Short-term exposure to fine particulate matter and its chemical constituents may affect arterial stiffness via inflammation: A panel study among healthy adults.

Cardiac remodeling and arterial stiffness progression in wild-type vs hereditary transthyretin amyloidosis in Crete.

Analysis of the relationship between different intensities of physical activity and pulse wave velocity in adults: an epidemiological study.

Risk Factors for Plaque Vulnerability in a Community Population: Endothelial Function and Arterial Stiffness Indexes.

Andrographolide ameliorates vascular injury in hypertension by suppressing EndMT via Sp1-Notch1 signaling.

Introduction: evidences demonstrated that subclinical HMOD is strongly associated with adverse cardiovascular outcomes, including left ventricular hypertrophy, reduced kidney function, microalbuminuria, and increased arterial stiffness and mortality. Therefore, this study is aimed to estimate prevalence of hypertension-mediated organ damage in Ethiopian adults. Methods and Material: PubMed, Scopus, web of science, and goggle scholar databases were used for this analysis. We assessed methodological quality using the Joanna Briggs Institute (JBI) critical appraisal checklist. An inverse variance-weighted random-effects model meta-analysis was performed to estimate the pooled prevalence with a 95% confidence interval (CI). The I2 test statistic was used to check between-study heterogeneity, and the Egger's regression statistical test was used to check publication bias. A p-value of less than 0.05 used to declare statistical significance. Result: Ten studies with3751 participants were included in this analysis. Most of the included studies were cross-sectional studies with prevalence of hypertension-mediated organ damage among adults in Ethiopia were ranged from 14.2% to 92.1%. The pooled Prevalence of hypertension-mediated organ damage among adults in Ethiopia with a random-effects model was 37.2 2% (95% CI: 21.9-52.2). Conclusion: This study showed that more than one-third of adults with hypertension in Ethiopia experience hypertension-mediated organ damage. Therefore, critical need of early diagnosis of hypertension, routine screening for target organ damage, and strengthened blood pressure management strategies is recommended.

Obesity and insulin resistance promote arterial stiffening and hypertension, increasing cardiovascular risk. Activation of the epithelial sodium channel (ENAC) contributes to vascular stiffening in preclinical models, but the vascular effects of ENAC inhibition in adults with obesity and insulin resistance are not well defined. In this Phase II, 24-week, randomized, double-blind, single-center, placebo-controlled trial, 137 adults aged 30-70 years with overweight or obesity and at least one metabolic syndrome feature were randomized (2:1) to the ENAC inhibitor amiloride (5 mg daily) or placebo. Carotid-femoral pulse wave velocity (cfPWV), blood pressure, and vascular function were assessed at baseline, 12 weeks, and 24 weeks. Amiloride significantly reduced arterial stiffness, with decreases in cfPWV at 12 and 24 weeks, whereas no changes were observed with placebo. Systolic blood pressure was also reduced, with a mean reduction of 5.6 mmHg at 24 weeks. Older age was associated with greater reductions in cfPWV and systolic blood pressure. Amiloride increased serum potassium and lowered fasting glucose but did not significantly affect brachial artery flow-mediated dilation. No severe adverse events were observed. In conclusion, low-dose amiloride improves blood pressure and arterial stiffness in adults with overweight or obesity and features of metabolic syndrome, without major safety concerns. These findings suggest that blood pressure lowering with amiloride is associated with favorable changes in vascular stiffness in this population.

Systemic lupus erythematosus (SLE) is an autoimmune disorder characterised by multisystem involvement, frequently including cardiovascular manifestations. Interleukin 2 (IL-2), a key cytokine in immune regulation, plays a pivotal role in maintaining tolerance by promoting regulatory T cell function. The relationship between serum IL-2 levels and specific SLE features remains incompletely defined. The aim of our study was to investigate the associations between serum IL-2 concentrations and disease activity, inflammatory markers, autoantibody profiles as well as cardiovascular and metabolic parameters in a well-characterised cohort of patients with SLE. In this cross-sectional study, 235 patients with SLE were recruited and characterised, including assessment of autoantibody profiles, disease activity indices (SLE Disease Activity Index-2000 (SLEDAI-2K)), Damage Index and remission status. Cardiovascular characteristics were evaluated, encompassing lipid profiles, insulin resistance indices and carotid ultrasound parameters such as plaque presence, intima-media thickness and arterial stiffness. Serum IL-2 concentrations were quantified using an ultrasensitive technique, the Single Molecule Array (Simoa). Multivariable linear regression was conducted to examine the associations between circulating IL-2 levels and clinical as well as cardiovascular manifestations of SLE. In multivariable analyses, serum IL-2 levels showed significant positive associations with inflammatory markers including C reactive protein and IL-6. Disease activity, assessed by SLEDAI-2K, was positively correlated with IL-2 levels. Positive and significant associations were also noted, after adjustment for covariates, between IL-2 and specific autoantibodies, including anti-DNA, anti-Sjögren's syndrome antigen A (SSA), anti-Sjögren's syndrome antigen B (SSB), anti-Smith (Sm) and antiribosome. Regarding cardiovascular disease factors, triglycerides were positively associated with IL-2 whereas high-density lipoprotein-cholesterol exhibited an inverse relationship. Significant correlations exist between serum IL-2 levels and markers of inflammation, lipid profile, disease activity and specific autoantibody profiles in patients with SLE. These findings underscore the pivotal role of IL-2 in SLE immunopathogenesis, reflecting its intricate involvement in modulating both inflammatory responses and metabolic pathways.

