Search Results (456)

Background and Objectives: Lipoprotein(a) [Lp(a)] is an established cardiovascular risk factor associated with atherosclerosis, vascular inflammation, and endothelial dysfunction. However, data regarding its relationship with hypertension-mediated organ damage and circadian blood pressure abnormalities remain limited. We aimed to investigate the association of elevated Lp(a) levels with carotid atherosclerosis and nocturnal blood pressure dipping patterns in patients with hypertension. Materials and Methods: This retrospective cross-sectional study included 80 nondiabetic patients with essential hypertension. Patients were categorized according to serum Lp(a) levels into elevated Lp(a) (≥50 mg/dL, n = 20) and lower Lp(a) (<50 mg/dL, n = 60) groups. All participants underwent carotid ultrasonography, transthoracic echocardiography, ambulatory blood pressure monitoring, and ophthalmologic evaluation. Multivariable logistic and linear regression analyses were performed to determine independent associations between Lp(a), carotid plaque presence, and nocturnal dipping percentage. Results: Patients with elevated Lp(a) levels had a significantly higher prevalence of carotid plaque (55.0% vs. 23.3%, p = 0.008) and non-dipper hypertension (75.0% vs. 46.7%, p = 0.028) compared with patients with lower Lp(a) levels. Serum Lp(a) concentrations were inversely correlated with nocturnal dipping percentage (r = −0.362, p = 0.001). In multivariable logistic regression analysis adjusted for age, sex, LDL cholesterol, and active smoking, elevated Lp(a) remained independently associated with carotid plaque presence (OR 3.24, 95% CI 1.06–9.80, p = 0.039). In multiple linear regression analysis adjusted for age, sex, LDL cholesterol, and office systolic blood pressure, higher Lp(a) levels remained independently associated with lower nocturnal dipping percentage (β = −0.294, p = 0.008). No significant associations were observed between Lp(a) and carotid intima–media thickness, left ventricular hypertrophy, hypertensive retinopathy, or renal functional parameters. Conclusions: Elevated Lp(a) levels were independently associated with carotid plaque presence and impaired nocturnal blood pressure decline in hypertensive patients. These findings suggest that Lp(a) may be more closely linked to focal macrovascular atherosclerosis and abnormal circadian blood pressure regulation rather than diffuse hypertensive structural remodeling. Full article

Background/Objectives: UNet-based models dominate medical image segmentation. Transformers have been added as an internal variant to these UNet-based architectures to improve feature learning. However, they have limitations in generalization and computational efficiency. Motivated by this idea, we have designed a two-stage novel hybrid segmentation framework, where tuners are added in cascade to the base architectures. Methods: Three sets of base UNets were designed, namely: B1: UNet1p, B2: UNet2p, and B3:UNet3p, and four sets of transformer-based tuners were designed, namely: T1:Transformer-augmented UNet, T2: Attention-guided UNet, T3: Swin Transformer-based UNet, and T4: Pyramid-based network, leading to 12 fused systems that combine three base UNets and four Tuners, namely: F1: B1 + T1, F2: B1 + T2, F3: B1 + T3, F4: B1 + T4; F5: B2 + T1, F6: B2 + T2, F7: B2 + T3, F8: B2 + T4, F9: B3 + T1, F10: B3 + T2, F11: B3 + T3, F12: B3 + T4. Results: The two-hybrid segmentation models are more effective and reliable than the single-stage UNet architecture. B3 + T4 achieved a Dice of 94.14% and Jaccard of 88.7%, surpassing prior baselines by 4.2% and 6.8%. It reduced cIMTE to 0.014 mm, a 36% improvement and the lowest reported to date, with cLIE and cMAE errors lowered by 40%. Conclusions: All 12 hybrid automated transformer-based models are highly accurate and reliable for wall segmentation in carotid ultrasound; they are a powerful paradigm for cardiovascular risk. Full article

