BackgroundDelayed cerebral ischemia (DCI) remains a major determinant of poor outcome after aneurysmal subarachnoid hemorrhage (aSAH). Growing evidence suggests that gut microbiota–derived metabolites, including short-chain fatty acids (SCFAs) and tryptophan-related indole compounds, modulate neuroinflammation and cerebrovascular vulnerability. However, their temporal dynamics and clinical relevance after aSAH are insufficiently characterized.MethodsIn this prospective observational study, 80 consecutive patients with aSAH were enrolled at a tertiary neurocritical care center. Serum concentrations of SCFAs (propionic, butyric, isobutyric, valeric, isovaleric, caproic acids) and tryptophan-derived metabolites (tryptophan, indole-3-propionic acid [IPA], indole-3-acetic acid, indole-3-lactic acid) were quantified using LC–MS on Day 1 and Day 9 after hemorrhage. Functional outcome at 3 months was assessed using the modified Rankin Scale (mRS), and DCI was diagnosed according to consensus criteria. Associations were analyzed using non-parametric statistics, ROC analyses, and multivariable logistic regression adjusted for established clinical confounders.ResultsPatients with unfavorable 3-month outcomes (mRS 4–6) showed significantly lower Day 1 levels of propionic, isobutyric, and isovaleric acids, persistently reduced tryptophan at both time points, and markedly lower IPA concentrations on Day 9. DCI was associated with reduced tryptophan and propionic acid levels on both days and a pronounced decrease in IPA on Day 9. Tryptophan and propionic acid demonstrated excellent discriminative performance for outcome and DCI (AUCs up to 0.99). In multivariable models, low Day 1 propionic acid and low Day 9 IPA independently predicted unfavorable outcome, while Day 9 tryptophan, IPA, and propionic acid independently predicted DCI.ConclusionDistinct temporal alterations in gut microbiota–derived metabolites after aSAH are strongly associated with functional outcome and DCI. SCFAs and tryptophan-related metabolites—particularly propionic acid, tryptophan, and IPA—emerge as promising biomarkers and potential mechanistic mediators in secondary brain injury after aSAH.

Long COVID affects a substantial proportion of individuals recovering from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, yet its underlying pathophysiology remains poorly understood. Although autoimmunity is increasingly implicated in disease pathogenesis, routine diagnostics frequently fail to detect relevant immune dysregulation. To address this gap, we analyzed sera from Long COVID patients (n = 114) and pre-pandemic controls (n = 36) using tissue-based Western blotting targeting cardiac, pulmonary, and vascular antigens, alongside standard ANA HEp-2 testing. Longitudinal samples were additionally evaluated to assess autoantibody dynamics. Autoantibodies were detected in the majority of patients (83

BackgroundNeuroinflammation and systemic immune dysregulation are increasingly recognized as key contributors to secondary brain injury after aneurysmal subarachnoid hemorrhage (aSAH). However, the temporal relationship between circulating cytokine responses and innate-like lymphocyte populations, particularly mucosal-associated invariant T (MAIT) cells, remains poorly characterized.MethodsIn this prospective observational study, peripheral blood cytokine profiles were longitudinally analyzed in 48 patients with aSAH on days 1, 5, and 9 after ictus and compared with healthy controls. Serum concentrations of IL-6, IL-7, IL-12p40, IL-12p70, IL-15, IL-17A, IL-18, IL-22, IP-10, and CXCL-9 were measured using multiplex immunoassay. Flow cytometric immunophenotyping was performed in a subgroup of 16 patients to evaluate MAIT cells, NK cells, γδ T cells, iNKT cells, and NKT-like cells. Associations between immune parameters and 3-month functional outcome were also assessed.ResultsPatients with aSAH demonstrated persistently elevated IL-6, IL-18, and IL-15 levels across all examined time points, while IL-7, IL-12p40, IP-10, and CXCL-9 showed delayed increases during the subacute phase. IL-6 and IL-15 concentrations were significantly higher in patients with unfavorable outcome, whereas IL-22 levels were increased in patients with favorable recovery. However, these associations were not independent of disease severity after adjustment for WFNS score and age. Flow cytometry revealed a persistent reduction in circulating MAIT-cell frequencies following aSAH, while other innate-like lymphocyte populations remained largely unchanged. DN MAIT-cell frequencies demonstrated significant negative correlations with circulating IL-18 levels across all examined time points.ConclusionaSAH is associated with sustained systemic inflammatory activation and selective alterations of MAIT-cell populations. Although several cytokines were associated with functional outcome in univariate analyses, these associations were attenuated after adjustment for WFNS score and age, suggesting that they primarily reflect disease severity rather than independent prognostic effects. The observed relationship between MAIT-cell dysregulation and IL-18–associated inflammation provides further evidence of altered innate-like immune responses following aSAH.

