Risk Factors For Hypertension Research Articles

Gut Microbe-Generated Metabolite Trimethylamine-N-Oxide and Ischemic Stroke

Trimethylamine-N-oxide (TMAO) is a gut microbiota-derived metabolite, the production of which in vivo is mainly regulated by dietary choices, gut microbiota, and the hepatic enzyme flavin monooxygenase (FMO), while its elimination occurs via the kidneys. The TMAO level is positively correlated with the risk of developing cardiovascular diseases. Recent studies have found that TMAO plays an important role in the development of ischemic stroke. In this review, we describe the relationship between TMAO and ischemic stroke risk factors (hypertension, diabetes, atrial fibrillation, atherosclerosis, thrombosis, etc.), disease risk, severity, prognostic outcomes, and recurrence and discuss the possible mechanisms by which they interact. Importantly, TMAO induces atherosclerosis and thrombosis through lipid metabolism, foam cell formation, endothelial dysfunction (via inflammation, oxidative stress, and pyroptosis), enhanced platelet hyper-reactivity, and the upregulation and activation of vascular endothelial tissue factors. Although the pathogenic mechanisms underlying TMAO’s aggravation of disease severity and its effects on post-stroke neurological recovery and recurrence risk remain unclear, they may involve inflammation, astrocyte function, and pro-inflammatory monocytes. In addition, this paper provides a summary and evaluation of relevant preclinical and clinical studies on interventions regarding the gut-microbiota-dependent TMAO level to provide evidence for the prevention and treatment of ischemic stroke through the gut microbe–TMAO pathway.

THE IMPACT OF VASCULAR RISK FACTORS ON CEREBRAL AMYLOID ANGIOPATHY: A COHORT STUDY IN HEREDITARY CAA AND A SYSTEMATIC REVIEW IN SPORADIC CAA

Background: Cerebral amyloid angiopathy (CAA) has a remarkably variable disease course, even in monogenetic hereditary forms. Our aim was to investigate the prevalence of vascular risk factors and their effect on disease onset and course in Dutch-type hereditary (D-)CAA and sporadic CAA. Methods: We performed a cohort study in D-CAA to investigate the association between vascular risk factors (hypertension, hypercholesterolemia, smoking and alcohol use) and age of intracerebral hemorrhage (ICH) onset and time of ICH recurrence with survival analyses. In addition, we performed a systematic review to assess the prevalence of vascular risk factors and their effect on clinical outcome in sporadic CAA. We searched PubMed, Embase, Web of Science and COCHRANE Library, from 1987-2022 and included cohorts with ≥10 patients. We created forest plots, calculated pooled estimates and reported variability (heterogeneity plus sampling variability) and risk of bias. Results: We included 70 participants with D-CAA (47% women, mean age 53y). Sixteen (23%) had hypertension, 15 (21%) hypercholesterolemia, 45 (64%) were smokers and 61 (87%) used alcohol. We found no clear effect of vascular risk factors on age of first ICH (log-rank test hypertension: p=0.35, hypercholesterolemia: p=0.41, smoking: p=0.61 and alcohol use: p=0.55) or time until ICH recurrence (log-rank test hypertension: p=0.71, hypercholesterolemia: p=0.20 and smoking: p=0.71). We identified 25 out of 1234 screened papers that assessed the prevalence of risk factors in CAA and 6 that reported clinical outcomes. The pooled prevalence estimates of hypertension was 62% (95%CI:55%-69%), diabetes 17% (95%CI:14%-20%), dyslipidemia 32% (95%CI:23%-41%), and tobacco use 27% (95%CI:18%-36%). One study reported study diabetes and hypertension to be associated with a lower risk of recurrent ICH, whereas another study reported hypertension to be associated with an increased risk. All other studies showed no association between vascular risk factors and clinical outcome. High quality studies focusing on vascular risk factors were lacking. Conclusions: In patients with D-CAA and sporadic CAA the prevalence of vascular risk factors is high. Although this suggests an opportunity for prevention, there is no clear association between these risk factors and CAA-related ICH onset and recurrence.

HIF-1α knockdown attenuates phenotypic transformation and oxidative stress induced by high salt in human aortic vascular smooth muscle cells.

