Search Results (155)

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

Background: Intracranial pressure (ICP) monitoring remains the cornerstone of neurocritical care in severe traumatic brain injury (TBI), yet its prognostic value as a standalone metric is limited. The Pressure Reactivity Index (PRx), a continuous measure of cerebrovascular reactivity derived from ICP and arterial blood pressure, may offer additional or complementary prognostic information. This systematic review aimed to compare the prognostic performance of PRx-derived metrics versus standard ICP monitoring for mortality and functional outcome in patients with TBI. Methods: A systematic search of PubMed, Web of Science, and Scopus was conducted for studies published between January 2000 and December 2025. Studies were eligible if they included adult TBI patients with continuous multimodal monitoring and reported comparative prognostic data for PRx- and ICP-based metrics. Risk of bias within the studies was appraised via the QUIPS tool, and the GRADE system was used to rate the strength of the evidence. Due to methodological heterogeneity, findings were synthesized narratively. Results: Nine studies were included. Applying a maximum-cohort estimation to account for overlapping registries, the pooled sample comprised a minimum of 1240 unique patients. In the majority of included studies, direct within-cohort head-to-head comparisons demonstrated that specific PRx-derived metrics—such as the individualized ICP threshold (iICP), Longest Continuous Duration of Autoregulatory Impairment (LCAI), Lower Limit of Reactivity (LLR), and time-integrated burdens (%Time > Threshold)—yielded stronger prognostic discrimination compared to standard ICP thresholds for both mortality (PRx: AUC 0.747–0.648 and ICP: AUC 0.660–0.614) and functional outcome. When added to established predictive models, PRx-derived metrics provided clinically meaningful incremental improvements in prognostic accuracy, with descriptive incremental AUC gains ranging from +0.039 to +0.170 across the six studies reporting model augmentation. Due to heterogeneity in baseline models, PRx-derived metrics, and patient populations, these findings are presented strictly as a descriptive range. Conclusions: PRx and PRx-derived cerebrovascular reactivity metrics-namely iICP, LCAI, LLR, and time-integrated burdens of autoregulatory failure—show potential to offer additive prognostic value beyond standard ICP monitoring in severe TBI. However, because current evidence is strictly observational and likely influenced by institutional confounders, it cannot currently support definitive clinical recommendations. Further prospective, multicenter studies utilizing standardized thresholds are necessary to confirm these associative findings and isolate their true prognostic value. Full article

Background/Objectives: Growth differentiation factor-15 (GDF-15) is a protein that belongs to the transforming growth factor beta superfamily and has been found elevated in cases of organ injury such as liver, kidney, heart, and lung, as well as cardiovascular diseases and cancer. Soluble urokinase plasminogen activator receptor (suPAR) is a protein which is expressed mainly on immune cells and endothelial and smooth muscle cells, and is a marker of severity and intensity of inflammation in acute and chronic diseases. The aim of the present study was to compare GDF-15 serum levels between patients with acute cerebrovascular incidents and healthy controls and to investigate the possible correlation of GDF-15 serum levels and inflammatory markers, such as serum C-reactive protein (CRP) and plasma suPAR, in the above-mentioned groups. Methods: This is a retrospective study. Thirty-one patients were included in the study, with a mean age ± SD of 67 ± 13 years, compared to 18 age-matched healthy controls. Results: In the patient group a statistically significant positive correlation of serum levels of GDF15 values with suPAR and CRP emerged (rs = 0.516, p = 0.003) and (rs = 0.409, p = 0.022), respectively, and no significant correlation was found in the group of controls (rs = 0.271, p = 0.277) and (rs = 0.423, p = 0.080), respectively. Conclusions: These findings support the role of inflammation as a key underlying mechanism in acute cerebrovascular injury and suggest that GDF-15 may serve as a valuable adjunct biomarker for assessing disease severity and inflammatory burden. Full article

Systemic inflammation plays a key role in cerebrovascular disease. While C-reactive protein (CRP) and white blood cell (WBC) count are individual risk markers, the predictive value of a combined inflammatory score (IS) for stroke prevalence remains unclear. This study aimed to investigate this association in a national population. Data were obtained from the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2010. An IS was calculated as the sum of standardized Z-scores for CRP and WBC. Weighted multivariable logistic regression assessed the IS-stroke association, adjusting for demographics and clinical confounders. Restricted cubic spline (RCS) models and subgroup analyses were performed. Among 9963 included participants, 345 reported a history of stroke. After full adjustment, individuals in the highest IS quartile had 1.60-fold higher odds of stroke (OR = 1.60, 95% CI: 1.08–2.36) compared to the lowest quartile. Each unit increase in IS was associated with 6% higher odds (OR = 1.06, 95% CI: 1.01–1.12). RCS analysis revealed that higher composite IS is independently associated with increased stroke prevalence, suggesting a nonlinear association. The composite IS remained a significant predictor in models where the individual CRP and WBC components did not. This combined index may capture inflammatory burden more comprehensively than either marker alone in cross-sectional analyses. However, given the cross-sectional design, these findings should be interpreted cautiously and require confirmation in prospective studies. Full article

