058, 95% CI: 1.022–1.095, padj = 0.004), and small vessel stroke (OR = 1.116, 95% CI: 1.041–1.196, padj = 0.004). Notably, PA also had a causal effect on adverse cardiac remodeling, including larger ventricular and atrial volumes, higher ventricular stroke volume, and reduced left atrial emptying fraction. Our findings support a causal role of PA in higher cardiovascular disease risk and adverse cardiac remodeling. Given the diagnostic delay and disease burden in PA, more attention should be paid to the screening and treatment of PA to reduce the incidence of cardiovascular outcomes.
尽管观察性研究发现原发性醛固酮增多症（PA）与心血管疾病（CVDs）有关，但其因果关系仍不确定。在本研究中，我们旨在利用孟德尔随机化（MR）方法研究 PA 是否与心血管疾病风险和心脏磁共振（CMR）参数存在因果关系。我们从全基因组关联研究（GWAS）的汇总统计中提取了与 PA 相关的独立的、全基因组意义重大的单核苷酸多态性。与心血管疾病和CMR参数相关的基因则来自近期的大规模GWAS或基因联盟。初步估计采用了逆方差加权（IVW）法，并进行了多种敏感性分析（包括加权中位数、Cochran's Q 检验、MR-Egger、MR-PRESSO 和 leave-one-out 分析）以验证结果的稳健性。使用 IVW 方法进行的 MR 分析表明，基因预测 PA 与心房颤动有显著相关性（OR = 1.046，95% CI：1.029-1.062，padj
{"title":"Primary Aldosteronism Influences Cardiac Structure, Function, and Disease Risk: Evidence From Mendelian Randomization Analysis","authors":"Rui Shen, Chengliang Pan, Jian Yu, Chen Dong, Zhiyang Li, Jiangmei Zhang, Qian Dong, Kunwu Yu, Qiutang Zeng","doi":"10.1111/jch.14912","DOIUrl":"10.1111/jch.14912","url":null,"abstract":"<p>Although observational studies have linked primary aldosteronism (PA) with cardiovascular diseases (CVDs), the causality remains uncertain. In this study, we aimed to investigate whether PA is causally associated with CVD risk and cardiac magnetic resonance (CMR) parameters using the Mendelian randomization (MR) method. Independent and genome-wide significant single nucleotide polymorphisms for PA were extracted from genome-wide association study (GWAS) summary statistics. Genetic associations with the CVDs and CMR parameters were obtained from recent large-scale GWASs or genetic consortia. Inverse-variance weighted (IVW) method was utilized for the preliminary estimates, and multiple sensitivity analyses (including weighted median, Cochran's Q test, MR-Egger, MR-PRESSO, and leave-one-out analysis) were conducted to verify the robustness of the results. The MR analyses using the IVW method showed that genetically predicated PA was significantly associated with atrial fibrillation (OR = 1.046, 95% CI: 1.029–1.062, padj < 0.001), myocardial infarction (OR = 1.029, 95% CI: 1.005–1.053, padj = 0.027), heart failure (OR = 1.023, 95% CI: 1.004–1.042, padj = 0.027), any stroke (OR = 1.062, 95% CI: 1.031–1.095, padj < 0.001), any ischemic stroke (OR = 1.058, 95% CI: 1.022–1.095, padj = 0.004), and small vessel stroke (OR = 1.116, 95% CI: 1.041–1.196, padj = 0.004). Notably, PA also had a causal effect on adverse cardiac remodeling, including larger ventricular and atrial volumes, higher ventricular stroke volume, and reduced left atrial emptying fraction. Our findings support a causal role of PA in higher cardiovascular disease risk and adverse cardiac remodeling. Given the diagnostic delay and disease burden in PA, more attention should be paid to the screening and treatment of PA to reduce the incidence of cardiovascular outcomes.</p>","PeriodicalId":50237,"journal":{"name":"Journal of Clinical Hypertension","volume":"26 11","pages":"1301-1309"},"PeriodicalIF":2.7,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11555523/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142382251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jaejin An, John J. Sim, Matt M. Zhou, Hui Zhou, Soon Kyu Choi, Jeffrey W. Brettler, Angeline L. Ong-Su, Kristi Reynolds
Sodium-glucose cotransporter-2 inhibitors (SGLT2i) have demonstrated a blood pressure (BP) reduction benefit despite other indications for use. We evaluated BP changes and antihypertensive medication use pre- and post-SGLT2i initiation among 12 960 patients with treated hypertension and among subgroups with apparent treatment-resistant hypertension (aTRH) and/or proteinuria. Post-SGLT2i initiation, the mean (SD) systolic blood pressure (SBP) was reduced from 133.9 (16.4) to 128.6 (15.5) mmHg and the mean diastolic blood pressure (DBP) was reduced from 70.8 (11.8) to 68.3 (11.3) mmHg among all patients. The mean SBP/DBP reduction was 5.3/2.5, 6.2/2.8, and 6.1/2.9 mmHg among all patients, patients with aTRH, and patients with proteinuria, respectively. Achieved BP < 130/80 mmHg increased by 12.5%, 16.9%, and 11.1% for all patients, patients with aTRH, and patients with proteinuria, respectively. Discontinuation of ≥ 1 antihypertensive medication within 12 months of SGLT2i initiation occurred in 33.4% overall, 47.6% of patients with aTRH, and 38.7% of patients with proteinuria.