Increased dietary salt intake is a well-established risk factor for hypertension and related cardiovascular diseases, involving complex vascular remodeling processes. However, the specific role of hypoxia-inducible factor-1α (HIF-1α) in vascular pathophysiology under high-salt conditions remains poorly understood. This study investigates the role of HIF-1α in high-salt-induced vascular remodeling using human aortic vascular smooth muscle cells (HA-VSMCs) cultured in vitro. HA-VSMCs were divided into three groups: high-salt with HIF-1α knockdown (shHIF-1α + HS), negative control (shcontrol), and high-salt (HS). Cell viability, migration, gene expression, and protein levels were evaluated. High-salt conditions significantly increased mRNA expression of α-smooth muscle actin (α-SMA), smooth muscle protein 22 (SM22), angiotensin II type 1 receptor (AT1R), collagen I, and collagen III (p < 0.0001). HIF-1α knockdown partially attenuated these increases, particularly for α-SMA, SM22, and AT1R (p < 0.01). At the protein level, high-salt exposure markedly elevated expression of collagen III, HIF-1α, osteopontin (OPN), and angiotensin II (Ang II) (p < 0.0001). HIF-1α knockdown significantly reduced the high-salt-induced increases in collagen III and HIF-1α protein levels (p < 0.001) but had a limited effect on OPN and Ang II upregulation. Interestingly, SM22 protein expression was significantly decreased under high-salt conditions (p < 0.0001), an effect partially reversed by HIF-1α knockdown (p < 0.0001). These findings demonstrate that high-salt conditions induce complex changes in gene and protein expression in HA-VSMCs, with HIF-1α playing a crucial role in mediating many of these alterations. The study highlights the differential effects of HIF-1α on various markers of vascular remodeling and suggests that HIF-1α may be a potential therapeutic target for mitigating salt-induced vascular pathology. Further research is warranted to elucidate the mechanisms underlying the HIF-1α-dependent and -independent effects observed in this study.

Effect of Different Dietary Patterns on Cardiometabolic Risk Factors: An Umbrella Review of Systematic Reviews and Meta-Analyses

Background/Objectives: Lifestyle interventions such as dietary changes have been proposed to control the cardiometabolic risk factors and thus prevent cardiovascular (CV) disease (CVD). We performed an umbrella review to investigate whether different dietary patterns affect CV risk in individuals with at least one cardiometabolic risk factor (hypertension, dyslipidemia, obesity, diabetes, metabolic syndrome) but not established CVD. Methods: We systematically searched the PubMed and Scopus databases (up to August 2024) for the systematic reviews and meta-analyses of randomized controlled trials (RCTs). Articles should be written in English and refer to a specific dietary pattern (such as Mediterranean diet, etc.). The population studied referred to adults with at least one cardiovascular (CV) risk factor. Results: From 4512 records identified, we finally included 25 meta-analyses with a total of 329 associations. Strong evidence for a benefit was found for LCD with reductions in BW [MD: −4.79 (95% CI −5.85, −3.72) kg, p ≤ 0.001], SBP [MD: −6.38 (95% CI −7.84, −4.93) mmHg, p ≤ 0.001], TG [WMD: −5.81 (95% CI −7.96, −3.66) mg/dL, p ≤ 0.001], and fasting plasma insulin [MD: −15.35 (95% CI −19.58, −11.12) pmol/L, p ≤ 0.001], as well as for low-GI diet for the reduction of BW [SMD: −0.66 (95% CI −0.90, −0.43) kg, p ≤ 0.001]. Conclusions: Across many dietary patterns, LCD showed strong or highly suggestive evidence for a benefit on SBP, BW reduction, and lipid profile improvement. Secondarily, low-GI, DASH, and Portfolio and Nordic diets suggested beneficial effects on controlling CV risk.

Abstract 4132249: Preoperative identification of respiratory viral genomes in the trachea but not in the nasopharynx is a risk factor for postoperative pulmonary hypertension in patients with congenital cardiac communications