The kidney and the brain share similarities in terms of structure and haemodynamic regime. The aim of the study was to assess a potential correlation of vascular endothelial growth factor (VEGF), soluble vascular endothelial growth factor receptor-1 (sFlt-1), and placental growth factor (PlGF) with biomarkers of podocyte damage, proximal tubular (PT) dysfunction, and endothelial dysfunction, as well as with cerebral vessels haemodynamic indices in neurologic asymptomatic type 2 DM patients. A cohort of 212 patients diagnosed with type 2 DM and 49 age- and gender-matched healthy controls were enrolled in the study. Parameters studied were urinary albumin/creatinine ratio (UACR), biomarkers of podocyte damage (synaptopodin, podocalyxin), PT dysfunction (kidney injury molecule-1-KIM-1, N-acetyl-β-(D)-glucosaminidase-NAG), endothelial dysfunction (P-selectin), VEGF, sFlt-1, and PlGF. The cerebrovascular hemodynamic indices evaluated were intima–media thickness (IMT) in the common carotid arteries (CCAs), the pulsatility index (PI), and the resistivity index (RI) in the internal carotid arteries (ICAs) and middle cerebral arteries (MCAs). Cerebrovascular reactivity (CVR) was assessed by the breath-holding index (BHI). In multivariable regression analysis, serum VEGF correlated directly with UACR, synaptopodin, NAG, serum P-selectin; serum sFlt-1 correlated directly with UACR, synaptopodin, podocalyxin, NAG, KIM-1; serum PlGF correlated negatively with eGFR and directly with UACR, synaptopodin, KIM-1. IMT-CCA correlated indirectly with eGFR and directly with UACR, serum P-selectin, and serum sFlt-1. The PI-ICAs correlated negatively with eGFR and positively with UACR, synaptopodin, serum P-selectin, and serum sFlt-1. The PI-MCAs correlated indirectly with eGFR and directly with synaptopodin, serum P-selectin, and serum sFlt-1. The RI-ICAs had a negative correlation with eGFR and a positive one with UACR, synaptopodin, NAG, KIM-1, urinary sFlt-1, and serum PlGF. The RI-MCAs displayed an indirect correlation with eGFR and a direct correlation with NAG, KIM-1, and serum sFlt-1. The BHT correlated directly with eGFR and negatively with serum P-selectin and serum PlGF. The study shows a significant association of VEGF, sFlt-1, and PlGF with biomarkers of podocyte injury, PT dysfunction, and endothelial dysfunction in early stages of DKD. These pro-angiogenic and anti-angiogenic factors correlated with cerebrovascular haemodynamic indices in neurologic asymptomatic type 2 DM, even in the normoalbuminuric stage of diabetic kidney disease. Full article

Hypertension remains a leading modifiable risk factor for cardiovascular morbidity and mortality. Nonetheless, blood pressure control rates remain suboptimal despite established treatment guidelines and effective pharmacologic therapies. In parallel, artificial intelligence (AI) has rapidly expanded within cardiovascular medicine, demonstrating promising capabilities in disease detection, risk prediction, and clinical decision support. However, most AI applications in hypertension have focused primarily on algorithmic performance rather than real-world implementation or measurable improvements in patient outcomes. This review examines artificial intelligence-driven hypertension management through the lens of quality improvement and prevention of end-organ damage. We summarize current applications of machine learning, deep learning, natural language processing, and imaging analytics in hypertension detection and risk stratification, and critically evaluate their integration into clinical workflows. Particular emphasis is placed on therapeutic inertia, primary care-centered implementation, and the use of AI to support continuous quality improvement frameworks. Beyond blood pressure reduction alone, we explore the potential of AI to identify patients at risk for hypertensive heart disease, heart failure, aortic pathology, renal dysfunction, and cerebrovascular events. We discuss implementation challenges, including external validation, algorithmic bias, workflow integration, and regulatory considerations, which must be addressed to ensure safe and equitable deployment. Artificial intelligence offers the opportunity to transform hypertension management from reactive blood pressure control to proactive organ protection. Critically, AI-driven quality improvement interventions must be evaluated against established non-AI strategies, including pharmacist-led management and team-based care, which provide the benchmarks for demonstrating added clinical value. Achieving this shift will require embedding predictive analytics within structured, outcome-oriented systems of care and rigorously evaluating their impact on cardiovascular morbidity and mortality. Full article