{"title":"Blood Pressure Reduction and Changes in Antihypertensive Medication Use Among Patients With Hypertension Who Initiated Sodium-Glucose Cotransporter-2 Inhibitors","authors":"Jaejin An, John J. Sim, Matt M. Zhou, Hui Zhou, Soon Kyu Choi, Jeffrey W. Brettler, Angeline L. Ong-Su, Kristi Reynolds","doi":"10.1111/jch.14915","DOIUrl":"10.1111/jch.14915","url":null,"abstract":"<p>Sodium-glucose cotransporter-2 inhibitors (SGLT2i) have demonstrated a blood pressure (BP) reduction benefit despite other indications for use. We evaluated BP changes and antihypertensive medication use pre- and post-SGLT2i initiation among 12 960 patients with treated hypertension and among subgroups with apparent treatment-resistant hypertension (aTRH) and/or proteinuria. Post-SGLT2i initiation, the mean (SD) systolic blood pressure (SBP) was reduced from 133.9 (16.4) to 128.6 (15.5) mmHg and the mean diastolic blood pressure (DBP) was reduced from 70.8 (11.8) to 68.3 (11.3) mmHg among all patients. The mean SBP/DBP reduction was 5.3/2.5, 6.2/2.8, and 6.1/2.9 mmHg among all patients, patients with aTRH, and patients with proteinuria, respectively. Achieved BP < 130/80 mmHg increased by 12.5%, 16.9%, and 11.1% for all patients, patients with aTRH, and patients with proteinuria, respectively. Discontinuation of ≥ 1 antihypertensive medication within 12 months of SGLT2i initiation occurred in 33.4% overall, 47.6% of patients with aTRH, and 38.7% of patients with proteinuria.</p>","PeriodicalId":50237,"journal":{"name":"Journal of Clinical Hypertension","volume":"26 11","pages":"1318-1321"},"PeriodicalIF":2.7,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11555531/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142382250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anja Degenaar, Ruan Kruger, Adriaan Jacobs, Catharina M. C. Mels
Biomarkers of kidney function, including glomerular, tubular, and fibrotic markers, have been associated with blood pressure in elderly populations and individuals with kidney and cardiovascular diseases. However, limited information is available in young adults. In this study, we compared levels of several kidney function biomarkers between normotensive and hypertensive young adults and explored the associations of these biomarkers with blood pressure within these groups. In this cross-sectional assessment, twenty-four-hour (24-h) blood pressure measurements of 1055 participants (mean age = 24.6 years) were used to classify hypertension as per the 2018 ESC/ESH guidelines. Biomarkers of kidney function included estimated glomerular filtration rate, urinary albumin, alpha-1 microglobulin (uA1M), neutrophil gelatinase-associated lipocalin (uNGAL), uromodulin (uUMOD), and the CKD273 classifier. All urinary biomarkers, except for the CKD273 classifier, were standardized for urinary creatinine (Cr). In the hypertensive group (61.0% White; 73.2% men), urinary albumin-to-creatinine ratio (uACR), uNGAL/Cr and uUMOD/Cr were lower than the normotensive group. In multiple regression analyses, 24-h systolic blood pressure (SBP) (β = 0.14; p = 0.042), 24-h diastolic blood pressure (DBP) (β = 0.14; p = 0.040), and 24-h mean arterial pressure (MAP) (β = 0.16; p = 0.020) associated positively with uA1M/Cr in the hypertensive group, while 24-h MAP positively associated with uACR (β = 0.17; p = 0.017). In exploratory factor analysis, positive associations of 24-h DBP and 24-h MAP with a factor pattern including tubular biomarkers were observed in the hypertensive group (24-h DBP: β = 0.18; p = 0.026, 24-h MAP: β = 0.17; p = 0.032). In the setting of hypertension, high perfusion pressure in the kidneys may play a role in the development of proximal tubule damage and promote early deterioration in kidney function in young adults.