Obstructive sleep apnea syndrome (OSAS) is heavily implicated in subclinical cardiovascular disease; however, traditional polysomnographic metrics fail to capture the localized mechanical trauma exerted on the carotid artery. To address this methodological gap, this study evaluated exploratory associations between frequency-domain snoring characteristics and right carotid artery alterations in 50 patients with OSAS. Snoring was quantified using a dual-modality bioelectronic approach: an ambient microphone captured airborne snoring sound energy (SSE), while a portable neck-surface piezoelectric sensor recorded tissue-conducted snoring vibratory energy (SVE). Subclinical vascular changes, including carotid intima-media thickness (CIMT) and atherosclerosis, were assessed via ultrasonography. Hierarchical multivariable regression demonstrated that acoustic SSE%-404–500 Hz and mechanical SVE%-112–144 Hz independently correlated with preliminary CIMT increases (adjusted β = 0.033 and 0.021, respectively; both p < 0.05), alongside neck circumference. Conversely, SSE%-404–500 Hz emerged as an exploratory marker for focal carotid atherosclerosis (adjusted odds ratio = 1.828; p = 0.009). Integrating this metric with baseline parameters yielded exploratory diagnostic capacity (area under the curve = 0.833; p < 0.001), achieving 89% sensitivity and 69% specificity. These findings suggest that dual-modality spectral analysis provides a non-invasive exploratory framework for cardiovascular risk stratification, isolating localized mechanotransduction phenotypes independently of systemic hypoxia. Full article

Congenital hypothyroidism (CH) is a common endocrine disorder characterized by thyroid hormone deficiency and has dramatic consequences if diagnosis and treatment are delayed. Although neonatal screening (NNS) and early levothyroxine (L-T4) treatment have markedly improved neurodevelopmental outcomes, evidence suggests that cardiovascular alterations may persist into later life. Thyroid hormones regulate lipid metabolism, endothelial nitric oxide (NO) availability, myocardial relaxation, vascular tone and arterial wall homeostasis. Early clinical studies in patients with CH reported variable lipid and lipoprotein abnormalities, whereas more recent studies have demonstrated endothelial dysfunction, increased arterial stiffness, and elevated carotid intima–media thickness (IMT), even in the absence of classical cardiovascular risk factors. These alterations appear to be associated with cumulative exposure to thyroid-stimulating hormone (TSH) abnormalities rather than isolated biochemical measurements. These findings suggest that CH may affect cardiovascular biology through multiple pathways, including dyslipidemia, endothelial dysfunction, vascular remodeling, and cumulative exposure to thyroid-stimulating hormone abnormalities. This review summarizes the available evidence linking congenital hypothyroidism to early vascular and atherosclerotic changes and discusses its conceptual relationship to familial hypercholesterolemia as another model of early-life cumulative cardiovascular risk. Full article

Subclinical atherosclerosis (SCA) has been associated with lung function in many populations. Accordingly, those factors involved in respiratory health may contribute to the mechanisms linking pulmonary and cardiovascular disorders. Since the airway microbiome plays a key role in respiratory pathophysiology, microbial abundance and diversity in the upper airway may be associated with SCA risk. This study aimed to assess the association of upper airway microbiome abundance and diversity with SCA risk. A nested case–control study was carried out among adults from the Southern Caribbean. SCA was defined by carotid Doppler ultrasound as a carotid intima-media thickness ≥ 0.8 mm or the presence of carotid plaque. Oropharyngeal mucosal samples were collected under fasting conditions, and the V3-V4 region of the 16SRNA gene was sequenced. Differences in genus-level abundance were assessed using Microbiome Multivariable Association with Linear Models 2 (MaAsLin2). Alpha-diversity indices were compared through Wilcoxon tests. Principal coordinates analysis (PCoA) and Permutational Multivariate Analysis of Variance (PERMANOVA), adjusted for age, body mass index, and smoking status, were performed to assess associations between Bray–Curtis distances and SCA. MaAsLin2 was also applied to determine predicted metabolic pathway enrichment. A total of 40 cases and 40 controls were analyzed. The oropharyngeal microbiomes composition was dominated by three genera: Prevotella (cases: 26.0%; controls: 29.8%), Veillonella (cases: 16.3%; controls: 13.7%) and Fusobacterium (cases: 7.5%; controls: 8.0%). Significant differences in relative abundance were found for Streptococcus, Aureimonas, Mogibaecterium, Candidatus Saccharimonas, Pseudomonas, Segatella, Stomatobaculum, Oribacterium and Lachnoanaerobaculum, with lower abundance in cases for all these genera. Alpha-diversity was lower in cases than in controls, as reflected by the Shannon index (cases: 5.95 IQR [4.87; 6.35] vs. controls: 6.49 IQR [6.29; 6.75], p < 0.001), Simpson index (cases: 0.994, IQR [0.989; 0.996] vs. controls: 0.997 IQR [0.997; 0.998], p < 0.001) and Chao1 richness (cases: 1076.2 IQR [345.2; 1473.4] vs. controls: 1136.1, IQR [841.1; 1635.3], p = 0.04) were compared. In adjusted-PERMANOVA, 8.2% of microbiome variations were associated with SCA (pseudo-F = 7.49, R² = 0.082, p < 0.001), although this finding may have been influenced by intra-group dispersion among cases (PERMDISP: pseudo-F = 5.62, p = 0.018; Tukey’s HSD test: mean difference = −0.071, 95% CI [−0.118, −0.025], p = 0.003) Predicted enrichment of phenylalanine metabolism and indole alkaloid biosynthesis was higher in cases. In conclusion, these exploratory analyses suggest that reduced oropharyngeal microbiome diversity is associated with SCA. Further studies are warranted to clarify the role of the airway microbiome on cardiovascular outcomes. Full article

