Accuracy of oscillometric noninvasive blood pressure at the ankle in the lateral position during general anesthesia.

BACKGROUND: This study aimed to evaluate the accuracy of ankle blood pressure measurements in relation to invasive blood pressure in the lateral position. METHODS: This prospective observational study included adult patients scheduled for elective non-cardiac surgery under general anesthesia in the lateral position. Paired radial artery invasive and ankle noninvasive blood pressure readings were recorded in the lateral position using GE Carescape B650 monitor. The primary outcome was the ability of ankle mean arterial pressure (MAP) to detect hypotension (MAP < 70 mmHg) using area under the receiver operating characteristic curve (AUC) analysis. The secondary outcomes were the ability of ankle systolic blood pressure (SBP) to detect hypertension (SBP > 140 mmHg) as well as bias (invasive measurement - noninvasive measurement), and agreement between the two methods using the Bland-Altman analysis. RESULTS: We analyzed 415 paired readings from 30 patients. The AUC (95% confidence interval [CI]) of ankle MAP for detecting hypotension was 0.88 (0.83-0.93). An ankle MAP of ≤ 86 mmHg had negative and positive predictive values (95% CI) of 99 (97-100)% and 21 (15-29)%, respectively, for detecting hypotension. The AUC (95% CI) of ankle SBP to detect hypertension was 0.83 (0.79-0.86) with negative and positive predictive values (95% CI) of 95 (92-97)% and 36 (26-46)%, respectively, at a cutoff value of > 144 mmHg. The mean bias between the two methods was - 12 ± 17, 3 ± 12, and - 1 ± 11 mmHg for the SBP, diastolic blood pressure, and MAP, respectively. CONCLUSION: In patients under general anesthesia in the lateral position, ankle blood pressure measurements are not interchangeable with the corresponding invasive measurements. However, an ankle MAP > 86 mmHg can exclude hypotension with 99% accuracy, and an ankle SBP < 144 mmHg can exclude hypertension with 95% accuracy.

Cardiovascular events according to blood pressure thresholds recommended by ACC/AHA.

AIM: The latest guidelines from ACC/AHA define hypertension at systolic blood pressure (SBP) 130-139 mmHg or diastolic blood pressure (DBP) 80-89 mmHg in contrast to guidelines from ESC/ESH defining hypertension at SBP ≥ 140 mmHg or DBP ≥ 90 mmHg. The aim was to determine whether the ACC/AHA definition of hypertension identifies persons at elevated risk for future cardiovascular outcome. METHODS: In a Danish prospective cardiovascular study, 19,721 white men and women aged 20-98 years were examined up to five occasions between 1976 and 2015. The population was followed until December 2018. The ACC/AHA definition of the BP levels were applied: Normal: SBP <120 mmHg and DBP <80 mmHg, Elevated: SBP 120-129 mmHg and DBP <80 mmHg, Stage 1: SBP 130-139 mmHg or DBP 80-89 mmHg, Stage 2: SBP ≥140 mmHg or DBP ≥90 mmHg. Absolute 10-year risk was calculated taking repeated examinations, covariates, and competing risk into account. RESULTS: For all outcomes, the 10-year risk in stage 1 hypertension did not differ significantly from risk in subjects with normal BP: The 10-year risk of cardiovascular events in stage 1 hypertension was 14.1% [95% CI 13.2;15.0] and did not differ significantly from the risk in normal BP at 12.8% [95% CI 11.1;14.5] (p = 0.19). The risk was highest in stage 2 hypertension 19.4% [95% CI 18.9;20.0] and differed significantly from normal BP, elevated BP, and stage 1 hypertension (p < 0.001). The 10-year risk of cardiovascular death was 6.6% [95% CI 5.9;7.4] in stage 1 hypertension and did not differ significantly from the risk in normal BP at 5.7% [95% CI 4.1;7.3] (p = 0.33). CONCLUSIONS: Stage 1 hypertension as defined by the ACC/AHA guidelines has the same risk for future cardiovascular events as normal BP. In contrast, the definition of hypertension as suggested by ESC/ESH identifies patients with elevated risk of cardiovascular events.