{"title":"Phenotyping Kidney Function in Young Adults With High Blood Pressure: The African-PREDICT Study","authors":"Anja Degenaar, Ruan Kruger, Adriaan Jacobs, Catharina M. C. Mels","doi":"10.1111/jch.14911","DOIUrl":"10.1111/jch.14911","url":null,"abstract":"<p>Biomarkers of kidney function, including glomerular, tubular, and fibrotic markers, have been associated with blood pressure in elderly populations and individuals with kidney and cardiovascular diseases. However, limited information is available in young adults. In this study, we compared levels of several kidney function biomarkers between normotensive and hypertensive young adults and explored the associations of these biomarkers with blood pressure within these groups. In this cross-sectional assessment, twenty-four-hour (24-h) blood pressure measurements of 1055 participants (mean age = 24.6 years) were used to classify hypertension as per the 2018 ESC/ESH guidelines. Biomarkers of kidney function included estimated glomerular filtration rate, urinary albumin, alpha-1 microglobulin (uA1M), neutrophil gelatinase-associated lipocalin (uNGAL), uromodulin (uUMOD), and the CKD273 classifier. All urinary biomarkers, except for the CKD273 classifier, were standardized for urinary creatinine (Cr). In the hypertensive group (61.0% White; 73.2% men), urinary albumin-to-creatinine ratio (uACR), uNGAL/Cr and uUMOD/Cr were lower than the normotensive group. In multiple regression analyses, 24-h systolic blood pressure (SBP) (<i>β</i> = 0.14; <i>p</i> = 0.042), 24-h diastolic blood pressure (DBP) (<i>β</i> = 0.14; <i>p</i> = 0.040), and 24-h mean arterial pressure (MAP) (<i>β</i> = 0.16; <i>p</i> = 0.020) associated positively with uA1M/Cr in the hypertensive group, while 24-h MAP positively associated with uACR (<i>β</i> = 0.17; <i>p</i> = 0.017). In exploratory factor analysis, positive associations of 24-h DBP and 24-h MAP with a factor pattern including tubular biomarkers were observed in the hypertensive group (24-h DBP: <i>β</i> = 0.18; <i>p</i> = 0.026, 24-h MAP: <i>β</i> = 0.17; <i>p</i> = 0.032). In the setting of hypertension, high perfusion pressure in the kidneys may play a role in the development of proximal tubule damage and promote early deterioration in kidney function in young adults.</p><p><b>Trial Registration</b>: ClinicalTrials.gov identifier: NCT03292094</p>","PeriodicalId":50237,"journal":{"name":"Journal of Clinical Hypertension","volume":"26 11","pages":"1291-1300"},"PeriodicalIF":2.7,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11555542/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142378491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Addressing sources of bias in the GRAND study protocol in India.","authors":"Narsingh Verma, Noriko Matsushita, Ebtehal Salman, Takayoshi Ohkubo, Yutaka Imai","doi":"10.1111/jch.14901","DOIUrl":"https://doi.org/10.1111/jch.14901","url":null,"abstract":"","PeriodicalId":50237,"journal":{"name":"Journal of Clinical Hypertension","volume":" ","pages":""},"PeriodicalIF":2.7,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142373427","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}
<p>Dear Sir,</p><p>Li et al. investigated in their study the association between primary aldosteronism (PA) and target organ damage (TOD) among patients with newly diagnosed hypertension.<span><sup>1</sup></span> The authors wrote, “Clinical studies have shown that PA is associated with an increased risk of TOD, including left ventricular hypertrophy (LVH), microalbuminuria and increased carotid intima-media thickness (CIMT), compared with essential hypertension (EH)”.<span><sup>1</sup></span> Fifty-seven patients with PA (mean age 44 years, 56% male gender) and 987 individuals (matched for age/gender) without PA were included.<span><sup>1</sup></span> As surrogate marker for preclinical atherosclerosis the CIMT was used.<span><sup>1</sup></span> The authors concluded that their research demonstrated “that individuals with PA had more severe TOD than those without PA, including LVH, carotid atherosclerosis, and microalbuminuria”.