BACKGROUND:Aneurysmal subarachnoid hemorrhage (aSAH) is associated with high mortality and poor functional outcome, driven in part by neuroinflammatory mechanisms. Inflammasome activation has emerged as a key contributor to early brain injury and delayed cerebral ischemia (DCI), yet the prognostic value of circulating inflammasome-related biomarkers remains incompletely defined. This study aimed to evaluate the temporal dynamics and clinical relevance of serum interleukin-18 (IL-18), caspase-1 p20, and gasdermin D N-terminal (GSDMN) in aSAH, and to determine their incremental prognostic value beyond established clinical severity scores. METHODS:In this single-center prospective observational cohort study, 183 patients with aSAH were enrolled. Serum levels of IL-18, caspase-1 p20, and GSDMN were measured on days 1, 5, and 9 after ictus using ELISA. Clinical severity was assessed using WFNS and modified Fisher scores. The primary outcome was 3-month functional status (modified Rankin Scale). Associations were analyzed using mixed-effects models and multivariable logistic regression adjusted for clinical covariates. Model performance was evaluated using ROC analysis. RESULTS:Caspase-1 p20 levels were significantly elevated in patients and consistently higher in those with unfavorable outcome across all time points. In multivariable analyses, caspase-1 p20 (day 1 and day 5) independently predicted poor outcome and DCI, improving model performance beyond clinical variables (AUC increase from 0.880 to 0.919). IL-18 showed time-dependent changes but lacked independent prognostic significance, while GSDMN levels did not differentiate outcome groups. Longitudinal analyses revealed distinct biomarker trajectories, with significant time-outcome interactions for caspase-1 p20 only. CONCLUSION:Circulating caspase-1 p20 is a robust and independent biomarker of inflammasome activation with significant prognostic value in aSAH. Its integration into clinical models enhances outcome prediction, supporting its potential role in risk stratification and biomarker-guided therapeutic strategies.

BACKGROUND:Aneurysmal subarachnoid hemorrhage (aSAH) and perimesencephalic subarachnoid hemorrhage (PM-SAH) share similar acute clinical presentations but differ markedly in etiology, vascular pathology, and outcome. The molecular mechanisms underlying these differences remain poorly defined. METHODS:In this prospective observational study, circulating levels of matrix metalloproteinases (MMP-1, MMP-2, MMP-7, MMP-9, MMP-10) and growth factors (EGF, FGF-2, PDGF-AA, PDGF-AB/BB, TGF-α, VEGF-A) were analyzed in patients with aSAH (n = 38) and PM-SAH (n = 40) within 24 h after ictus. Serum biomarker concentrations were quantified and compared between groups, and inter-marker correlations were evaluated. RESULTS:Serum levels of MMP-1, MMP-7, and MMP-9 were significantly higher in the aSAH group than in the PM-SAH group, whereas MMP-2 and MMP-10 showed no significant difference. Among growth factors, EGF, PDGF-AA, PDGF-AB/BB, and VEGF-A were markedly elevated in aSAH, while FGF-2 and TGF-α levels remained comparable across groups. Distinct correlation patterns between MMPs and growth factors were observed in the two cohorts. CONCLUSIONS:The observed biomarker differences between aSAH and PM-SAH likely reflect the presence of an aneurysmal lesion and its associated vascular injury, rather than a generalized response to subarachnoid blood. Elevated MMP and growth factor levels in aSAH point to enhanced extracellular matrix degradation, blood-brain barrier disruption, and a more pronounced aneurysm-associated vascular remodeling and endothelial activation signature, processes not evident in PM-SAH. These findings provide clinical evidence supporting the hypothesis that aneurysm rupture initiates a unique cascade of molecular events contributing to the distinct pathophysiology and poorer outcomes of aSAH.