Until 2017, there was worldwide agreement on defining hypertension at systolic blood pressure (SBP) ≥ 140 mmHg or diastolic blood pressure (DBP) ≥ 90 mmHg.In 2017, the American Cardiology Societies (ACC and AHA) lowered the threshold for defining hypertension at SBP 130-139 mmHg or DBP 80-89 mmHg.Lowering the threshold might make healthy persons sick if the thresholds do not identify persons at high risk.Unnecessary medical treatment is associated with high economic cost for the health care systems.We wanted to explore whether applying the American BP definition in a Scandinavian population identified persons with elevated risk for cardiovascular disease.As part of the Copenhagen City Heart study, 19,721 men and women aged 20-98 years were followed from 1976.They went through up to five examinations between 1976 and 2018 including BP measurements.We applied the American BP thresholds and followed the persons until death or 2018.In Denmark all citizens have a unique identification number which is linked to all health care contacts and administrative registers.We used advanced statistical methods and linked the BP measurements with the data for cardiovascular disease and death date from the Danish registries for each person.The results showed that the American definition of hypertension has same risk for future cardiovascular disease as the definition of normal BP.This means that healthy persons will be diagnosed with hypertension if the US guidelines were applied in Denmark.

Differential changes in end organ immune cells and inflammation in salt-sensitive hypertension: effects of increasing M2 macrophages.

Salt-sensitive hypertension (SSHTN) is associated with M1 macrophage polarization and inflammatory responses, leading to inflammation-associated lymphangiogenesis and functional impairment across multiple organs, including kidneys and gonads. However, it remains unclear whether promoting M2 macrophage polarization can alleviate the hypertension, inflammation, and end organ damage in mice with salt sensitive hypertension (SSHTN). Male and female mice were made hypertensive by administering nitro-L-arginine methyl ester hydrochloride (L-NAME; 0.5 mg/ml) for 2 weeks in the drinking water, followed by a 2-week interval without any treatments, and a subsequent high salt diet for 3 weeks (SSHTN). AVE0991 (AVE) was intraperitoneally administered concurrently with the high salt diet. Control mice were provided standard diet and tap water. AVE treatment significantly attenuated BP and inflammation in mice with SSHTN. Notably, AVE promoted M2 macrophage polarization, decreased pro-inflammatory immune cell populations, and improved function in renal and gonadal tissues of mice with SSHTN. Additionally, AVE decreased lymphangiogenesis in the kidneys and testes of male SSHTN mice and the ovaries of female SSHTN mice. These findings highlight the effectiveness of AVE in mitigating SSHTN-induced elevated BP, inflammation, and end organ damage by promoting M2 macrophage polarization and suppressing pro-inflammatory immune responses. Targeting macrophage polarization emerges as a promising therapeutic approach for alleviating inflammation and organ damage in SSHTN. Further studies are warranted to elucidate the precise mechanisms underlying AVE-mediated effects and to assess its clinical potential in managing SSHTN.

Differential changes in end organ immune cells and inflammation in salt-sensitive hypertension: effects of lowering blood pressure.

We reported that salt-sensitive hypertension (SSHTN) is associated with increased pro-inflammatory immune cells, inflammation, and inflammation-associated lymphangiogenesis in the kidneys and gonads of male and female mice. However, it is unknown whether these adverse end organ effects result from increased blood pressure (BP), elevated levels of salt, or both. We hypothesized that pharmaceutically lowering BP would not fully alleviate the renal and gonadal immune cell accumulation, inflammation, and lymphangiogenesis associated with SSHTN. SSHTN was induced in male and female C57BL6/J mice by administering nitro-L-arginine methyl ester hydrochloride (L-NAME; 0.5 mg/ml) in their drinking water for 2 weeks, followed by a 2-week washout period. Subsequently, the mice received a 3-week 4% high salt diet (SSHTN). The treatment group underwent the same SSHTN induction protocol but received hydralazine (HYD; 250 mg/L) in their drinking water during the diet phase (SSHTN+HYD). Control mice received tap water and a standard diet for 7 weeks. In addition to decreasing systolic BP, HYD treatment generally decreased pro-inflammatory immune cells and inflammation in the kidneys and gonads of SSHTN mice. Furthermore, the decrease in BP partially alleviated elevated renal and gonadal lymphatics and improved renal and gonadal function in mice with SSHTN. These data demonstrate that high systemic pressure and salt differentially act on end organ immune cells, contributing to the broader understanding of how BP and salt intake collectively shape immune responses and highlight implications for targeted therapeutic interventions.