The American Academy of Pediatrics Clinical Practice Guidelines (AAPCPG) recommend 24-h ambulatory blood pressure monitoring (ABPM) for diagnosing hypertension (HTN) in pediatric kidney transplant recipients. The ABPM guidelines were updated in 2022 to incorporate the 2017 AAPCPG thresholds for those ≥ 13years and exclude blood pressure loads. The effect of the 2022 update on ABPM phenotype and its association with end-organ damage in this population remains unexplored. We retrospectively evaluated pediatric kidney transplant recipients (age < 22years) who underwent 24-h ABPM for HTN surveillance between 1/2021 and 9/2024. We grouped ABPM phenotypes into two categories: HTN (masked, ambulatory, and 2014-specific severe ambulatory) and no HTN (normal, white-coat, and 2014-specific uncategorized). We assessed systematic differences between the two guidelines using McNemar's test and agreement using Cohen's Kappa coefficient. Our cohort included 105 recipients. Compared to 2014, the 2022 guidelines identified more recipients with HTN (49.5% vs. 36.2%; McNemar's p < 0.001); however, the overall agreement remained substantial (kappa: 0.73, 95% CI: 0.61, 0.86). Among the 10 recipients with elevated ambulatory arterial stiffness index (AASI), the 2022 guidelines identified 80.0% as abnormal compared to only 30.0% under the 2014 guidelines (McNemar's p = 0.025), reflecting no significant agreement (Kappa: 0.19; 95% CI: -0.1, 0.49). Compared to the 2014 criteria, the 2022 guidelines identified a higher proportion of pediatric kidney transplant recipients with HTN and more effectively identified abnormalities in recipients with elevated AASI. Our findings indicate that 2022 guidelines are better aligned with markers of arterial stiffness and cardiovascular risk.

Evidence of sex-related differences in vascular health among people with cystic fibrosis.

Introduction: Metabolic acidosis is common after kidney transplantation and is associated with adverse outcomes. However, its vascular and functional correlates in kidney transplant recipients remain insufficiently characterized. Methods: We conducted a cross-sectional study of adult kidney transplant recipients attending routine outpatient visits at a tertiary transplant center. Metabolic acidosis was defined as serum bicarbonate < 22 mmol/L. Arterial stiffness was assessed by carotid-femoral pulse wave velocity (PWV), and physical frailty was evaluated using the Fried frailty phenotype. Multivariable regression models were used to identify determinants of metabolic acidosis and to examine its association with arterial stiffness and frailty severity. Results: Among 239 patients (median age 46 years), 154 (64%) had metabolic acidosis. Lower estimated glomerular filtration rate and higher systemic inflammation were independently associated with metabolic acidosis. Metabolic acidosis was independently associated with higher arterial stiffness, with a 1.41 m/s higher PWV after adjustment for age, sex, blood pressure, kidney function, and diabetes mellitus (p < 0.001). Although metabolic acidosis was associated with greater frailty severity in minimally adjusted models, this association was attenuated and no longer statistically significant after further adjustment for kidney function, diabetes, and inflammation. In stable kidney transplant recipients, metabolic acidosis is independently associated with increased arterial stiffness but not with frailty after accounting for key clinical confounders. Conclusions: These findings highlight metabolic acidosis as a marker of vascular vulnerability and a potential therapeutic target after kidney transplantation.