<span><sup>1</sup></span></p><p>Some comments are needed to evaluate the results and conclusions of this study in a more exhaustive way. As to their measurement, the authors wrote, “the vertical distance from the upper margin of vascular intima to the upper margin of the vascular adventitia of the distal common carotid artery (with an up–and–down range of 1.0 to 1.5 cm below the level of the bifurcation) or the initial segment of the internal carotid artery was measured as the intima-media thickness (IMT)”.<span><sup>1</sup></span> From the methodological description, namely the use of the word “or”, it appears that the authors measured not uniformly in (a) preestablished carotid artery (CA) segment(s) (e.g., common carotid artery (CCA) and internal carotid artery (ICA), CCA solely, ICA solely), but apparently chose for each subject a different segment of the CA, that is, the CCA or the ICA. Ultrasonography cannot differentiate intermediate stages between IMT and atherosclerotic plaque, whereby such conditions, while occasionally present at the CCA, are common at the bifurcation and the ICA.<span><sup>4</sup></span> In the “Mannheim Carotid Intima-Media Thickness and Plaque Consensus paper” the important differentiation between IMT and plaque formation is made, “Epidemiological and intervention studies have shown that although both share common risk factors of atherosclerosis, its natural history, patterns of risk factors and the prediction of cardiac and cerebral events are different for carotid IMT and carotid plaque”.<span><sup>4</sup></span> Ling et al., wrote in their meta-analysis, “CCA-IMT is more likely linked to systemic atherosclerosis and vascular remodeling in response to hemodynamic changes rather than ICA-IMT, which is related to localized atherosclerosis”.<span><sup>2</sup></span> It is not comprehensible why Li et al.<span><sup>1</sup></span> did not perform uniformly their CIMT measures at the same CA location(s) and instead adopted a highly heterogenic data acquisition. As to their selected cutoff, Li et
Christian Saleh撰写并修改了手稿。作者声明没有利益冲突。
{"title":"Carotid intima-media thickness, primary aldosteronism, and target organ damage in untreated hypertensive patients","authors":"Christian Saleh MD","doi":"10.1111/jch.14896","DOIUrl":"10.1111/jch.14896","url":null,"abstract":"<p>Dear Sir,</p><p>Li et al. investigated in their study the association between primary aldosteronism (PA) and target organ damage (TOD) among patients with newly diagnosed hypertension.<span><sup>1</sup></span> The authors wrote, “Clinical studies have shown that PA is associated with an increased risk of TOD, including left ventricular hypertrophy (LVH), microalbuminuria and increased carotid intima-media thickness (CIMT), compared with essential hypertension (EH)”.<span><sup>1</sup></span> Fifty-seven patients with PA (mean age 44 years, 56% male gender) and 987 individuals (matched for age/gender) without PA were included.<span><sup>1</sup></span> As surrogate marker for preclinical atherosclerosis the CIMT was used.<span><sup>1</sup></span> The authors concluded that their research demonstrated “that individuals with PA had more severe TOD than those without PA, including LVH, carotid atherosclerosis, and microalbuminuria”.<span><sup>1</sup></span></p><p>Some comments are needed to evaluate the results and conclusions of this study in a more exhaustive way. As to their measurement, the authors wrote, “the vertical distance from the upper margin of vascular intima to the upper margin of the vascular adventitia of the distal common carotid artery (with an up–and–down range of 1.0 to 1.5 cm below the level of the bifurcation) or the initial segment of the internal carotid artery was measured as the intima-media thickness (IMT)”.<span><sup>1</sup></span> From the methodological description, namely the use of the word “or”, it appears that the authors measured not uniformly in (a) preestablished carotid artery (CA) segment(s) (e.g., common carotid artery (CCA) and internal carotid artery (ICA), CCA solely, ICA solely), but apparently chose for each subject a different segment of the CA, that is, the CCA or the ICA. Ultrasonography cannot differentiate intermediate stages between IMT and atherosclerotic plaque, whereby such conditions, while occasionally present at the CCA, are common at the bifurcation and the ICA.