Introduction: Pulmonary vascular remodeling is a key determinant of outcomes in patients undergoing surgery for congenital cardiac communications (CCCs). Respiratory epithelial cells infected by viruses express cytokines and growth factors with potential impact on airway and vascular remodeling. Hypothesis: Preoperative exposure to respiratory viruses renders CCC patients susceptible to postoperative pulmonary hypertension. Aims: To investigate if asymptomatic patients carrying respiratory viral genomes (RVGs) in the airways are at risk for pulmonary hypertension following cardiac surgery. To analyze the role of postoperative inflammatory reaction. Methods: The study comprised patients with unrestrictive CCCs undergoing surgery under cardiopulmonary bypass (CPB). In the absence of any signs of recent infection, RVGs were searched for in nasopharyngeal aspirates 2-3 days before surgery, and in tracheal aspirates collected in the operating room (RT-PCR, panel for 19 viruses). Serum levels of 36 inflammatory proteins were measured by chemiluminescence preoperatively and 4 hours post CPB. Pulmonary/systemic mean arterial pressure ratio (PAP/SAP) computed during the first 12 hours postoperatively (invasive assessment) was defined as the study outcome. A cutoff level was set at 0.40. Results: Sixty patients were enrolled (age 11 [7-16] months, median with interquartile range). Preoperative PAP/SAP was 0.78 (0.63-0.88). RVGs were present in nasopharyngeal and tracheal aspirates in 64% and 38% of patients, respectively. The presence of RVGs in tracheal aspirates was associated with an upward shift of postoperative PAP/SAP curve (p=0.006). The same was not observed for positive tests in nasopharyngeal aspirates (p=0.343). Of all factors analyzed as possible predictors of postoperative PAP/SAP &gt;0.40, only preoperative peripheral oxygen saturation and the presence of RVGs in the trachea were selected at multivariate analysis (respective OR with 95% CI, 0.40 [0.23-0.72] and 4.42 [1.17-16.78]. Heightened post-CPB levels of interleukin-1 receptor antagonist and chemokines MIF and MCP-1 were found to increase the risk of having a PAP/SAP &gt;0.40 in RVG carriers (respective OR with 95% CI, 2.04 [1.09-3.81], 2.34 [1.15-4.74] and 2.18 [1.07-4.43]. Conclusion: The observed relation of postoperative hemodynamics to respiratory viruses and post-CPB inflammatory reaction may have pathophysiological and therapeutic implications in pulmonary hypertension associated with congenital heart disease.

Abstract 4136776: Prognostic Value of Resting Heart Rate and Heart Rate Variability in the 12-lead Electrocardiogram: Mortality Data From the CODE Nationwide Database

Introduction: Resting Heart Rate (HR) and Heart Rate Variability (HRV) reflect autonomic control, and are implicated as prognostic factors. We aimed to evaluate the prognostic value of HR and HRV in a cohort from a nationwide telemedicine network. Methods: We assessed unique ECGs recorded from patients ≥16 years-old, from the tele-ECG database of the Telehealth Network of Minas Gerais, Brazil, between 2010 and 2017. Variables of interest were HR and standard deviation of normal RR intervals (SDNN). Self-informed data were collected: sex, age, risk factors (hypertension, dyslipidemia, diabetes, smoking) and comorbidities (myocardial infarction, Chronic Obstructive Pulmonary Disease, and Chagas disease). Outcomes of interest were all-cause and cardiovascular mortality, assessed by ICD codes reported in death certificates, through linkage with the Mortality Information System. Cox regression was applied to evaluate the association between HR and HRV and the outcomes, in 4 models: 1. Unadjusted; 2. Adjusted for sex and age; 3. Model 2 + risk factors + clinical comorbidities; 4. Model 3 + HRV or HR, respectively. Results: At total 992.611 individuals were included, median age of 55 years, 60% women. In 6 years, there were 33.292 deaths (3,37%), 21% due to cardiovascular causes. Patients who died had higher prevalence of all risk factors and comorbidities, as well as higher HR: 76 (IQR 66-87) vs. 74 (IQR 65-83) bpm, p&lt;0.001 and lower HRV: 84 (IQR 51-127) vs. 114 (IQR 74-153), p&lt;0.001. After adjustments (model 4), all HR quartiles were independently associated a progressively increased risk of all-cause mortality, being 88% higher for the 4 th quartile (HR=1.88 (95%CI 1.77–1.89). Similarly, the 1 st and 2 nd HRV quartiles remained associated with increased all-cause mortality (1 st quartile HR=1.42 (95%CI 1.37–1.47) in the final model. For cardiovascular mortality, HR was also an independent predictor, with a progressively higher risk, with a 77% increase (HR=1.77 95%CI 1.65–1.91) in the 4 th quartile. HRV was also an independent predictor of cardiovascular death, with a 33% risk increase (HR=1.33, 95%CI 1.23–1.44) for the 1 st quartile. Male gender, age, and all risk factors and comorbidities were also independent predictors of all-cause and cardiovascular mortality. Conclusions: In a large cohort of Brazilian adults, baseline HR and HRV were independent predictors of all-cause and cardiovascular mortality, after adjustment for clinical variables and autonomic indexes.