Gstp1 negatively regulates blood pressure in hypertensive rat via promoting APLNR ubiquitination degradation mediated by Nedd4.

Hypertension is a leading risk factor for disease burden worldwide. Vascular contraction and remodeling contribute to the development of hypertension. Glutathione S-transferase P1 (Gstp1) plays several critical roles in both normal and neoplastic cells. In this study, we investigated the effect of Gstp1 on hypertension as well as on vascular smooth muscle cell (VSMC) contraction and phenotypic switching. We identified the higher level of Gstp1 in arteries and VSMCs from hypertensive rats compared with normotensive rats for the first time. We then developed Adeno-associated virus 9 (AAV9) mediated Gstp1 down-regulation and overexpression in rats and measured rat blood pressure by using the tail-cuff and the carotid catheter method. We found that the blood pressure of spontaneously hypertensive rats (SHR) rose significantly with Gstp1 down-regulation and reduced apparently after Gstp1 overexpression. Similar results were obtained from the observations of 2-kidney-1-clip renovascular (2K1C) hypertensive rats. Gstp1 did not influence blood pressure of normotensive Wistar-Kyoto (WKY) rats and Sprague-Dawley (SD) rats. Further in vitro study indicated that Gstp1 knockdown in SHR-VSMCs promoted cell proliferation, migration, dedifferentiation and contraction, while Gstp1 overexpression showed opposite effects. Results from bioinformatic analysis showed that the Apelin/APLNR system was involved in the effect of Gstp1 on SHR-VSMCs. The rise in blood pressure of SHR induced by Gstp1 knockdown could be reversed by APLNR antagonist F13A. We further found that Gstp1 enhanced the association between APLNR and Nedd4 E3 ubiquitin ligases to induce APLNR ubiquitination degradation. Thus, in the present study, we discovered a novel anti-hypertensive role of Gstp1 in hypertensive rats and provided the experimental basis for designing an effective anti-hypertensive therapeutic strategy.

Patient-Specific Factors Predicting Renal Denervation Response in Patients With Hypertension: A Systematic Review and Meta-Analysis.

BACKGROUND: The accurate selection of patients likely to respond to renal denervation (RDN) is crucial for optimizing treatment outcomes in patients with hypertension. This systematic review was designed to evaluate patient-specific factors predicting the RDN response. METHODS AND RESULTS: We focused on individuals with hypertension who underwent RDN. Patients were categorized based on their baseline characteristics. The primary outcome was blood pressure (BP) reduction after RDN. Both randomized controlled trials and nonrandomized studies were included. We assessed the risk of bias using corresponding tools and further employed the Grading of Recommendations Assessment, Development, and Evaluation approach to assess the overall quality of evidence. A total of 50 studies were ultimately included in this systematic review, among which 17 studies were for meta-analysis. Higher baseline heart rate and lower pulse wave velocity were shown to be associated with significant antihypertensive efficacy of RDN on 24-hour systolic BP reduction (weighted mean difference, -4.05 [95% CI, -7.33 to -0.77]; weighted mean difference, -7.20 [95% CI, -9.79 to -4.62], respectively). In addition, based on qualitative analysis, higher baseline BP, orthostatic hypertension, impaired baroreflex sensitivity, and several biomarkers are also reported to be associated with significant BP reduction after RDN. CONCLUSIONS: In patients with hypertension treated with the RDN, higher heart rate, and lower pulse wave velocity were associated with significant BP reduction after RDN. Other factors, including higher baseline BP, hypertensive patients with orthostatic hypertension, BP variability, impaired cardiac baroreflex sensitivity, and some biomarkers are also reported to be associated with a better BP response to RDN.

Interrelation of daily blood pressure profile with left ventricular myocardial hypertrophy in men of working age with hypertension.