Background and Objectives: Despite the presence of atherosclerosis risk factors and symptoms associated with occlusive atherosclerotic cardiovascular disease (ASCVD), up to 30% of individuals do not present significant atherosclerotic lesions at the point of diagnostic evaluation. Those in whom ASCVD was ruled out once might be believed to be at low risk of future major cerebral and cardiac events (MACCEs). Despite this, they might still have some residual risk for MACCEs. Therefore, in the present study we aimed to evaluate risk factors for atherosclerosis progression to the stage of occlusive arterial disease in patients with cardiovascular risk factors but initially free from significant ASCVD. Materials and Methods: Between March 2012 and February 2014, a total of 686 consecutive patients presenting with clinical suspicion of significant coronary artery disease were evaluated. The actual status of atherosclerosis burden was verified in four major arterial territories (coronary, carotid, renal, lower limb arteries) with the use of angiography, computed tomography and ultrasonography. For the present study purpose, 188 (27.4%) patients were enrolled, in whom significant ASCVD (in any of the examined territories) was ruled out. In all patients, the incidence and severity of atherosclerotic risk factors, carotid intima–media complex thickness (CIMT) and carotid plaque presence were evaluated during first hospital admission. A ten-year follow-up period for a composite endpoint of MACCEs was included. Univariate and multivariate Cox proportional hazard analyses with the Simon–Makuch method for new-onset type 2 diabetes mellitus (T2DM) were performed for MACCEs. Results: MACCEs occurred in 30 (16%) of 188 patients, including 5 cardiovascular deaths, 19 non-fatal myocardial infarctions, and 6 non-fatal ischemic strokes, in a median of 48 (Q1; Q3: 25; 86) months. Univariate Cox proportional hazard analysis revealed that individuals who presented with baseline LDL cholesterol > 3.2 mmol/L, CIMT > 1 mm, carotid plaque, or experienced new-onset T2DM were predisposed to MACCE with hazard ratios (HRs) of 3.21 (p = 0.003), 3.82 (p = 0.001), 5.41 (p < 0.001), and 36.89 (p < 0.001), respectively. In multivariate Cox analysis, its associations with MACCEs were retained (HRs between 2.19 and 21.47), respectively. Conclusions: Our findings support the need for continued risk factor optimization despite the initial exclusion of obstructive ASCVD. In this study, we identified new-onset T2DM, initial LDL cholesterol, and the presence of subclinical atherosclerosis as risk factors for MACCEs. Full article