Background/Objectives: Adults with congenital heart disease (CHD) have a substantially higher risk of ischemic stroke than the general population. Circulating biomarkers such as N-terminal pro B-type natriuretic peptide (NT-pro-BNP), high-sensitivity C-reactive protein (hs-CRP), and microalbuminuria have been associated with adverse cardiovascular outcomes in CHD, but their role in predicting cerebrovascular events remains uncertain. Methods: Prospective cohort study including 372 adults with CHD [median age 34 years (IQR 23–42); 57.8% male] followed at a tertiary center between 2017 and 2022. Baseline assessments included demographic characteristics, CHD anatomical complexity, cardiovascular risk factors, NT-pro-BNP, hs-CRP, lipid profile, and 24-h urinary albumin excretion. The primary endpoint was incident ischemic stroke during a median follow-up of 6.3 years (IQR 3.9–8.3). Univariable Cox proportional hazards models were used to identify predictors of stroke. Results: During follow-up, 13 patients (3.5%) experienced ischemic stroke. Patients with stroke were significantly older [51 (46–64) vs. 30 (23–40) years; p < 0.001] and had a higher prevalence of dyslipidemia (61.5% vs. 15.0%; p < 0.001). NT-pro-BNP levels were markedly higher in patients with stroke [369 (218–604) vs. 64 (21–172) pg/mL; p < 0.001]. No significant differences were observed between groups in renal function parameters, hs-CRP, thyroid-stimulating hormone, or urinary albumin excretion rate. In Cox analyses, older age and dyslipidemia were the strongest predictors of stroke (p < 0.001). Arterial hypertension, diabetes mellitus, and higher NT-pro-BNP levels were also associated with increased stroke risk (p < 0.05), whereas CHD anatomical complexity, NYHA functional class, and cyanosis were not. Conclusions: In adults with CHD, ischemic stroke was mainly associated with traditional cardiovascular risk factors and elevated NT-pro-BNP levels rather than anatomical disease complexity or functional status. Full article

Background/Objectives: Several therapeutic approaches, including phlebotomy and rheopheresis, are used to improve hemorheological parameters. While the effects of phlebotomy on cerebral circulation have been described, the impact of rheopheresis on cerebral hemodynamics remains poorly understood. This study primarily aimed to evaluate the within-group effects of phlebotomy and rheopheresis on cerebral blood flow velocity changes evoked by neuronal activation and on cerebrovascular reactivity in patients with elevated hematocrit or hyperviscosity, respectively. Methods: In our present study, we used transcranial Doppler to examine the effects of phlebotomy (n = 11) and rheopheresis (n = 9) on cerebral hemodynamics in patients with elevated hematocrit and hyperviscosity, respectively. Measurements included resting flow velocity (FV) in the posterior cerebral artery (PCA) and middle cerebral artery (MCA), the visually evoked FV response in the PCA (neurovascular coupling) and the hypercapnia-induced FV response in the MCA (cerebral vasoreactivity). In addition to flow velocity data, visual evoked potential (VEP) parameters were also recorded to assess neuronal activation. Results: Phlebotomy significantly reduced hematocrit and hemoglobin levels, while rheopheresis led to a significant decrease in both blood and plasma viscosity. Although we observed no differences in resting FV values before and after either intervention, the FV increase in response to visual stimulation and hypercapnia was greater after rheopheresis than before, whereas no such difference was observed following phlebotomy. VEP parameters remained similar before and after both phlebotomy and rheopheresis. Conclusions: Our data indicate that rheopheresis reduces blood and plasma viscosity in patients with hyperviscosity and leads to a significant improvement in cerebral vasoreactivity and neurovascular coupling, without affecting VEP parameters. The improvement in cerebral vasoreactivity, but no changes in VEP parameters, suggests that the improved FV response to visual stimulation after rheopheresis is most likely caused by better vascular response rather than improved neuronal activation. Full article