OBJECTIVE: Aim: To analyze the relationship between daily blood pressure biorhythms and left ventricular myocardial hypertrophy in working-age men with arterial hypertension. PATIENTS AND METHODS: Materials and Methods: Fifty-seven men with AH (mean age: 44.6±1.3 years) underwent Echo-CG and daily ABPM. Non-dipper and night-peaker patterns indicated BP biorhythm disturbances, while normal dipper and over-dipper patterns indicated undisturbed BP biorhythms. LVH was defined as LMMI > 115 g/m^2. RESULTS: Results: About 60% of participants exhibited diurnal BP rhythm disorders, with a higher prevalence of LVH in this group compared to those with normal BP biorhythms (32% vs. 22%, p>0,05). Patients with normal daily BP biorhythms had significantly higher circadian indices of HR, systolic and diastolic BP, and double product compared to those with disturbed BP rhythms. CONCLUSION: Conclusions: In young men with "non-dipper" and "night-peaker" patterns, LVH appears to be more pronounced than in those with normal daily BP biorhythms. This approach may optimize the timing of antihypertensive drug administration.

Blood pressure is associated with knee pain severity in middle-aged and elderly individuals with or at risks for osteoarthritis: data from the Osteoarthritis Initiative.

BACKGROUND: Hypertension is a common comorbidity of osteoarthritis (OA). Joint pain is the main clinical manifestation of OA. Knowledge about the relationship between hypertension and OA pain is limited. This study aimed to investigate whether blood pressure parameters are associated with knee pain severity in individuals with or at risks for OA. METHODS: Our sample consisted of 2598 subjects (60.7% female, aged 45-79 years) collected from the Osteoarthritis Initiative. Blood pressure parameters included blood pressure stage, systolic blood pressure (SBP), diastolic blood pressure (DBP) and pulse pressure (PP). Radiographic evaluation using Kellgren-Lawrence system and pain severity evaluation using Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC), Knee Injury and Osteoarthritis Outcome Score (KOOS), and Numeric Rating Scale (NRS) were performed for right knee. Linear regression was used to examine the relationship between blood pressure parameters and knee pain severity. RESULTS: For the overall sample, blood pressure stage, SBP, and PP were positively correlated with WOMAC and NRS pain scores when adjusting for age, sex, and body mass index (BMI) (p ≤ 0.024) and were inversely correlated with KOOS score (p ≤ 0.004). After further adjusting for all covariates, PP remained a positive correlation with WOMAC score (p = 0.037) while other associations between blood pressure parameters and pain scores did not reach the statistical significance. In female, higher blood pressure stage, SBP, and PP were significantly associated with increased WOMAC and NRS scores and decreased KOOS score after adjustments of age and BMI (p ≤ 0.018). When adjusting for all covariates, the correlations of PP with WOMAC, KOOS and NRS scores remained significant (p = 0.008-0.049). In male sample, SBP was positively correlated with WOMAC score when adjusting for age and BMI (p = 0.050), but other associations between blood pressure parameters and pain scores were not statistically significant. No significant correlation was observed in male when further adjusting for other covariates. CONCLUSIONS: Increased PP is a risk factor for knee pain and mainly affects females, which suggested that controlling PP may be beneficial in preventing or reducing knee pain in females with or at risks for OA.

Comparable cerebral cortex activity and gait performance in elderly hypertensive and healthy individuals during dual-task walking: A fNIRS study.

BACKGROUND: Hypertension increases the risk of cognitive impairment and related dementia, causing impaired executive function and unusual gait parameters. However, the mechanism of neural function illustrating this is unclear. Our research aimed to explore the differences of cerebral cortex activation, gait parameters, and working memory performance between healthy older adults (HA) and older hypertensive (HT) patients when performing cognitive and walking tasks. METHOD: A total of 36 subjects, including 12 healthy older adults and 24 older hypertensive patients were asked to perform series conditions including single cognitive task (SC), single walking task (SW), and dual-task (DT), wearing functional near-infrared spectroscopy (fNIRS) equipment and Intelligent Device for Energy Expenditure and Activity equipment to record cortical hemodynamic reactions and various gait parameters. RESULTS: The left somatosensory cortex (L-S1) and bilateral supplementary motor area (SMA) showed higher cortical activation (p < .05) than HA when HT performed DT. The intragroup comparison showed that HT had higher cortical activation (p < .05) when performing DT as SW. The cognitive performance of HT was significantly worse (p < .05) than HA when executing SC. The activation of the L-S1, L-M1, and bilateral SMA in HT were significantly higher during SW (p < .05). CONCLUSION: Hypertension can lead to cognitive impairment in the elderly, including executive function and walking function decline. As a result of these functional declines, elderly patients with hypertension are unable to efficiently allocate brain resources to support more difficult cognitive interference tasks and need to meet more complex task demands by activating more brain regions.