<span><sup>4</sup></span> In the “Mannheim Carotid Intima-Media Thickness and Plaque Consensus paper” the important differentiation between IMT and plaque formation is made, “Epidemiological and intervention studies have shown that although both share common risk factors of atherosclerosis, its natural history, patterns of risk factors and the prediction of cardiac and cerebral events are different for carotid IMT and carotid plaque”.<span><sup>4</sup></span> Ling et al., wrote in their meta-analysis, “CCA-IMT is more likely linked to systemic atherosclerosis and vascular remodeling in response to hemodynamic changes rather than ICA-IMT, which is related to localized atherosclerosis”.<span><sup>2</sup></span> It is not comprehensible why Li et al.<span><sup>1</sup></span> did not perform uniformly their CIMT measures at the same CA location(s) and instead adopted a highly heterogenic data acquisition. As to their selected cutoff, Li et","PeriodicalId":50237,"journal":{"name":"Journal of Clinical Hypertension","volume":"26 10","pages":"1201-1202"},"PeriodicalIF":2.7,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11466350/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142331560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p>I read with great interest the study by Peng et al. which examined the relationship between coagulation and platelet parameters and pregnancy outcome in patients with preeclampsia [<span>1</span>]. In this study, it was found that platelet count, mean platelet volume (MPV), and plateletcrit (PCT) values were significantly reduced with the severity of preeclampsia, and the researchers argued that their study showed a significant relationship between coagulation and platelet parameters and the severity of preeclampsia and adverse pregnancy outcome. I want to emphasize the existence of some factors that negatively affect the evaluation of platelet parameters in this study.</p><p>Since the measurement of MPV, a platelet parameter, has not yet been standardized, the use of these values for purposes such as diagnosis or prognosis, especially in acquired diseases, is definitely not recommended [<span>2</span>]. The main factors affecting MPV measurement standardization are the type of anticoagulant used in the measurement, the time between blood collection and measurement, and the devices used in the measurement [<span>3-5</span>]. As in this study, the most commonly used anticoagulant in complete blood counts is ethylenediaminetetraacetic acid (EDTA), and when platelets come into contact with EDTA in the blood tube, they undergo rapid growth, change shape, and develop pseudopods [<span>3</span>]. The increase in MPV caused by EDTA contact can be up to 30% in the first 5 min and 40%–45% in the first 2 h [<span>3</span>]. In studies using EDTA as an anticoagulant, increases of 2%–50% in MPV values have been reported [<span>3-5</span>]. Deviations in MPV values have also been reported with other anticoagulants [<span>4, 5</span>]. Differences in the devices used in the measurement can cause deviations of up to 40% in MPV values [<span>5-7</span>]. Since the determination of another platelet parameter, PCT (=platelet count × MPV/10 000), is made by calculation based on MPV values, any factor that negatively affects the measurement of MPV values also negatively affects PCT values. In the study by Peng et al., the time between blood collection and MPV measurement and the devices used in MPV measurement were not specified, thus negatively affecting the reliability of the MPV data and therefore the PCT data of the study. Also, in the study by Peng et al., comparisons were made between pregnants with and without preeclampsia, and the absence of a non-pregnant healthy women group in the comparisons made it difficult to understand whether pregnancy had an effect on the deviations detected in platelet parameters.</p><p>Another issue is that it was stated in the discussion section of the article that the change in platelet parameters reflects the decrease in platelet function. The gold standard test used to measure platelet function is light transmission platelet aggregation in platelet-rich plasma, and studies using this method have shown that there is no corre