Per- and polyfluoroalkyl substances (PFAS) are persistent environmental contaminants increasingly associated with cardiovascular disease. Identifying early manifestations of vascular aging before the onset of overt disease is essential for improving cardiovascular risk stratification and prevention. Emerging evidence suggests that PFAS exposure contributes to early vascular and atherosclerotic alterations detectable by imaging techniques, including increased carotid intima–media thickness (CIMT), arterial stiffness, and endothelial dysfunction. In contrast, evidence for associations with coronary artery calcium progression and coronary stenosis remains scarce. Mechanistically, PFAS exposure promotes endothelial dysfunction, oxidative stress, chronic inflammation, lipid dysregulation, and genetic and epigenetic modifications, all of which contribute to premature vascular aging and metabolic disturbances. The integration of imaging and molecular biomarkers may provide complementary insights into the structural, functional, and biological processes underlying PFAS-related vascular damage; however, to date, this field remains largely unexplored. This narrative review summarizes current evidence on imaging and molecular biomarkers of PFAS-induced vascular aging and discusses their potential role in cardiovascular risk assessment. It also highlights key knowledge gaps and the need for robust epidemiological and multi-omics studies to validate these biomarkers, clarify causal mechanisms, and support their application in cardiovascular and environmental health surveillance. Full article

Background/Objectives: Polycystic ovary syndrome (PCOS) is increasingly recognized as a condition associated with cardiometabolic risk, yet its relationship with subclinical atherosclerosis in premenopausal women remains unclear. This systematic review aimed to synthesize and critically appraise the available evidence on the association between PCOS and markers of subclinical atherosclerosis. Methods: A systematic search of PubMed/MEDLINE, Embase, Scopus, Web of Science, and the Cochrane Library was conducted for studies published between January 2021 and January 2026. Eligible studies included premenopausal women with PCOS and assessed direct vascular markers or validated surrogate indicators of subclinical atherosclerosis. Data were synthesized narratively following PRISMA guidelines. Results: Nine studies were included, comprising five human clinical studies and four bioinformatics analyses. Evidence from imaging-based studies demonstrated increased carotid intima-media thickness, reduced wall shear stress, and a higher prevalence of subclinical vascular abnormalities in women with PCOS, particularly in some hyperandrogenic phenotypes. In contrast, adolescent populations showed predominantly metabolic and inflammatory alterations without clear structural vascular changes. Biochemical studies reported adverse lipid profiles and elevated atherogenic markers, while mechanistic studies highlighted inflammatory and mitochondrial pathways. Conclusions: Current evidence suggests that PCOS may be associated with early vascular alterations in premenopausal women; however, findings are limited by heterogeneity and observational designs. Further large-scale, phenotype-stratified prospective studies using standardized vascular assessments are needed to clarify cardiovascular risk in this population. Full article

Background: Recent research has drawn attention to potential systemic inflammation in patients with inherited epidermal differentiation disorders (EDD)—rare genetic skin conditions that may contribute to vascular dysfunction. Objective: This study assessed selected vascular, inflammatory, and biochemical parameters in 20 patients with selected EDD and 20 matched healthy controls. Methods: Assessments included Doppler ultrasound, ankle-brachial index, intima-media thickness (IMT), and laboratory profiling focused on lipid metabolism and systemic inflammation. Results: EDD patients showed significantly lower LDL cholesterol and higher interleukin-17A (IL-17A) than controls. IMT values were similar across groups and disease types, but correlated positively with age, body weight, waist circumference, triglycerides, and glucose, and negatively with reactive lymphocytes. No link was found between IMT and self-reported cardiovascular symptoms. Conclusions: In patients with selected EDD, we observed a distinct biochemical profile characterized by lower LDL cholesterol and higher IL-17A concentrations, without accompanying structural arterial changes—carotid IMT and ABI did not differ from controls and remained stable at short-term follow-up. These alterations may reflect disease-specific disturbances of lipid and inflammatory homeostasis rather than classical atherosclerosis. Although they could be of theoretical relevance to long-term vascular health, no structural arterial abnormality was demonstrated. Longitudinal studies incorporating endothelial function testing are needed to clarify their significance. Full article