Effect of early endothelial function improvement on subclinical target organ damage in hypertensives.

Endothelial dysfunction is acknowledged as a marker for subclinical target organ damage (STOD) in hypertension, though its therapeutic potential has not yet been clarified. This study assessed whether early endothelial function improvement (EEFI) reduced STOD in patients with essential hypertension (EH). We conducted a retrospective cohort analysis of 456 EH patients initially free from STOD. Endothelial function was assessed using brachial artery flow-mediated dilation (FMD), with values ≤ 7.1% indicating dysfunction. Patients were initially categorized by endothelial status (dysfunction: n = 180, normal: n = 276), and further divided into improved or unimproved groups based on changes within three months post-enrollment. During a median follow-up of 25 months, 177 patients developed STOD. The incidence of STOD was significantly higher in patients with initial dysfunction compared to those with normal function. Kaplan-Meier analysis indicated that the improved group had a lower cumulative incidence of STOD compared to the unimproved group (p < 0.05). Multivariable Cox regression confirmed EEFI as an independent protective factor against STOD in EH patients (p < 0.05), regardless of their baseline endothelial status, especially in those under 65 years old, non-smokers, and with low-density lipoprotein cholesterol levels ≤ 3.4 mmol/L. In conclusion, EEFI significantly reduces STOD incidence in EH patients, particularly in specific subgroups, emphasizing the need for early intervention in endothelial function to prevent STOD.

miPEP31 alleviates Ang II-induced hypertension in mice by occupying Cebpα binding sites in the pri-miR-31 promoter.

BACKGROUND: Previous studies have shown that peptides encoded by noncoding RNAs (ncRNAs) can be used as peptide drugs to alleviate diseases. We found that microRNA-31 (miR-31) is involved in the regulation of hypertension and that the peptide miPEP31, which is encoded by the primary transcript of miR-31 (pri-miR-31), can inhibit miR-31 expression. However, the role and mechanism of miPEP31 in hypertension have not been elucidated. METHODS: miPEP31 expression was determined by western blot analysis. miPEP31-deficient mice (miPEP31-/-) were used, and synthetic miPEP31 was injected into Ang II-induced hypertensive mice. Blood pressure was monitored through the tail-cuff method. Histological staining was used to evaluate renal damage. Regulatory T (Treg) cells were assessed by flow cytometry. Differentially expressed genes were analysed through RNA sequencing. The transcription factors were predicted by JASPAR. Luciferase reporter and electrophoretic mobility shift assays (EMSAs) were used to determine the effect of pri-miR-31 on the promoter activity of miPEP31. Images were taken to track the entry of miPEP31 into the cell. RESULTS: miPEP31 is endogenously expressed in target organs and cells related to hypertension. miPEP31 deficiency exacerbated but exogenous miPEP31 administration mitigated the Ang II-induced systolic blood pressure (SBP) elevation, renal impairment and Treg cell decreases in the kidney. Moreover, miPEP31 deletion increased the expression of genes related to Ang II-induced renal fibrosis. miPEP31 inhibited the transcription of miR-31 and promoted Treg differentiation by occupying the Cebpα binding site. The minimal functional domain of miPEP31 was identified and shown to regulate miR-31. CONCLUSION: miPEP31 was identified as a potential therapeutic peptide for treating hypertension by promoting Treg cell differentiation in vivo. Mechanistically, we found that miPEP31 acted as a transcriptional repressor to specifically inhibit miR-31 transcription by competitively occupying the Cebpα binding site in the pri-miR-31 promoter. Our study highlights the significant therapeutic effect of miPEP31 on hypertension and provides novel insight into the role and mechanism of miPEPs.

Body Mass Index and Hypertension as Mediators of the Association Between Age at Menarche and Subclinical Atherosclerosis: A Sex-Specific Mendelian Randomization Analysis.