Abstract 4123373: Estimating obesity-attributable cardiovascular disease burden in the United States: a Bayesian network analysis

Background: Obesity is a known contributor to the development of cardiovascular disease (CVD) and increases the risk of subsequent mortality. To fully understand the burden of obesity, accurate information regarding its effects on CVD is necessary. Current estimates are limited by a focus on direct effects, use of non-representative data sources, and a reliance on inaccurate diagnosis codes. Aim: To determine the size of CVD burden attributable to obesity in the US and identify the mechanisms through which obesity affects CVD. Methods: This study used data collected from US adults (aged ≥35 years) participating in the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2020 and US Census projections. NHANES data were longitudinally adapted, and participants were excluded if they had missing data for weight history, risk factors, or a given outcome of interest. Bayesian networks (BNs) mapping out the relationship between risk factors and each outcome were constructed to estimate current CVD risk and expected CVD risk in the absence of obesity. Obesity-attributable CVD burden was then calculated for each outcome, and the direct and indirect pathways through which changes in CVD risk occur were characterized. A subgroup analysis was conducted in non-smoking participants aged ≤65 years for whom obesity is likely the primary CVD risk factor. Results: The final sample included data from approximately 29,000 participants. Of these, 1286 (4.3%) had a history of myocardial infarction (MI), 1283 (4.4%) had a history of stroke, 1092 (3.7%) had a history of heart failure (HF), and 1992 (6.7%) had a history of CVD (composite of MI, stroke, angina, coronary heart disease, and HF). Results from the fitted BN indicate that 21% of MI, 16% of stroke, 38% of HF, and 19% of CVD cases were attributable to obesity, with ≥80% of this burden due to the effect of obesity on intermediate risk factors (hypertension, type 2 diabetes, and prior cardiovascular events). In the subgroup analysis, the obesity-attributable CVD burden was approximately twice as high for non-smokers aged ≤65 years, with 39% of MI, 32% of stroke, 65% of HF, and 38% of CVD cases attributable to obesity. Conclusion: Through a sophisticated network modeling approach, we generated estimates of obesity-attributable CVD burden in the US. Results highlight the importance of obesity as a CVD risk factor, particularly in younger non-smokers, and provide insight into the nature of this relationship.

Abstract 4136145: All-cause and Cause-specific Mortality Disparities in the District of Columbia: Temporal Trends from 2000 to 2020

Background: A report evaluating all-cause mortality in 30 major U.S. cities documented that inequality between Black and White populations in Washington, D.C. was the greatest. However, little is known about disparities in cause-specific mortality over time or by racial groups. Aims: Evaluate trends in all-cause and cause-specific mortality in D.C. from 2000 to 2020 by race, and concurrently examine trends in cardiovascular (CV) risk factors. Methods: Using the CDC WONDER database, we calculated age-adjusted mortality rates per 100,000 persons (2000-2020) for Non-Hispanic Black and Non-Hispanic White populations in D.C. and corresponding rate ratios. Average Annual Percentage Change (AAPC) was examined with joinpoint regression. We examined the prevalence of risk factors (obesity, hypertension, diabetes, smoking, and hypercholesterolemia) using the Behavioral Risk Factor Surveillance System (2000-2020). Results: Among 102,710 deaths that occurred in D.C. (80% Black), cardiovascular diseases (CVD, 32%) and cancer (22%) accounted for over half of the deaths. All-cause mortality declined between 2000-2012 (AAPC: -2.9%, 95% CI: -5.6, 1.0) but stagnated between 2012-2018 (AAPC:-1.1%, 95% CI: -4.6, 0.9) and increased after 2018 (AAPC: 7.7%, 95% CI: 0.6, 11.9). CVD mortality declined between 2000-2011 and plateaued thereafter among Black individuals, contrasting with a monotonous decline (AAPC: -4.7%, 95% CI: -5.3, -4.0) among White individuals, resulting in a magnification of the disparities. Cancer mortality decreased over time for both White and Black individuals (AAPC: -3.4%, 95% CI: -3.9, -2.9 vs. AAPC: -1.8%, 95% CI: -2.1, -1.4, respectively), with a greater magnitude in White individuals. Risk factors were more prevalent among Black individuals over the period. Conclusion: In D.C., the mortality rate is higher in Black vs. White populations, and disparities are increasing over time. While CVD and cancer mortality rates declined overall, profound disparities remain. CVD risk factors are more common in Black populations, with persisting disparities. There is an urgent need for CVD prevention and management, tailored to Black populations in D.C.