To ascertain the cross-sectional association between cardiovascular autonomic dysfunction and arterial stiffness across glucose metabolism status. We performed a cross-sectional analysis of participants of the Maastricht study. Cardiovascular autonomic function was based on heart rate variability (HRV) indices from 24-hour ECG recordings and summarized in z-scores for time and frequency domains. Aortic and carotid stiffness were assessed by carotid-femoral pulse wave velocity (PWV) and carotid artery distensibility (CD), respectively. We used multiple linear regression to study the associations and adjusted for demographic and lifestyle factors and a range of cardiovascular risk factors. We tested for effect modification of the associations by glucose metabolism status. PWV and CD measures were available in 3673 and 1802 participants, respectively (median (25th; 75th percentile) age: 60 years (53; 66), 51% women, 20% type 2 diabetes by design. Participants with lower HRV had higher aortic stiffness. Per SD lower time-domain and frequency-domain HRV z-scores were associated with 2.8% (95% CI 2.1% to 3.4%) and 2.8% (95% CI 2.1% to 3.5%) higher PWV, respectively. Similar trends were observed for carotid stiffness, with 3.2% (95% CI 1.4% to 5.0%) and 3.1% (95% CI 1.2% to 5.0%) lower CD per SD lower time-domain and frequency-domain HRV, respectively. The magnitude of these associations was higher in groups with prediabetes and type 2 diabetes compared with those with normal glucose metabolism, with evidence of effect modification by glucose metabolism status (p value for interaction: <0.01 for prediabetes and <0.05 to <0.10 for type 2 diabetes, both compared with normal glucose metabolism). Cardiovascular autonomic dysfunction is associated with higher aortic and carotid stiffness, especially in people with dysglycemia.

ABSTRACT Vascular calcification represents an active multifactorial process that mirrors several key features of skeletal bone mineralization. Clinically, it is characterized by diminished arterial compliance and increased arterial wall stiffness, both of which serve as independent predictors of significant adverse cardiovascular events. The primary cellular mechanism involves the phenotypic transformation of contractile vascular smooth muscle cells (VSMCs) into osteo/chondrogenic‐like cells, which produce an extracellular matrix conducive to hydroxyapatite deposition. This transdifferentiation is regulated by intricate cellular signaling networks, including the BMP‐Smad signaling pathway, both canonical and non‐canonical Wnt/β‐catenin pathways, Stat3 activated by inflammatory cytokines, the Notch signaling pathway, and ROS‐activated MAPK (ERK/p38) and NF‐κB pathways. In contrast, the SIRT family proteins (such as nuclear SIRT1/SIRT6), extracellular pyrophosphate (PPi), and matrix Gla protein (MGP) exert inhibitory effects on vascular calcification. Anatomically, calcification can be localized to the intimal layer, often superimposed on advanced atherosclerotic plaques in large conduit arteries, or to the medial layer, a pattern characteristic of small‐ to medium‐sized muscular arteries, known as Mönckeberg's sclerosis. Despite extensive research efforts, the molecular mechanisms governing mineral deposition in vascular tissues remain inadequately understood, and no pharmacological intervention has yet been demonstrated to be both safe and effective in preventing or reversing established calcification. In this review, we examine current insights into the pathobiology of vascular calcification, critically evaluate available in vitro models (including human aortic smooth muscle cells, endothelial cells, and valvular interstitial cell calcification models) and in vivo models (such as pharmacologically induced and genetically modified or surgical models) and highlight emerging therapeutic targets and agents that are currently under preclinical or early clinical investigation.

Effect of the Alto Endovascular Aneurysm Repair Device on Postoperative Large Artery Stiffness.

Active arterial mechanics, governed by vascular smooth muscle contraction, are critical to physiological regulation, cardiovascular disease progression, and clinical diagnosis. Although various in vivo methods have been developed to assess arterial stiffness, most cannot distinguish the contribution of smooth muscle tone; therefore, quantitative characterization of arterial activity remains challenging. In this study, we developed a pressure-area analysis framework integrating ultrasound imaging, blood pressure measurement, neural network-based segmentation of arterial cross-sectional area, and biomechanical model-driven inversion to infer active mechanical properties. A total of 233 volunteers (aged 18-65 year) were recruited to acquire cross-sectional ultrasound videos of the right common carotid artery for training the neural network. The segmentation results demonstrate good spatial and temporal performance of the neural network. We further recruited 10 additional volunteers (aged 25 ± 3year) to perform a 1min step test, followed by pressure-area measurements over a 30min recovery period. Using the proposed approach, we quantified post-exercise changes in carotid arterial active mechanics relative to baseline (i.e., the resting state). Results showed that active mechanics remained elevated for approximately 15min compared to baseline (p < 0.05), whereas systolic pressure differed significantly only within the first approximately 5min post-exercise (p < 0.001). These results indicate a dissociation between blood pressure and smooth muscle recovery, which may offer new insight into vascular smooth muscle regulation during physiological stress.