BACKGROUND: Early age at menarche (AAM) has been associated with a higher risk of carotid artery intima-media thickness (cIMT), an indicator of subclinical vascular disease, albeit the mechanisms underlying this association remain elusive. A better understanding of the relationship between AAM, modifiable cardiometabolic risk factors, and subclinical atherosclerosis may contribute to improved primary prevention and cardiovascular disease treatment. We aimed to investigate the putative causal role of AAM on cIMT, and to identify and quantify the potentially mediatory effects of cardiometabolic risk factors underlying this relationship. METHODS AND RESULTS: We conducted linkage disequilibrium score regression analyses between our exposure of interest, AAM, our outcome of interest, cIMT and potential mediators of the AAM-cIMT association to gauge cross-trait genetic overlap. We considered as mediators the modifiable anthropometric risk factors body mass index (BMI), systolic blood pressure (SBP), lipid traits (total cholesterol, triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol), and glycemic traits (fasting glucose). We then leveraged the paradigm of Mendelian randomization to infer causality between AAM and cIMT, and to identify whether cardiometabolic risk factors served as potential mediators of this effect. Our analyses showed that genetically predicted AAM was inversely associated with cIMT, BMI, SBP, and triglycerides, and positively associated with high-density lipoprotein, low-density lipoprotein, and total cholesterol. We showed that the effect of genetically predicted AAM on cIMT may be partially mediated through BMI (20.1% [95% CI, 1.4% to 38.9%]) and SBP (13.5% [95% CI, 0.5%-26.6%]). Our cluster-specific Mendelian randomization revealed heterogeneous causal effect estimates of age at menarche on BMI and SBP. CONCLUSIONS: We highlight supporting evidence for a potential causal association between earlier AAM and cIMT, and almost one third of the effect of AAM on cIMT may be mediated by BMI and SBP. Early intervention aimed at lowering BMI and hypertension may be beneficial in reducing the risk of developing subclinical atherosclerosis due to earlier age at menarche.

Multiethnic Perspectives of Shared Decision-Making in Hypertension: A Mixed-Methods Study.

BACKGROUND: Shared decision-making (SDM) has the potential to improve hypertension care quality and equity. However, research lacks diverse representation and evidence about how race and ethnicity affect SDM. Therefore, this study aims to explore SDM in the context of hypertension management. METHODS AND RESULTS: Explanatory sequential mixed-methods design was used. Quantitative data were sourced at baseline and 12-month follow up from RICH LIFE (Reducing Inequities in Care of Hypertension: Lifestyle Improvement for Everyone) participants (n=1212) with hypertension. Qualitative data were collected from semistructured individual interviews, at 12-month follow-up, with participants (n=36) selected based on their SDM scores and blood pressure outcome. Patients were cross- categorized based on high or low SDM scores and systolic blood pressure reduction of ≥10 or <10 mm Hg. Multinomial logistic regression analysis showed that predictors of SDM scores and blood pressure outcome were race and ethnicity (relative risk ratio [RRR], 1.64; P=0.029), age (RRR, 1.03; P=0.002), educational level (RRR, 1.87; P=0.016), patient activation (RRR, 0.98; P<0.001; RRR, 0.99; P=0.039), and hypertension knowledge (RRR, 2.2; P<0.001; and RRR, 1.57; P=0.045). Qualitative and mixed-methods findings highlight that provider-patient communication and relationship influenced SDM, being emphasized both as facilitators and barriers. Other facilitators were patients' understanding of hypertension; clinicians' interest in the patient, and clinicians' personality and attitudes; and barriers included perceived lack of compassion, relationship hierarchy, and time constraints. CONCLUSIONS: Participants with different SDM scores and blood pressure outcomes varied in determinants of decision and descriptions of contextual factors influencing SDM. Results provide actionable information, are novel, and expand our understanding of factors influencing SDM in hypertension.

Deep Learning-Based Vascular Aging Prediction From Retinal Fundus Images.