Abstract 4137620: Serum Acylcarnitines Predict Longitudinal Deteriorations in Cardiac Function and Adverse Outcomes in Older Adults

Background: Circulating acylcarnitines (ACs), biomarkers of mitochondrial β-oxidative function, are linked to cardiovascular diseases (CVD) yet the extent to which ACs relate to prospective cardiac aging remains uncertain. We investigate the longitudinal associations between ACs, cardiac function, and clinical outcomes. Methods: A population-based sample of community older adults without CVD underwent baseline serum metabolomic profiling and interval echocardiography at five years. Incident hospitalizations were prospectively tracked from 2014 to 2021. Multiple linear regression adjusted for significant clinical variables. Results: Of 202 participants (baseline 65±11.9 years, 49.3% women), we observed interval increases in risk factors (hypertension 39% vs 52.2% p&lt;0.001; dyslipidemia 39% vs 50% p=0.034; diabetes 11.7% vs 18.8% p=0.035; smoking 13.2% vs 24.7% p=0.003; waist circumference 81±10.1 vs 86±9.9cm p&lt;0.001) during follow-up (4.9±0.4 years). These changes paralleled E/e’ increases (8.9±2.6 vs 11.1±3.3 p&lt;0.001) and E/A decreases (1.09±0.4 vs 1.0±0.4 p&lt;0.001). Baseline C8:1 (β=0.182 p=0.011), C22:3 (β=0.148 p=0.047), C22:5 (β=0.210 p=0.003), C5:1 (β=-0.142 p=0.048), and C16-OH (β=-0.156 p=0.028) levels were associated with E/e’ change over time while C6 (β=0.163 adj. p=0.019), C8:1 (β=0.137 adj. p=0.047), C10:2 (β=0.153 adj. p=0.035), C14:3 (β=0.147 adj. p=0.031), and C16:1-OH/C14:1-DC (β=0.158 adj. p=0.022) were associated with E/A change. At follow-up, baseline C8:1 (β=0.178 adj. p=0.006) and C10:3 (β=0.145 adj. p=0.024) were associated with E/e’ while C4-DC/C6-OH (β=-0.004 adj. p=0.034) was associated with E/A. Baseline C22:2 predicted incident hospitalizations (HR=1.20 95%CI 1.03-1.39, adj. p=0.018). Conclusion: Circulating ACs independently predicted declining cardiac function and adverse outcomes over five years among older adults without CVD. The prognostic effect of ACs should be translated to strategies targeting mitochondrial health in cardiac aging prevention.

Impact of smoking status on incident hypertension in a Japanese occupational population.

Hypertension and tobacco smoking pose independent risks for cardiovascular diseases, but their association is unclear especially in Japanese. We investigated the impact of smoking status on the risk of new-onset hypertension in male and female Japanese workers. We evaluated 5439 subjects without hypertension who participated in medical check-ups in 2007-2018. The outcome was the development of hypertension (blood pressure ≥140/90 mmHg or initiation of antihypertensive drugs). Cox's proportional hazards models were used to assess the association between smoking status and the hypertension incidence. During the average 6.0-year follow-up, 1395 individuals (25.6%) developed hypertension. The crude incidence rates of hypertension (per 100 person-years) were: current non-smokers (n = 3033), 3.4; quitters (n = 445), 4.2; and sustained smokers (n = 1961), 5.7. The multivariable-adjusted hazard ratio was 1.34 (1.20-1.50) for sustained smokers and 1.03 (0.86-1.24) for quitters compared to current non-smokers (P for trend <0.01). In stratified analyses, the risk of incident hypertension was significantly higher in the sustained smokers with lower blood pressure or without diabetes at baseline versus the current non-smokers. A significant risk reduction of hypertension development due to smoking cessation was revealed in the subjects with higher blood pressure levels at baseline or without body weight gain after smoking cessation. Smoking was an independent risk factor for incident hypertension. Smoking cessation reduced the risk of hypertension development compared to sustained smoking, especially among the subjects with higher blood pressure levels. Maintaining one's body weight after smoking cessation would also help prevent hypertension development.

Psidium guajava leaves extract alters colonic microbiome composition and reduces intestinal sodium absorption in rats exposed to a high-sodium diet.

High sodium intake is a major risk factor for hypertension and renal diseases. Previous studies have shown that a suspension of ethanolic extract of Psidium guajava (guava) leaves (PsE) has antihypertensive effects in rats on a high-sodium diet (HSD), but some mechanisms to that remain unexplored. This study explored whether oral PsE treatment affects sodium handling by the intestine and alters the gut microbiome in HSD-fed rats. Male Wistar rats were divided into two groups: standard salt diet (SSD) and HSD (0.9% Na+), from weaning. After 12 weeks, both groups received PsE (200mg/kg) or a vehicle for an additional 4 weeks. Sodium excretion was measured using flame photometry, and sodium absorption was assessed by intestinal perfusion technique. The gut microbiome was analysed through 16S ribosomal gene sequencing. HSD increased faecal sodium, further elevated by PsE, which inhibited intestinal sodium absorption in HSD rats. HSD altered the abundance of specific bacterial families, which PsE partially reversed. No changes in alpha diversity were noted among groups. These findings suggest that PsE inhibited intestinal sodium handling and that PsE, combined with increased faecal sodium, may reshape the gut microbiome of HSD rats to resemble that of SSD rats.