Background/Objectives: Quantifying cerebrovascular reactivity (CVR) is essential for stroke risk assessment in patients with Moyamoya Angiopathy (MMA). Breath-hold functional MRI (bh-fMRI) is an easily implementable method to assess CVR. Determining the optimal time period of the BOLD signal for analyzing the best bh-fMRI data quality remains an open question. Methods: A retrospective analysis of 46 bh-fMRI data sets of MMA patients was conducted. The percentage BOLD signal changes were evaluated at different time periods (time point of the maximum cerebellar signal peak (TP_{cereb. max}) ± 0 s, TP_{cereb. max} ± 1 s, TP_{cereb. max} ± 2 s, TP_{cereb. max} ± 3 s, TP_{cereb. max} ± 4 s, TP_{cereb. max} ± 5 s). The agreement between the bh-fMRI maps and [¹⁵O]water PET maps was independently and consensually rated on a 4-point Likert scale (1 = poor, 2 = moderate, 3 = good, 4 = excellent) and compared with the Friedman test. The inter-rater agreement was calculated separately for each time period using quadratic weighted Cohen’s kappa κ_w. Results: The selected time period had a significant impact on the agreement between bh-fMRI and [¹⁵O]water PET (χ²(5) = 79.448, p < 0.001, W = 0.345). Short time periods of TP_cereb.max ± 0 s or TP_cereb.max ±1 s demonstrated the highest level of concordance between bh-fMRI and [¹⁵O]water PET (median = 3.5 for TP_cereb.max ± 0 s; median = 3 for TP_cereb.max ± 1 s, modus = 4 in both cases). The agreement between bh-fMRI and [¹⁵O]water PET was significantly higher when evaluating time periods of TP_cereb.max ± 0 s than when evaluating all time periods ≥ TP_{cereb. max} ± 2 s. The inter-rater agreement was almost perfect for all time periods except one (TP_{cereb. max} ± 1 s). Conclusions: Short time periods should be selected when evaluating CVR with bh-fMRI, as this study suggests a high level of validity in comparison to [¹⁵O]water PET. Full article

Background: In patients with severe atherosclerotic internal carotid artery stenosis (ICAS), the capacity of cerebral vasoreactivity (CVR)—an independent risk factor for cerebral ischemia—is reduced, and dysregulation of arterial blood pressure (ABP) may also be present. Thus, this study assessed the relationship between changes in cerebral blood flow velocity (BFV) in response to vasoactive stimuli (as measured by transcranial Doppler (TCD)), characterizing CVR and cardiovascular autonomic nervous system (CANS) function. Methods: Common carotid artery compression (CCC n = 26), hyperventilation (HV) and breath-holding (BH) tests (n = 31), and the Valsalva maneuver (VM n = 34) were used to assess CVR in patients with ICAS. In the middle cerebral arteries, BFV was monitored by TCD, whereas ABP was registered non-invasively. For statistical analysis, validated indices describing CANS function—namely, sympathetic index (SI), pressure recovery time (PRT), and Valsalva heart rate ratio (VHRR)—were selected based on the VM response. Several parameters were defined in order to evaluate CVR responses, including cerebral arterial resistance (CAR = ABP/BFV), which was correlated with the CVR indices using Spearman’s pairwise correlation and canonical correlation. Results: A significant correlation was found between several CVR indices of the HV-BH and VM tests and CANS indices of VM using Spearman’s pairwise correlation test. Regarding the HV-BH CVR and CANS indices of VM, a significant correlation was found between CAR values until it reached its maximum on the to-be-operated side (CAR_{timetomaxICAop}) and VHRR (p = 0.041). A significant correlation was also found between the time elapsed until the CAR minimum value (CAR_{timetominICAop}) and SI (p = 0.019). Concerning the CVR and CANS indices of the VM, a significant correlation was found between cerebrovascular Valsalva ratio on the to-be-operated side (CVAR_ICAop) and PRT (p = 0.002). Canonical correlation analysis confirmed that impairments of CANS and CVR may be associated. Conclusions: In patients with severe ICAS, the potentially concomitant dysregulation of cerebrovascular reactivity and the cardiovascular autonomic nervous system can further increase cerebral ischemic risk. Full article