Purpose: The purpose of this study was to establish and validate a deep learning model to screen vascular aging using retinal fundus images. Although vascular aging is considered a novel cardiovascular risk factor, the assessment methods are currently limited and often only available in developed regions. Methods: We used 8865 retinal fundus images and clinical parameters of 4376 patients from two independent datasets for training a deep learning algorithm. The gold standard for vascular aging was defined as a pulse wave velocity ≥1400 cm/s. The probability of the presence of vascular aging was defined as deep learning retinal vascular aging score, the Reti-aging score. We compared the performance of the deep learning model and clinical parameters by calculating the area under the receiver operating characteristics curve (AUC). We recruited clinical specialists, including ophthalmologists and geriatricians, to assess vascular aging in patients using retinal fundus images, aiming to compare the diagnostic performance between deep learning models and clinical specialists. Finally, the potential of Reti-aging score for identifying new-onset hypertension (NH) and new-onset carotid artery plaque (NCP) in the subsequent three years was examined. Results: The Reti-aging score model achieved an AUC of 0.826 (95% confidence interval [CI] = 0.793-0.855) and 0.779 (95% CI = 0.765-0.794) in the internal and external dataset. It showed better performance in predicting vascular aging compared with the prediction with clinical parameters. The average accuracy of ophthalmologists (66.3%) was lower than that of the Reti-aging score model, whereas geriatricians were unable to make predictions based on retinal fundus images. The Reti-aging score was associated with the risk of NH and NCP (P < 0.05). Conclusions: The Reti-aging score model might serve as a novel method to predict vascular aging through analysis of retinal fundus images. Reti-aging score provides a novel indicator to predict new-onset cardiovascular diseases. Translational Relevance: Given the robust performance of our model, it provides a new and reliable method for screening vascular aging, especially in undeveloped areas.

Leptin in reproduction and hypertension in pregnancy.

Leptin has important roles in numerous physiological functions, including those in the regulation of energy balance, and in immune and reproductive systems. However, in the recent years, evidence has implicated it in a number of obesity-related diseases, where its concentrations in serum are significantly elevated. Elevated serum leptin concentrations and increased placental leptin secretion have been reported in women with hypertensive disorders of pregnancy. Whether leptin is responsible for this disorder remains to be established. Leptin injections in healthy rats and mice during pregnancy result in endothelial activation, increased blood pressure and proteinuria. A potential role for leptin in the pathogenesis of pre-eclampsia is hypothesised, particularly in women who are overweight or obese where serum leptin concentrations are often elevated. This review summarises pertinent information in the literature on the role of leptin in puberty, pregnancy, and hypertensive disorders of pregnancy. In particular, the possible mechanism that may be involved in leptin-induced increase in blood pressure and proteinuria during pregnancy and the potential role of marinobufagenin in this disease entity. We hypothesise a significant role for oxidative stress in this, and propose a conceptual framework on the events that lead to endothelial activation, raised blood pressure and proteinuria following leptin administration.

Sex disparities in hypertension prevalence, blood pressure trajectories and the effects of anti-hypertensive treatment.

INTRODUCTION: Sex differences in blood pressure (BP), hypertension and hypertension mediated cardiovascular complications have become an increasingly important focus of attention. This narrative review gives an overview of current studies on this topic, with the aim to provide a deeper understanding of the sex-based disparities in hypertension with essential insights for refining prevention and management strategies for both men and women. METHODS AND RESULTS: We searched Medline, Embase and the Cochrane libray on sex differences in BP-trajectories and hypertension prevalence. In the past decade various population-based studies have revealed substantial sex-disparities in BP-trajectories throughout life with women having a larger increase in hypertension prevalence after 30 years of age and a stronger association between BP and cardiovascular disease (CVD). In general, the effects of antihypertensive treatment appear to be consistent across sexes in different populations, although there remains uncertainty about differences in the efficacy of BP lowering drugs below 55 years of age. CONCLUSION: The current uniform approach to the diagnosis and management of hypertension in both sexes neglects the distinctions in hypertension, while the differences underscore the need for sex-specific recommendations, particularly for younger individuals. A major limitation hampering insights into sex differences in BP-related outcomes is the lack of sex-stratified analyses or an adequate representation of women. Additional large-scale, longitudinal studies are imperative.

PERSONIFICATION OF ANTIHYPERTENSIVE THERAPY IN ISCHEMIC CEREBRAL STROKE.