Impact of Overweight on Renal Prognosis in Malignant Hypertension Patients With Thrombotic Microangiopathy.

Overweight and obesity is a risk factor for hypertension. Malignant hypertension (MHT) is the most severe form of hypertension, and thrombotic microangiopathy (TMA), one of its complications, has been linked to significant renal outcomes. However, the impact of overweight and obesity on renal prognosis in MHT patients with TMA is not well understood. This was a prospective cohort enrolled 288 MHT patients with renal TMA from 2008 to 2023. The clinical and histopathological characteristics were recorded based on body mass index (BMI, < 25 and ≥ 25 kg/m2). The outcome was the incidence of kidney failure. The associations of BMI with kidney failure were examined in logistic regression models. Among 288 patients, 180 (62.5%) progressed to kidney failure, including 113 (68.5%) patients with BMI < 25 kg/m2. Participants with obesity had higher levels of hemoglobin, estimated glomerular filtration rate and C3, but lower levels of serum creatinine and IgA nephropathy. BMI ≥ 25 kg/m2 was associated with a better outcome of kidney failure in MHT patients with TMA (odd ratios [ORs]: 0.49 [95% confidence interval (CI): 0.27-0.91], p = 0.025). Male, uric acid, onion skin lesions, and global sclerosis ratio were correlated with higher risk of kidney failure; serum albumin and treatment with renin-angiotensin system blockers were related to lower risk of kidney failure. In MHT patients with renal TMA, normal-weight rather than overweight was found to associate with a worse renal prognosis. Management efforts for MHT may be directed toward controlling body weight within a reasonable range for patients.

Inhaling Poor Health: The Impact of Air Pollution on Cardiovascular Kidney Metabolic Syndrome.

Air pollution, mostly from fossil fuel sources, is the leading environmental cause of global morbidity and mortality and is intricately linked to climate change. There is emerging evidence indicating that air pollution imposes most of its risk through proximate cardiovascular kidney and metabolic (CKM) etiologies. Indeed, there is compelling evidence linking air pollution to the genesis of insulin resistance, type 2 diabetes, hypertension, and other risk factors. Air pollution frequently coexists with factors such as noise, with levels and risks influenced substantially by additional factors such as social determinants and natural and built environment features. Persistent disparities regarding the impact and new sources of air pollution, such as wildfires attributable to climate change, have renewed the urgency to better understand root sources, characterize their health effects, and disseminate this information for personal protection and policy impacts. In this review, we summarize evidence associating air pollution with cardiovascular health, the impact of air pollution on CKM health, and how interactions with other exposures and personal characteristics may modify these associations. Finally, we discuss new integrated approaches to capture risk from air pollution in the context of an exposomic framework.

QUERCETIN AS A POTENTIAL THERAPEUTIC AGENT IN HYPERTENSION COMPLICATED BY CONNECTIVE TISSUE DYSPLASIA

This article summarizes data on the effect of quercetin during the treatment of arterial hypertension, complicated by connective tissue dysplasia. Currently, numerous studies are being conducted to study the role of various genes in the development of arterial hypertension. One of the risk factors for hypertension, which remains insufficiently studied, is collagen pathology - undifferentiated connective tissue dysplasia (UND). The presence of connective tissue in all organs and systems, its common origin with mesenchyme, smooth muscle, blood, and lymph leads to dysplastic changes in any organ and system. Among the many metabolic agents in the treatment of hypertension in combination with DST, the bioflavonoid quercetin, which has a pronounced antioxidant effect, deserves the most attention. The use of water-soluble quercetin in the complex therapy of patients with hypertension in combination with DST reduces the frequency of recurrence of hypertensive crises in the post-hospital period, reduces the number of complications, leads to a decrease in blood stabilization, pressure, additional hypotensive effect.