{"title":"Mean Platelet Volume and Plateletcrit Values May Not Be Associated With the Severity of Preeclampsia","authors":"Cengiz Beyan","doi":"10.1111/jch.14907","DOIUrl":"10.1111/jch.14907","url":null,"abstract":"<p>I read with great interest the study by Peng et al. which examined the relationship between coagulation and platelet parameters and pregnancy outcome in patients with preeclampsia [<span>1</span>]. In this study, it was found that platelet count, mean platelet volume (MPV), and plateletcrit (PCT) values were significantly reduced with the severity of preeclampsia, and the researchers argued that their study showed a significant relationship between coagulation and platelet parameters and the severity of preeclampsia and adverse pregnancy outcome. I want to emphasize the existence of some factors that negatively affect the evaluation of platelet parameters in this study.</p><p>Since the measurement of MPV, a platelet parameter, has not yet been standardized, the use of these values for purposes such as diagnosis or prognosis, especially in acquired diseases, is definitely not recommended [<span>2</span>]. The main factors affecting MPV measurement standardization are the type of anticoagulant used in the measurement, the time between blood collection and measurement, and the devices used in the measurement [<span>3-5</span>]. As in this study, the most commonly used anticoagulant in complete blood counts is ethylenediaminetetraacetic acid (EDTA), and when platelets come into contact with EDTA in the blood tube, they undergo rapid growth, change shape, and develop pseudopods [<span>3</span>]. The increase in MPV caused by EDTA contact can be up to 30% in the first 5 min and 40%–45% in the first 2 h [<span>3</span>]. In studies using EDTA as an anticoagulant, increases of 2%–50% in MPV values have been reported [<span>3-5</span>]. Deviations in MPV values have also been reported with other anticoagulants [<span>4, 5</span>]. Differences in the devices used in the measurement can cause deviations of up to 40% in MPV values [<span>5-7</span>]. Since the determination of another platelet parameter, PCT (=platelet count × MPV/10 000), is made by calculation based on MPV values, any factor that negatively affects the measurement of MPV values also negatively affects PCT values. In the study by Peng et al., the time between blood collection and MPV measurement and the devices used in MPV measurement were not specified, thus negatively affecting the reliability of the MPV data and therefore the PCT data of the study. Also, in the study by Peng et al., comparisons were made between pregnants with and without preeclampsia, and the absence of a non-pregnant healthy women group in the comparisons made it difficult to understand whether pregnancy had an effect on the deviations detected in platelet parameters.</p><p>Another issue is that it was stated in the discussion section of the article that the change in platelet parameters reflects the decrease in platelet function. The gold standard test used to measure platelet function is light transmission platelet aggregation in platelet-rich plasma, and studies using this method have shown that there is no corre","PeriodicalId":50237,"journal":{"name":"Journal of Clinical Hypertension","volume":"26 10","pages":"1203-1204"},"PeriodicalIF":2.7,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11466356/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142331562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ali Çoner MD, Can Ramazan Öncel MD, Cemal Köseoğlu MD, Göksel Dağaşan MD
To the Editor,
I read with great interest the article titled “Usability of myocardial work parameters to demonstrate subclinical myocardial involvement in normotensive individuals with exaggerated hypertensive response in treadmill exercise testing” by Efe et al. In their detailed statistical analysis, Efe et al. reported that myocardial work parameters such as global myocardial work index (GWI) might be used to identify early signs of myocardial involvement in normotensive patients with an exaggerated blood pressure response to exercise (EBPRE).1 Accordingly, the increase in GWI value predicts the presence of EBPRE. Myocardial work parameters are related to myocardial deformation and distortion independent from pressure and volume load which is different from previous myocardial performance parameters such as global longitudinal strain (GLS) and left ventricular ejection fraction (LVEF).2