Background/Objectives: Long COVID-19 (LC) has been associated with persistent inflammation and impaired vascular health. Dietary minerals are involved in oxidative stress, endothelial homeostasis, and arterial stiffness; however, their relationship with vascular health in LC remains poorly explored. This study aimed to examine the association between energy-adjusted dietary mineral intake and markers of vascular stiffness and vascular aging in adults with LC, while exploring potential sex-specific patterns. Methods: A total of 304 adults with LC from the BioICOPER study were included. Dietary mineral intake was assessed using a validated 7-day dietary record from the EVIDENT tool and expressed as mineral density per 1000 kcal for the regression analyses. Vascular assessment included carotid intima-media thickness (cIMT), carotid-femoral pulse wave velocity (cfPWV), brachial-ankle pulse wave velocity (baPWV), and the vascular aging index (VAI). Hierarchical multivariable linear regression models, false discovery rate (FDR) correction, restricted cubic spline analyses, sensitivity analyses excluding supplement users, and formal sex × mineral interaction tests were performed. Results: In descriptive adequacy analyses, adequate iron intake was associated with lower baPWV. In energy-adjusted linear regression models, no mineral-outcome association remained statistically significant after FDR correction. In the fully adjusted sensitivity model, zinc density showed a nominal positive association with cfPWV, but this association did not survive FDR correction. Restricted cubic spline analyses suggested possible non-linear associations of magnesium and potassium density with cfPWV and VAI. Formal interaction analyses did not provide robust evidence of sex-related effect modification. Conclusions: After energy adjustment and correction for multiple testing, the evidence for independent linear associations between dietary mineral density and vascular outcomes in adults with LC was limited. These exploratory findings suggest that mineral intake, dietary sources, and non-linear patterns deserve further evaluation in prospective studies and nutritional intervention trials. Full article

Background: Rheumatoid arthritis (RA) is associated with increased cardiovascular risk beyond traditional risk factors. Carotid intima–media thickness (IMT) is a marker of subclinical atherosclerosis and may be influenced by chronic inflammation in RA. Objectives: This study aimed to compare carotid IMT between women with RA and age-matched controls, and to investigate the associations between IMT and RA-related factors, including disease duration, menopausal status, anti-cyclic citrullinated peptide (anti-CCP) antibodies and the CD4/CD8 T-cell ratio. Methods: This cross-sectional study included 59 women with RA and 55 age-matched controls. All RA patients received methotrexate and had no recent biologic DMARD exposure. Carotid IMT was measured by B-mode ultrasonography. Clinical, laboratory, and immunologic parameters, including anti-CCP antibodies and CD4/CD8 ratio, were analyzed. Results: Mean carotid IMT was significantly higher in RA patients than in controls (0.85 ± 0.09 vs. 0.63 ± 0.08 mm, p < 0.0001). Within the RA group, IMT correlated positively with disease duration (r = 0.48, p < 0.001), years since menopause (ρ = 0.44, p = 0.001), anti-CCP titers (r = 0.31, p = 0.018) and CD4/CD8 ratio (r = 0.42, p < 0.001), and inversely with CD8 T-cell counts (r = −0.34, p = 0.009). In multivariable analysis, RA duration and CD4/CD8 ratio remained independently associated with IMT after adjustment for age, lipids and blood pressure. Conclusions: Women with RA had greater carotid IMT than age-matched controls. Longer disease duration and a higher CD4/CD8 ratio were independently associated with IMT, supporting a link between cumulative disease burden, T-cell imbalance and subclinical carotid atherosclerosis in RA. These findings support routine cardiovascular risk assessment and consideration of vascular imaging in high-risk RA subgroups. Full article