Background: Mitophagy is a critical mitochondrial quality control mechanism that limits neuronal injury following cerebral ischemia/reperfusion injury (CI/RI). Tetramethylpyrazine (TMP), a bioactive alkaloid from Ligusticum chuanxiong Hort., exhibits neuroprotective effects in cerebrovascular disorders. However, whether these effects involve mitophagy regulation remains unclear. Methods: CI/RI was induced using a middle cerebral artery occlusion/reperfusion (MCAO/R) model in mice and an oxygen–glucose deprivation/reoxygenation (OGD/R) model in HT22 cells. Neurological function, infarct volume, mitochondrial function, and mitophagy-related markers were assessed. Pharmacological inhibitors and genetic manipulation of YAP and Parkin were used to investigate underlying mechanisms. Results: TMP treatment significantly reduced infarct volume and improved neurological deficits in MCAO/R mice, accompanied by enhanced mitophagy, as indicated by increased mitochondrial LC3 recruitment and Parkin expression. In OGD/R-injured HT22 cells, TMP promoted mitophagosome and mitolysosome formation, reduced mitochondrial reactive oxygen species, and restored mitochondrial membrane potential. Inhibition of mitophagy with Mdivi-1 attenuated TMP-mediated neuroprotection. Mechanistically, TMP promoted YAP nuclear localization, and inhibition of YAP or silencing of Parkin abolished TMP-induced mitophagy, while Parkin overexpression restored mitophagy under YAP inhibition. Conclusions: TMP alleviates CI/RI by promoting mitophagy through the YAP/Parkin signaling pathway, suggesting mitophagy modulation as a potential therapeutic strategy for ischemic brain injury. Full article

Background/Objectives: Despite increasing interest in high-intensity exercise and cerebrovascular function, the effects of maximal sprint exercise on cerebrovascular reactivity (CVR), a key indicator of vascular health, remain unclear. Methods: This study investigated the acute effects of a 30-s all-out cycling sprint (Wingate Anaerobic Test, WAnT), on CVR to hypocapnia in 24 healthy young adults (12 males). Following familiarisation and a $\dot{\mathrm{V}}$O_2max test, participants completed an experimental session where CVR was assessed at rest and 30 min post-WAnT. CVR was evaluated using a 1-min voluntary hyperventilation protocol (25 breaths·min⁻¹), with middle cerebral artery blood velocity (MCAv) measured via transcranial Doppler ultrasound and end-tidal CO₂ (P_ETCO₂) recorded breath-by-breath. CVR was calculated as the absolute change in MCAv per 1 mmHg change in P_ETCO₂ from the final 10 s of hyperventilation. Results: Resting MCAv and P_ETCO₂ were significantly reduced post-WAnT (p < 0.01 and p < 0.001 respectively). Consequently, the reductions in MCAv and P_ETCO₂ during hyperventilation were attenuated after exercise in both males and females (p < 0.01 and p < 0.001 respectively). Despite these changes, CVR remained unaltered in both sexes following WAnT (males: 1.79 ± 0.35 vs. 1.59 ± 0.26 cm·s⁻¹·mmHg⁻¹, p = 0.09; females: 2.01 ± 0.44 vs. 2.01 ± 0.46 cm·s⁻¹·mmHg⁻¹, p = 0.97). However, post-exercise CVR was significantly lower in males than females, despite no baseline sex differences (p = 0.01). Conclusions: Cerebrovascular reactivity to hypocapnia is preserved 30 min after a single bout of maximal sprint exercise in healthy young adults. Notably, females demonstrated a more favorable maintenance of CVR post-exercise compared to males, suggesting potential sex differences in CVR following maximal sprint exercise. Full article

Type 1 diabetes (T1D) increases the risk for cerebral microangiopathy. However, the association between gender and cerebral microcirculatory dysfunction in T1D remains undetermined. Therefore, we have conducted a comparative analysis of cerebral endothelial-mediated microcirculatory parameters between middle-aged Caucasian females and males with type 1 diabetes. The present study examined the nitric oxide-induced vasomotor reactivity of middle cerebral arteries (MCA using transcranial Doppler and L–arginine infusion (L–arg VMR)). The study compared L–arg VMR between 23 males and 26 females with type 1 diabetes without a history of overt cerebrovascular disease. Mean L–arg VMR and baseline MCA flow velocity (V rest) were higher in females than in males (20.1 ± 5.4 vs. 14.6 ± 7.1% p < 0.01 and 73, 54–106 vs. 60.7–77 cm/s p < 0.01, respectively). Males were older than females (39.7 [range: 31.3–55.7] vs. 36.5 [range: 25.0–45.5] years, p = 0.02) and were characterized by later T1D onset and higher insulin/24 h, triglyceride levels and body mass index (BMI). Higher L–arg VMR in females persisted when co-variated with patients’ age, age of onset, BMI, triglyceride level and V rest. Cerebral vasomotor reactivity to L–arginine showed greater efficacy in middle-aged females than in males with T1D, independent of age and disease course. The protective effect of the female gender on cerebral endothelium function has been demonstrated in type 1 diabetes. Full article