Introduction: The co-prevalence of cerebrovascular and cardiovascular diseases is not uncommon among patients. In most cases, the symptoms can be clearly differentiated; however, in certain situations, establishing the correct diagnosis and selecting the appropriate therapy can be particularly challenging. Case report: A 74-year-old diabetic patient was admitted to the Emergency Department with limb numbness and blurred vision. During observation, he experienced two episodes of staring blankly ahead with unresponsiveness and transient impairment of consciousness. Simultaneous ECG recordings showed significant ST-segment elevation in inferior leads, which nearly resolved by the end of each episode. Neurological evaluation considered absence seizures unlikely, and native brain CT excluded intracranial tumor or hemorrhage; therefore, the patient was admitted to the cardiology department. Echocardiography revealed a reduced left ventricular ejection fraction (37%) with diffuse hypokinesis. Carotid ultrasound, followed by contrast-enhanced CT, demonstrated a significant occlusion of the left internal carotid artery and a marked stenosis of the right internal carotid artery. Although no further seizure-like episodes were observed during cardiology hospitalization, an urgent coronary angiography was performed due to non-sustained ventricular tachycardia (NSVT). Coronarography revealed significant stenosis of the left main coronary artery and chronic total occlusion of the right coronary artery; thus, urgent coronary artery bypass graft (CABG) surgery was recommended. Based on these findings, we concluded that the transient ischemic episodes were caused by angina-induced severe reductions in cardiac output, leading to critically decreased cerebral perfusion. Prior to triple bypass surgery, right carotid artery stenting was successfully performed. Follow-up echocardiography showed an improved ejection fraction (47%). The patient was discharged in good general condition to cardiac rehabilitation, with only mild residual neurological symptoms. Conclusion: This case illustrates that severe concomitant cardiovascular and cerebrovascular diseases can be effectively managed through timely diagnosis and close interdisciplinary collaboration.

Bevezetés: A cerebro- és kardiovaszkuláris betegségek együttes előfordulása nem ritka betegeink körében. Az esetek többségében a két tünetegyüttes jól elkülöníthető, bizonyos helyzetekben azonban a helyes diagnózis felállítása kihívást jelenthet. Esetismertetés: A 74 éves, diabéteszes férfi beteg végtagzsibbadás és szemkáprázás miatt kereste fel a Sürgősségi Betegellátó Osztályt (SBO). Két ízben „elrévedéssel” járó rosszulléte jelentkezett, amely során a beteg érdemi kontaktusba nem volt vonható. A rosszulléti EKG-n az inferior elvezetésekben szignifikáns ST-eleváció volt látható, amely a rosszullét terminálódásával szinte teljesen megszűnt. A tünetek hátterében felmerült Jackson-roham kóroki szerepét a neurológiai konzílium elvetette. Az akut natív koponya-CT vérzést, illetve térfoglalást nem igazolt, így a beteget a kardiológiai osztályra vettük fel. Echokardiográfia során csökkent szisztolés balkamra-funkciót (EF: 37%) és kiterjedt hipokinézist írtunk le. A carotisultrahang, majd a kontrasztanyagos koponya-CT a bal oldali carotis interna okklúzióját és a jobb oldali carotis interna szűkületét igazolta. Osztályunkon ismételt rosszullét nem jelentkezett, EKG-eltérések és monitorozása során észlelt, nem tartós kamrai tachycardia miatt sürgető koronarográfia történt, amely szignifikáns szűkülettel eredő főtörzset, illetve krónikusan elzárt RCA-t írt le, így sürgető koronária-bypass- (CABG-) műtétet javasoltak. Mindezen eredmények alapján a beteg panaszainak hátterében az anginás rosszullétek alatti csökkent pumpafunkció, illetve a súlyos carotisbetegség következtében fellépő agyi perfúziós zavar kóroki szerepe állhatott. A hármas CABG-műtét előtt megtörtént a jobb oldali carotis sztentelése. A kontrollszívultrahangon jelentősen javult, 47%-os ejekciós frakció írtunk le. A beteget kardiológiai rehabilitáció után otthonába emittáltuk jó állapotban, enyhe neurológiai maradványtünetekkel. Következtetés: Esetünk megmutatja, hogy súlyos cerebro- és kardiovaszkuláris betegségek együttállása esetén is a korai diagnózis és az interdiszciplináris együttműködés sikeres kimenetelhez vezethet.