Background and Objectives: A relationship between cognitive decline (CD) and chronic coronary syndrome (CCS), common among the elderly population, has not yet been clearly established. Our study aims to evaluate the link between severe cognitive impairment and cognitive impairment, as measured by various neuropsychological tests in patients with or without CCS. In addition, we sought to identify cardiovascular risk factors (CVRFs) that influence the severity of CD and severe cognitive impairment. Materials and Methods: This observational study was conducted on 264 people with CVRFs. Of the 264, 132 were classified as patients with CCS and 132 as control subjects without CCS. Neuropsychological assessment tools included the Instrumental Activities of Daily Living (IADL) and Activities of Daily Living (ADL) scales, the Montreal Cognitive Assessment (MoCA), the Mini-Mental State Examination (MMSE), and the Geriatric Depression Scale (GDS-15). Clinical characteristics, echocardiographic measures, and vascular parameters of all subjects were also evaluated. Results: Patients with CCS had significantly lower cognitive performance (MMSE, p = 0.010; MoCA, p = 0.021), reduced functional status (IADL, p = 0.030; ADL, p = 0.012), and higher depression scores (p = 0.004) compared with controls. They also had worse cardiovascular profiles, including lower left ventricular ejection fraction (LVEF) (p = 0.001), higher NT-proBNP levels (p = 0.005), and increased carotid intima-media thickness (IMT) (p < 0.05). IMT and blood pressure values were negatively correlated with cognitive and functional scores and positively correlated with depression severity (p < 0.001). Multivariate analysis identified systolic and diastolic blood pressure, age, body mass index, heart rate, reduced daily activity, and depression as independent predictors of cognitive decline in patients with CCS. In the GDS-15 score, each unit increase was associated with a 32.1% higher risk of cognitive decline and a 37.1% higher risk of MMSE-defined severe cognitive impairment, while improved ADL scores significantly reduced this risk. Conclusions: CCS is associated with an increased risk of severe cognitive impairment and also with cognitive decline, influenced by hypertension, subclinical atherosclerosis, depression, and reduced functional status. These findings emphasize the importance of early identification and multidisciplinary management of cognitive impairment in patients with CCS to prevent progression to severe cognitive impairment. Full article

Background: Long COVID (LC) has been associated with persistent endothelial dysfunction and vascular impairment. Although nutrition is a key modifiable determinant of cardiovascular health, the relationship between dietary macronutrient intake and vascular alterations in LC remains poorly understood. Objective: To evaluate the association between dietary macronutrient intake and markers of vascular structure, arterial stiffness, and vascular aging in patients with LC, including potential sex differences. Methods: We conducted a cross-sectional study including 304 patients with LC. Dietary intake was assessed using a validated 7-day dietary record (EVIDENT study). Vascular evaluation included carotid intima–media thickness (cIMT), carotid–femoral pulse wave velocity (cfPWV), brachial–ankle pulse wave velocity (baPWV), cardio-ankle vascular index (CAVI), augmentation index adjusted to a heart rate of 75 beats per minute (AIx@75), and vascular aging index (VAI), measured using carotid ultrasound and validated devices (SphygmoCor^® and VaSera^®). Results: The mean age was 53 ± 12, higher in men (p = 0.001). The study included 207 women (68%) and 97 men (32%). Energy intake and carbohydrate intake in g/day showed a negative association with cfPWV in Model 2 (energy intake: β = −0.06; 95% CI: −0.11 to −0.01; p = 0.02; carbohydrate intake: β = −0.47; 95% CI: −0.87 to −0.07; p = 0.02). The percentage of carbohydrate/total energy intake was positively associated with AIx@75 in Model 2 (β = 0.8; 95% CI 0.12 to 1.49; p = 0.02), and percentage of fat/total energy intake showed a consistent inverse association (β = −0.30; 95% CI: −0.49 to −0.11; p = 0.002). No significant associations were observed for cIMT, baPWV, CAVI or VAI. Conclusions: In patients with LC, total energy intake and absolute carbohydrate intake were negatively associated with cfPWV, whereas the relative contribution of carbohydrates and fats to total energy intake showed divergent associations with AIx@75. These findings suggest that both absolute macronutrient intake and relative macronutrient distribution may be related to central arterial stiffness and wave reflection parameters LC. However, given the cross-sectional design of the study, these results should be interpreted as exploratory and do not allow causal inference. Further longitudinal and interventional studies are needed to confirm these findings and to assess whether nutritional strategies may contribute to modulating vascular risk in this population. Full article