In recent clinical studies, EBPRE has been found to be associated with subclinical target organ damage in normotensive individuals.3, 4 In addition, it has been suggested that EBPRE may be a predictor of future overt hypertension.5 It is suggested that the most probable mechanism that plays a role in the development of EBPRE is the lack of enough decrement in peripheral vascular resistance in response to increased cardiac output with exercise. This inadequate decrease in peripheral vascular resistance may be related to endothelial dysfunction and subclinical vascular inflammation.4, 6 Closely related to this inadequate response in peripheral vascular resistance, various metabolic parameters (such as central adiposity, fasting blood sugar, triglyceride, total cholesterol, and impaired glucose tolerance) were also found to be associated with the development of EBPRE.4, 6, 7 When deciding whether the possible role of load-independent myocardial work parameters predicts the presence of EBPRE, metabolic variables that may accompany the pathophysiology should be taken into consideration and clinicians may also interact with the manageable metabolic variables to manage the personal risk stratification.
{"title":"Multiple factors are related to the development of exaggerated blood pressure response to exercise","authors":"Ali Çoner MD, Can Ramazan Öncel MD, Cemal Köseoğlu MD, Göksel Dağaşan MD","doi":"10.1111/jch.14899","DOIUrl":"10.1111/jch.14899","url":null,"abstract":"<p>To the Editor,</p><p>I read with great interest the article titled “Usability of myocardial work parameters to demonstrate subclinical myocardial involvement in normotensive individuals with exaggerated hypertensive response in treadmill exercise testing” by Efe et al. In their detailed statistical analysis, Efe et al. reported that myocardial work parameters such as global myocardial work index (GWI) might be used to identify early signs of myocardial involvement in normotensive patients with an exaggerated blood pressure response to exercise (EBPRE).<span><sup>1</sup></span> Accordingly, the increase in GWI value predicts the presence of EBPRE. Myocardial work parameters are related to myocardial deformation and distortion independent from pressure and volume load which is different from previous myocardial performance parameters such as global longitudinal strain (GLS) and left ventricular ejection fraction (LVEF).<span><sup>2</sup></span></p><p>In recent clinical studies, EBPRE has been found to be associated with subclinical target organ damage in normotensive individuals.<span><sup>3, 4</sup></span> In addition, it has been suggested that EBPRE may be a predictor of future overt hypertension.<span><sup>5</sup></span> It is suggested that the most probable mechanism that plays a role in the development of EBPRE is the lack of enough decrement in peripheral vascular resistance in response to increased cardiac output with exercise. This inadequate decrease in peripheral vascular resistance may be related to endothelial dysfunction and subclinical vascular inflammation.<span><sup>4, 6</sup></span> Closely related to this inadequate response in peripheral vascular resistance, various metabolic parameters (such as central adiposity, fasting blood sugar, triglyceride, total cholesterol, and impaired glucose tolerance) were also found to be associated with the development of EBPRE.<span><sup>4, 6, 7</sup></span> When deciding whether the possible role of load-independent myocardial work parameters predicts the presence of EBPRE, metabolic variables that may accompany the pathophysiology should be taken into consideration and clinicians may also interact with the manageable metabolic variables to manage the personal risk stratification.</p>","PeriodicalId":50237,"journal":{"name":"Journal of Clinical Hypertension","volume":"26 11","pages":"1322"},"PeriodicalIF":2.7,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11555529/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142331563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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