Construction of OSA-related hypertension prediction model based on nomogram

Objective:This study aimed to construct a risk prediction model for obstructive sleep apnea（OSA） related hypertension based on the nomogram, and to explore the independent risk factors for OSA-related hypertension, so as to provide reference for clinical treatment decision-making. Methods:The clinical data of OSA patients diagnosed by polysomnography from October 2019 to December 2021 were collected retrospectively and randomly divided into training sets and validation sets. A total of 1 493 OSA patients with 27 variables were included. The least absolute shrinkage and selection operator（Lasso） logistic regression model was used to select potentially relevant features and establish a nomogram for OSA-related hypertension.The performance and clinical benefits of this nomogram were verified in terms of discrimination, calibration ability and clinical net benefit. Results:Multivariate logistic regression showed that body mass index（BMI）, family history of hypertension, lowest oxygen saturation（LSaO2）, age and cumulative percentage of total sleep time with oxygen saturation below 90% were independent risk factors for OSA-related hypertension. Lasso logistic regression identified BMI, family history of hypertension, LSaO2 and age as predictive factors for inclusion in the nomogram. The nomogram provided a favorable discrimination, with a C-indexes of 0.835（95% confidence interval[CI ]0.806-0.863） 0.865（95%CI 0.829-0.900） for the training and validation cohort, respectively, and well calibrated. The clinical decision curve analysis displayed that the nomogram was clinically useful. Conclusion:Compared with cumulative percentage of total sleep time with blood oxygen saturation below 90%, LSaO2 may have a greater impact on the incidence of OSA-related hypertension, and the effects of different times and degrees of hypoxia on OSA-related hypertension should be further explored in the future. Apnea hypopnea index involvement is weak in predicting OSA-related hypertension, and the blood oxygen index may be a better predictor variable. Furthermore, we established a risk prediction model for OSA-related hypertension patients using nomogram, and demonstrated that this prediction model was helpful to identify high-risk OSA-related hypertension patients. This model can provide early and individualized diagnosis and treatment plans, protect patients from the serious.

Prevalence and risk factors associated with undiagnosed hypertension among adults aged 15–49 years in India: insights from the National Family Health Survey (NFHS-5)

ObjectivesTo estimate the prevalence and identify the factors associated with undiagnosed hypertension in India. Study designA secondary data analysis using the National Family Health Survey (NFHS-5) covering the period 2019–2021. MethodsInformation on hypertension among individuals aged 15–49 years was extracted from the survey dataset. We estimated the prevalence of undiagnosed hypertension using physical measurements along with self-reported data from the survey. A log-binomial model with survey-adjusted Poisson regression was used to estimate the prevalence ratio between undiagnosed and diagnosed hypertension. Multinomial logistic regression analysis examined the factors associated with diagnosed hypertension (vs healthy) and undiagnosed hypertension (vs healthy). All the analyses were survey-weight adjusted and stratified by gender. ResultsThe survey-adjusted prevalence of undiagnosed hypertension was 8.75% (8.62%–8.87%) and was higher among males [13.56% (13.03%–14.12%)] than in females [8.14% (8.03%–8.25%)]. The proportion of individuals with undiagnosed hypertension among total hypertension was 44.99% (44.44%–45.55%) and was higher in males [65.94% (64.25%–67.60%)] than in females [42.18% (41.66%–42.71%)]. ConclusionsOur findings revealed that age, higher body mass index, no access to health care, and having no comorbidities were risk factors for undiagnosed hypertension. One in twelve people had undiagnosed hypertension, and of those with hypertension, one in two were undiagnosed, with males being disproportionately affected. Targeted public health interventions are crucial to improve hypertension screening, particularly among middle-aged and obese individuals without comorbidities.

Consumption of Milk a Probable Risk Factor of Hypertension in India: A Study Based on National Family Health Survey-5

Introduction: Chronic high blood pressure, often known as hypertension, can cause a number of cardiovascular issues due to its higher blood pressure levels. A growing body of research points to a possible link between the use of dairy products and a higher risk of hypertension. Objectives: The present study aims to provide information regarding a probable association between dairy consumption and hypertension among the population of India. Methodology: The current study uses data from the fifth series of the National Family Health Survey (NFHS-5) 2019–21 in order to examine this association. The sample size is 724115 in total. This study included eight factors in total: systolic and diastolic blood pressure, age, religion, ethnicity, education, wealth index, and frequency of milk/curd consumption. IMB-SPSS version 26.0 was used for all data analysis. Results: It was found that those consuming milk products daily and weekly have very strong chances of having stage 1(95.3% and 93.2%, respectively in 95% CI) and stage 2 hypertension (92.4% and 90.4%, respectively in 95% CI). daily consumption of milk products also significantly increases 80.3% the chance of having stage 3 hypertension as well (95% CI). Conclusion: It is abundantly obvious from the current study that consuming milk and curd on a daily and weekly basis considerably raises your risk of developing stage 1, stage 2, and stage 3 hypertension. Given that India consumes the most milk globally and that the bulk of it is unpasteurized, it is crucial to consider the connection between milk consumption and hypertension discovered in the current study.