Background: Aneurysmal subarachnoid hemorrhage (aSAH) induces complex systemic inflammatory and metabolic responses that may influence clinical outcome. DSC provides an integrative biophysical readout of proteome-level thermodynamic behavior rather than protein-specific identification or quantification; however, its applicability in neurocritical conditions remains largely unexplored. This pilot study aimed to explore whether serum DSC profiles show preliminary associations with clinical severity and neurological outcomes after aSAH. Methods: Serum samples collected on day 1 after aSAH were analyzed by DSC and compared with healthy control samples. A small patient cohort was stratified according to clinical severity and neurological outcome. Thermograms were evaluated based on melting temperatures (Tm), calorimetric enthalpy (ΔHcal), heat capacity changes (ΔCp), and the relative contributions of major serum protein components. Results: Healthy controls exhibited characteristic DSC profiles dominated by a cooperative albumin transition at approximately 65-66 °C. In this limited cohort, patients with severe clinical conditions and unfavorable outcomes displayed marked thermogram reorganization, including increased albumin Tm, reduced unfolding cooperativity, decreased ΔCp, and enhanced high-temperature immunoglobulin-related contributions. Patients with mild condition and favorable outcome showed profiles more similar to those of the controls. Notably, patients with severe conditions but favorable outcomes demonstrated heterogeneous albumin-related thermal domains, which may reflect individual-level variability and suggesting dynamic proteomic heterogeneity at the early post-ictus phase. Given the small group sizes, these patterns should be interpreted as exploratory and hypothesis-generating. Conclusions: This pilot exploratory study suggests that serum DSC may capture preliminary thermoanalytical patterns associated with clinical outcomes after aSAH. While the findings indicate the potential of DSC as a systems-level tool in neurocritical care, larger, well-powered studies are required to validate these observations and assess their robustness and generalizability.

Background: Periodontitis has been associated with systemic diseases such as cerebrovascular events. Emerging research highlights the potential role of the microbiome in intracranial aneurysm formation and rupture. Aims: We aimed to explore the associations among periodontal pathogens and the outcomes in patients with aneurysmal subarachnoid hemorrhage (aSAH). Materials and Methods: A total of 43 aSAH patients were enrolled. Clinical probing depth measurement and microbiological culture were performed for all participants. The markers of systemic immune response (IL-6, hsCRP) and brain injury (NSE, S100B) were measured between 24 and 48 h after admission. Development of delayed cerebral ischemia (DCI) as the primary and clinical outcome, based on modified Rankin Scale as secondary endpoints, comprised the chosen metrics. Results: A significant association was observed between patients with periodontal pocket depth PPD ≥ 5 mm (n = 28) and DCI, which developed in 19 patients (p = 0.007). In the subgroup of patients with PPD ≥ 5 mm significant associations were found between certain periodontal pathogens and DCI. Higher hsCRP (p = 0.05), IL-6 (p = 0.037) levels were observed in cases with periodontal pathogens, independent of the depth of the pocket, suggesting systemic inflammation. Conclusions: Elevated hsCRP and IL-6 levels, periodontal pocket depth ≥ 5 mm, and red-complex periodontal pathogens are associated with an increased risk of DCI after aSAH, suggesting a role for periodontal disease-related systemic inflammation in DCI risk stratification.