Background/Objectives: Cerebral angiography is a cornerstone diagnostic and therapeutic procedure for cerebrovascular diseases; however, its potential effects on vascular integrity and cellular homeostasis remain incompletely elucidated. This systematic review aims to comprehensively evaluate endothelial and histopathological alterations induced by cerebral angiographic procedures, with particular emphasis on oxidative stress, inflammation, endothelial dysfunction, and blood–brain barrier disruption. Methods: This systematic review was conducted in accordance with the PRISMA 2020 guidelines. PubMed, Scopus, and Web of Science databases were systematically searched for studies published between 1981 and 2025 using predefined keywords related to cerebral angiography, endothelial injury, oxidative stress, inflammation, and histopathological changes. A total of 1142 records were identified, and 216 duplicates were removed. Following title and abstract screening, 312 full-text articles were assessed for eligibility, of which 112 were excluded due to irrelevance or insufficient endothelial or histopathological data. Ultimately, 200 studies were included in the qualitative synthesis. The literature identification, screening, and selection process are summarized in the manuscript. The review protocol was not prospectively registered. Results: The included studies demonstrated that cerebral angiographic procedures induce endothelial and microvascular alterations through both mechanical and contrast-mediated mechanisms. Iodinated contrast agents were consistently associated with increased reactive oxygen species production, reduced endothelial nitric oxide bioavailability, mitochondrial dysfunction, and activation of pro-inflammatory signaling pathways, including nuclear factor kappa B (NF-κB). Histopathological findings revealed endothelial swelling, vacuolization, apoptosis, microthrombus formation, inflammatory cell infiltration, and disruption of endothelial junctions, leading to increased vascular permeability and blood–brain barrier impairment. Mechanical factors related to catheter manipulation and high-pressure contrast injection further exacerbated endothelial injury by altering shear stress and promoting leukocyte adhesion. The severity of endothelial damage and inflammatory responses was consistently greater in patients with comorbid conditions such as diabetes mellitus, hypertension, and atherosclerotic disease. Conclusions: Cerebral angiography may induce endothelial dysfunction and histopathological vascular injury predominantly through oxidative and inflammatory mechanisms. Optimization of contrast agent selection, refinement of procedural techniques, and implementation of endothelial-protective strategies may mitigate vascular injury and improve procedural safety. Further translational and clinical studies are warranted to identify biomarkers and protective interventions targeting angiography-induced endothelial damage. Full article

Diabetes mellitus (DM) is a complex, heterogeneous, hyperglycemic chronic metabolic disorder. Type 2 diabetes mellitus (T2DM) is characterized by progressive loss of insulin secretion from pancreatic islet β-cells due to IR (insulin resistance), which is a feature of metabolic syndrome (MetS). Chronic hyperglycemia in patients with T2DM in synergy with other metabolic abnormalities causes complications such as diabetic ketoacidosis, osmotic diuresis and hyperglycemic diabetic coma, as well as chronic microvascular and macrovascular complications such as atherosclerotic cardiovascular disease (ASCVD), peripheral artery disease (PAD) and cerebrovascular events, which implicate the formation of reactive species and the promotion of inflammatory pathways. In these events, natural or synthetic antioxidants and minerals seem to have ameliorative effects and may serve as beneficial co-treatment options. In view of these terms, the aim of this study is to investigate the underlying mechanisms of T2DM, its clinical presentation, and its complications. Additionally, the association of the pathogenesis of T2DM and the occurrence of its complications with obesity, chronic inflammation, oxidative stress (OS), insulin resistance (IR), hepatic steatosis, and dyslipidemia is examined, whilst molecular pathways, such as NF-κB and JAK/STAT, are also summarized, under the scope of the effects of several antioxidant compounds and minerals on their progression. The interrelation of T2DM with these conditions, as well as the effects of antioxidant supplementation, seems to be bidirectional, and it is recommended that obese patients be screened for T2DM and adopt lifestyle changes, including exercise, diet modification, and weight loss, in addition to potentially taking multifunctional supplements that offer antioxidant and anti-inflammatory potential. However, many aspects of the protective mechanisms of such antioxidants remain to be elucidated, with more drawbacks in their pharmacokinetic behavior, such as their poor absorption and solubility, waiting to be resolved. Full article