Centrum semiovale perivascular spaces (CSO PVS) are common to different cerebral small vessel disease (CSVD) subtypes, yet their enlargement to the point of visibility on magnetic resonance imaging is thought to occur through distinct mechanisms. In cerebral amyloid angiopathy (CAA), CSO PVS are thought to reflect impaired perivascular Aβ (amyloid-β) drainage, whereas in deep perforator arteriopathy (DPA) they may result from microangiopathy-related arterial stiffening and altered fluid dynamics. The extent to which this can be confirmed in vivo remains unclear. We retrospectively analyzed 186 patients with CSVD and cerebrospinal fluid (CSF) Aβ biomarkers (n=111 probable CAA, n=75 DPA). CSO PVS were counted on axial T2-weighted images. Associations between CSO PVS and CSF biomarkers were assessed via Pearson correlation and multivariable linear regression, including an interaction term between CSF Aβ and CSVD subtype, adjusted for demographics and neuroimaging markers of CSVD. Patients with higher CSO PVS counts were generally younger, had lower white matter hyperintensity burden, higher basal ganglia PVS counts, and were more frequently affected by cortical superficial siderosis. CSO PVS counts were similar in patients with CAA and DPA. The association between CSF Aβ42/40 ratio and CSO PVS burden was observed in patients with CAA, but not in those with DPA (interaction term between CSF Aβ42/40 ratio and CAA: β=-0.27; P=0.016), independent of demographics and other neuroimaging markers of CSVD. CSF Aβ40 showed no association with CSO PVS counts in any model. Our findings strengthen the pathophysiological link between CSO PVS and Aβ pathology in CAA but not in DPA. These results extend previous histopathologic and neuroimaging work and underscore the need to interpret CSO PVS in the context of underlying CSVD subtype.

Vascular effects of achieving low disease activity in axial spondyloarthritis - A 2-year prospective treat-to-target study.

The relationship between the progression of arterial stiffness and the risk of chronic kidney disease (CKD) remains unclear. This study aimed to evaluate the time-dependent association between the progression of arterial stiffness and the risk of CKD. We followed 10,567 individuals in the Kailuan Study, who were free of CKD and CVD at baseline. Arterial stiffness was repeatedly measured by brachial-ankle pulse wave velocity (baPWV) from baseline to the subsequent follow-ups. Time-dependent Cox models were used to estimate the association between progression of arterial stiffness (△baPWV/years) and incident CKD, defined as an eGFR below 60 ml/min per 1.73 m2 and/or the presence of albuminuria. During a mean follow-up of 5.32 years, 1108 participants developed CKD. Lower quintiles in baPWV at baseline and the progression of baPWV over time were associated with a lower risk of CKD in a dose-dependent manner (p-trend <0.001). Compared with participants with the greatest deterioration in arterial stiffness (quintile 5), those with the greatest improvement in arterial stiffness (quintile 1) had a 45% (95% CI 34, 55) lower risk of CKD. Each SD increment in the progression of baPWV was associated with a 19% higher risk of CKD. Additionally, compared with participants who consistently had high baPWV (≥1400 cm/s), participants who maintained low baPWV (<1400 cm/s) or improved from high to low baPWV over time had a 46% (95% CI 33, 57) or 32% (95% CI 12, 48) lower risk of incident CKD, respectively. Adding progression of arterial stiffness to the CKD risk model modestly improved discrimination (optimism-adjusted C statistic from 0.690 to 0.709, p<0.001). In this cohort study, improvement in arterial stiffness, as indicated by a consistently low or decreased baPWV, might be associated with a lower risk of CKD. These findings underscore the potential importance of coordinated actions targeting cardiovascular health to improve kidney health in the general population.

Research on chronic aerobic exercise (AE) and arterial stiffness has yielded mixed results, largely due to differences in participant characteristics and training protocols. This meta-analysis included 26 trials (40 interventions; n=756; average age 42±15 y) to assess AE's effect on arterial stiffness, measured by pulse wave velocity (PWV) and to explore moderating factors. AE programs averaged 40±19 minutes/session, 3±1 d/wk, over 11±8 weeks, with intensities between 3 and 8 METs. Random-effects analysis showed AE significantly reduced central (- 1.02 m/s), mixed (- 0.34 m/s), and peripheral (- 0.72 m/s) PWV, with an overall mean reduction of-0.93 m/s and no differences between arterial beds. However, only a subset of studies showed significant reductions: 9/25 for central, 3/6 for mixed, and 4/8 for peripheral PWV. Studies with higher methodological quality yielded larger effect sizes. Reductions in PWV were consistent across participants with normal or high blood pressure, differing baseline PWV, and both younger and older adults, regardless of blood pressure changes. The impact of training components was inconsistent, suggesting AE benefits across a range of intensities and volumes. Overall, AE appears to reduce arterial stiffness across diverse populations and exercise protocols, supporting its role in improving vascular health.

Exercise and the hallmarks of cardiovascular aging.