Interaction of serum uric acid with overweight on hypertension: findings from the China Health and Nutrition Survey

BackgroundBoth serum uric acid (SUA) levels and body mass index (BMI) are recognized as important risk factors for hypertension. The current study aimed to investigate the interaction effects between SUA levels and overweight (defined as BMI ≥ 24 kg/m2 in Chinese) on the incidence of hypertension among Chinese adults.Methods1124 hypertensive participants and 7283 non-hypertensive participants, extracted from the China Health and Nutrition Survey (CHNS), were analyzed. Participants were categorized based on their SUA levels and BMI, to investigate the interaction effects between SUA levels and overweight on hypertension.ResultsIn comparison with the reference group (BMI < 24 kg/m2 and in the 1st quintile of SUA), multivariable adjusted analysis demonstrated that the odds ratio (OR) (95% confidence interval, 95% CI) of hypertension for participants with overweight alone was 2.18 (1.41–3.37); for elevated SUA levels alone, the ORs (95% CIs) were 1.57 (1.08–2.30), 1.84 (1.24–2.74), 2.21 (1.47–3.32), and 2.48 (1.55–3.96) across SUA quintiles; and for the combined effect of higher SUA levels and overweight, the ORs (95% CIs) were 3.25 (2.19–4.82), 3.73 (2.51–5.55), 5.17 (3.42–7.80), and 6.21 (4.01–9.60). The relative excess risk due to interaction (RERI) was 3.26 (1.43–5.09) at the 5th quintile of SUA, indicating the presence of additive interaction between overweight and SUA levels on hypertension.ConclusionInteraction between SUA levels and overweight on hypertension exists specifically at the highest quintile (Q5, > 6.39 mg/dL) of SUA among Chinese adults. Therefore, strategies to lower SUA levels could be considered as a potential approach to mitigate hypertension risk in overweight individuals within this specific subgroup.

Paradigm shift from glucocentric to organ protection for the management of hyperglycemia in patients with type 2 diabetes

The UK Prospective Diabetes Study was the first study to investigate the effectiveness of glycemic control in patients with type 2 diabetes. Since then, many studies have evaluated the impact of intensive glycemic control on diabetes-related morbidities and mortality. The results of these studies were intended to change the paradigm for controlling glycated hemoglobin and preventing diabetes-related complications, but the beneficial outcomes were limited to microvascular diseases rather than diabetes-related cardiorenal diseases and deaths. This has emphasized the need for comprehensive management of other risk factors (hypertension, dyslipidemia, renal failure, etc.) in addition to hyperglycemia to prevent atherosclerotic cardiovascular diseases and end-stage renal disease in type 2 diabetes. Since 2008, clinical trials to demonstrate cardiovascular safety have shown a beneficial effect of sodium-glucose transporter 2 inhibitors or glucagon-like peptide-1 receptor agonists on macrovascular or renal complications in patients with type 2 diabetes. Recently, major societies around the world including the Korean Diabetes Association, have shifted the goals of diabetes management from the typical glucocentric view to cardiorenal outcome-oriented (organ protection) care, which has been widely accepted and is gradually applied to primary care.

The association of second-hand smoke with hypertension among adult males in Bali, Indonesia

Second-hand smoke (SHS), also known as passive smoking, is a widely accepted risk factor for hypertension. This study aimed to determine the association of SHS and hypertension among a cohort of adult males in Bali, Indonesia. A nation-wide cross-sectional study of males aged ≥18 years was included in the study. We included 7,087 males in this study out of 14,494 subjects in Bali, that participated in the Indonesian Basic Health Survey (IBHS) 2018. Multivariate logistic regression was used to assess the association. The prevalence of hypertension among male adults was 32.3%. Among the hypertensive males, about 20.9% of the subjects was exposed to SHS. Multivariate logistic regression showed significant association between SHS (OR=1.16; 95%CI,1.02-1.32) and hypertension with adjusted odd ratio of age (aOR=1.03; 95%CI,1.02-1.04) and residence (aOR=1.10; 95%CI,0.99-1.23). The prevalence of hypertension among older males who were exposed to SHS was higher among urban residents. A public health campaign of anti-smoking is urgently needed to increase awareness of SHS exposure among older males who live in urban areas.