The purpose of the study is to optimize monitoring and personalize antihypertensive therapy in patients with severe ischemic cerebral stroke (ICS). We examined 37 patients with ICS, average age 74,1±1,3 years, who received treatment in intensive care wards of the stroke department with general neurology beds of the Municipal Non-Profit Enterprise "City Hospital № 9" of the Zaporizhzhia City Council. There were 16 men (43,2%), average age 71,9±2,1 years; women - 21 (56,8%), average age 75,8±1.6 years. Personification of antihypertensive therapy for severe ICS was carried out based on the etiology of hypertensive hemodynamic disorders: hyperkinetic type of arterial hypertension (Cardiac index ≥ 3,80 L×min-1×m-2) or hypokinetic type of arterial hypertension (Cardiac index ≤ 2,98 L×min-1×m-2). In patients with severe ICS and hyperkinetic type of arterial hypertension, initial hemodynamic parameters were characterized by Mean arterial pressure (MAP) of 111,4 ± 1,4 mm Hg; Heart rate (HR) of 107,2±1,6 min; Cardiac index (CI) 6,74±0,27 L×min-1×m-2; the Total peripheral vascular resistance (TPVR) is 674±36 dyn×sec-1×cm-5. For the purpose of antihypertensive correction of the hyperkinetic type of arterial hypertension (CI ≥ 3,80 L×min-1×m-2), a solution of Magnesium Sulfate was used intravenously at a dose of 2500-5000 mg×day-1 in combination with Bisoprolol 5-10 mg×day-1 orally. This made it possible to stabilize hemodynamic parameters by the end of intensive therapy within the limits of eukinetic values: MAP 95,2±1,5 mm Hg (p<0,05); HR 81,9±1,5 min (p<0,05); CI 3,60±0,15 L×min-1×m-2 (p<0,05); TPVR is 1079±58 dyn×sec-1×cm-5 (p<0,05). In patients with severe ICS and hypokinetic type of arterial hypertension, initial hemodynamic parameters were characterized by MAP of 117,7±2,8 mm Hg; HR of 76,7±1,5 min; CI 2,74±0,18 L×min-1×m-2; TPVR is 1754±123 dyn×sec-1×cm-5. For the purpose of antihypertensive correction of the hypokinetic type of arterial hypertension (CI≤2,98 L×min-1×m-2), a solution of Ebrantil was used intravenously as a bolus of 1,25-2,5 mg with a further infusion of 5-40 mg×hour-1. This made it possible to stabilize hemodynamic parameters by the end of intensive therapy within the limits of eukinetic values: MAP 92,7 ± 1,7 mm Hg (p<0,05); HR 81,4 ± 0,9 min (p<0,05); CI 3,65±0,16 L×min-1×m-2 (p<0,05); TPVR is 1036±46 dyn×sec-1×cm-5 (p<0,05).

Home blood pressure measurement days and changes in urinary sodium-to-potassium ratio, estimated salt and potassium intakes and blood pressure: 1-year prospective study.

OBJECTIVE: Current international guidelines recommend home blood pressure (BP) measurement and low sodium and high potassium intakes for the management of hypertension. We hypothesized that increased home BP measurement may result in more effective management of sodium and potassium intakes and BP. METHODS: We examined associations of home BP measurement days with changes in the urinary sodium-to-potassium (Na/K) ratio, estimated salt and potassium intakes and BP. We included 209 healthy participants (mean age, 55.9 years; 56.5% women) from a prospective cohort study. We examined 1-year data on self-measured home BP and spot urine samples. RESULTS: Median (interquartile range) days of home BP measurement was 324 (225-358) over 1-year. Baseline mean (SD) Na/K ratio, salt and potassium intakes, morning and evening SBP, and morning and evening DBP were 3.8 (2.3), 8.5 (1.9) g/day, 1833.5 (416.5) mg/day, 120.4 (14.0) mmHg, 118.2 (14.2) mmHg, 79.2 (10.1) mmHg, and 76.2 (10.1) mmHg, respectively. In multivariable-adjusted linear regression , ß (standard error) per 10 days increase in number of home BP measurement were -0.031 (0.017) for Na/K ratio, -0.036 (0.015) for salt intake, -1.357 (2.797) for potassium intake, -0.178 (0.064) for morning SBP, -0.079 (0.041) for morning DBP, -0.109 (0.067) for evening SBP and -0.099 (0.045) for evening DBP. Additionally, relationships persisted for men and women, but changes in salt intake were more pronounced among participants taking antihypertensive medication (interaction P = 0.002). CONCLUSION: Continuous measurement of home BP may lead not only to self-monitoring of BP, but also to declines in salt intakes and some BP indices.