Background: Chronic kidney disease presents a significant health challenge among the elderly, with recent data indicating a 13.9% prevalence for early stages (1–3) and a lower 0.6% prevalence for advanced stages. Notably, many geriatric patients die from cardiovascular complications before reaching end-stage kidney disease, highlighting the critical interplay between renal and cardiovascular health. Central to this connection is endothelial dysfunction, considered the initial trigger for cardiovascular mortality. We aimed to investigate the correlation between different measurement methods demonstrating endothelial dysfunction and sVE-cadherin levels. Another objective was to examine the relationship between decreased glomerular filtration rate (GFR) and sVE-cadherin levels. We hypothesized an inverse relationship between impaired renal function, endothelial dysfunction, and sVE-cadherin. Methods: The study included geriatric patients with CKD who were not receiving RRT. Non-geriatric patients, those with cardiovascular disease, atrial fibrillation, heart failure, active immunosuppressive use, active infection, history of active malignancy, Raynaud’s phenomenon, and renal transplantation patients were excluded. Demographic data of the patients, nailfold capillary measurements, carotid intima-media thickness, flow-mediated dilatation, sVE-cadherin, and serum fibroblast growth factor 23 (FGF23) levels were measured. Results: We analyzed 96 patients. Key findings revealed a significant inverse correlation between serum sVE-cadherin levels and glomerular filtration rate (GFR), suggesting that, as kidney function declines, endothelial integrity is compromised. Interestingly, patients treated with sodium–glucose co-transporter-2 inhibitors had notably lower sVE-cadherin levels, indicating the possible modulatory effect of these drugs on endothelial function. Additional correlations were observed: fibroblast growth factor 23 levels were positively related to capillary diameter, and carotid intima-media thickness was associated with mean platelet volume. Declining GFR corresponded to reductions in capillary count, while use of dipeptidyl peptidase-4 inhibitors was linked to higher capillary density. Over a 2.3-year follow-up, survivors had higher lymphocyte counts (p = 0.088, not statistically significant) and baseline sVE-cadherin levels tended to be higher in those who died, although this was not statistically significant. Conclusions: These findings suggest that uremic toxins may worsen endothelial injury by disrupting intercellular connections, highlighting the complex pathogenic environment in CKD. Given these insights, the need for standardized diagnostic thresholds for endothelial dysfunction in geriatric CKD patients is clear. Serum sVE-cadherin emerges as a promising novel biomarker for assessing endothelial health, offering potential for earlier intervention and improved cardiovascular outcomes. It may be a potent indicator of endothelial dysfunction and should be featured in future studies of elderly CKD patients. Full article

Background/Objectives: Rheumatoid arthritis (RA) has been associated with accelerated atherosclerosis and cerebrovascular alterations. Our 2017 study compared 60 RA patients to healthy controls, assessing vascular, neurological, and cognitive parameters. The present study is a follow-up of these RA patients to evaluate disease progression and vascular changes over time, using their 2017 results as baseline. Methods: In 2023, we reassessed 43 of the original 60 RA patients using laboratory testing, carotid ultrasound, functional transcranial Doppler (TCD) and brain magnetic resonance imaging (MRI) examinations. Changes over time were analyzed within the same individuals. Results: Inflammatory markers and lipid profiles showed a trend toward improvement, though changes were not statistically significant, except for a significant increase in vitamin D (p < 0.001) and a decrease in Disease Activity Score in 28 Joints (DAS28) scores (p < 0.001). Carotid ultrasound revealed a significant increase in plaque burden (p = 0.022 on the right side and p = 0.008 on the left), while carotid intima media thickness (cIMT) showed a non-significant rise. TCD measurements indicated significantly increased pulsatility (p < 0.001 on the right, p = 0.001 on the left side) and resistance (p = 0.001 on the right, p = 0.012 on the left side) indices and reduced flow velocities (p < 0.001 on the right and p = 0.001 on the left side) in bilateral middle cerebral arteries (MCAs). The cerebrovascular reserve capacity was significantly lower on the right side overall (p = 0.013), with further decline noted in the methotrexate (MTX)-treated subgroup on the left side (p = 0.043). MRI findings showed non-significant numerical trends toward worsening lacunar small-vessel disease (p = 0.405) and cerebral atrophy (p = 0.063), with higher but stable lacunar infarction scores among MTX users (p = 0.023). Conclusions: Despite improved inflammatory control, RA patients demonstrated progressive vascular and hemodynamic alterations over time, while MRI changes should be interpreted as trends. These findings support multimodal vascular monitoring in RA. Full article