Aneurysmal subarachnoid hemorrhage (aSAH) is a severe stroke subtype often complicated by symptomatic cerebral vasospasm (sVP), contributing to delayed cerebral ischemia and poor outcomes. Immune dysregulation, particularly T-cell imbalances and pro-inflammatory cytokines, is implicated in vasospasm development. Soluble immune checkpoint proteins-CTLA-4 (sCTLA-4) and PD-L1 (sPD-L1)-regulate immune homeostasis and may serve as biomarkers or modulators of inflammation in aSAH. This prospective cohort study included 179 aSAH patients, divided into sVP+ (n = 48) and sVP- (n = 131), plus 50 healthy controls. Serum sCTLA-4 and sPD-L1 levels were measured on days 1, 5, and 9 post-ictus using Luminex xMAP. Associations with clinical outcomes were analyzed using non-parametric statistics and hierarchical clustering. Both sCTLA-4 and sPD-L1 were significantly elevated in sVP+ patients versus sVP- and controls, increasing over time. sCTLA-4 was significantly higher in sVP+ on days 5 (p = 0.001) and 9 (p < 0.001), and sPD-L1 on days 5 and 9 (both p < 0.001). Clustering revealed distinct expression patterns between sVP+ and sVP- groups. Elevated sCTLA-4 and sPD-L1 levels are associated with sVP after aSAH and may serve as biomarkers for early immune dysfunction, offering insights into potential therapeutic targets.

Background: Aneurysmal subarachnoid hemorrhage (aSAH) is a disease associated with high mortality, caused by the rupture of a cerebral aneurysm. Decision-support scoring systems used for managing unruptured aneurysms (UIAs) include only radiological parameters related to the size and configuration of the aneurysm, without incorporating blood-based markers. Our aim is to identify a serum marker that shows a correlation with aneurysm size in patients with ruptured aneurysms. Methods: Arterial blood samples were collected from patients who experienced aSAH within 24 h of the ictus, and serum desmosine levels were determined using ELISA. The morphological parameters of the aneurysms were assessed during 3D DSA. A favorable outcome was defined as a 3-month mRS score of 0–3. Results: This study included 135 aSAH patients and 25 controls. (i) The desmosine level in serum collected within 24 h after aneurysm rupture in patients with aSAH was significantly higher compared to the serum level in the control group (aSAH: 0.737 ng/mL [IQR: 0.401–1.214], vs. control: 0.365 ng/mL [IQR: 0.251–0.531], p < 0.001); (ii) examining the size of ruptured aneurysms, patients with aneurysms larger than 7 mm had significantly higher serum desmosine levels than those with aneurysms smaller than 7 mm; (iii) in the group with aneurysms smaller than 7 mm, serum desmosine levels correlated with the aneurysm neck width and the size ratio. Conclusions: Serum desmosine shows a strong correlation with the size of ruptured aneurysms in aSAH patients.

Background/Objectives: Cerebral subarachnoid hemorrhage (SAH) from ruptured aneurysms poses significant morbidity and mortality risks. Among survivors, cerebral vasospasm can develop, increasing complications. This study investigates the relationship between blood parameters and the risk of vasospasm. Methods: We analyzed clinical data from patients with SAH—both with and without vasospasm—and healthy controls. Statistical analyses, including Spearman’s rank correlation and univariate analysis, were conducted. Results: Significant differences were observed between patients with and without vasospasm. Elevated white blood cell counts, a higher neutrophil-to-lymphocyte ratio, and lower platelet counts showed a significant association with symptomatic vasospasm. Younger age and female gender were associated with a higher risk. Conclusions: These preliminary findings highlight the importance of specific blood parameters and demographic factors in assessing the risk of cerebral vasospasm in SAH patients, supporting early risk stratification and monitoring to improve outcomes; however, these results require validation in larger cohorts.

Background: Aneurysmal subarachnoid hemorrhage (aSAH) is a critical condition characterized by blood-brain barrier (BBB) disruption. Tight junction proteins, claudin-3 (CLDN3) and claudin-5 (CLDN5), are key regulators of BBB integrity and may serve as biomarkers of hemorrhage severity. Methods: In this prospective cohort study, 200 patients with aSAH were evaluated. Serum CLDN3 and CLDN5 levels were measured on days 1, 5, and 9 post-ictus and compared with healthy and aneurysm-bearing controls. Patients were stratified by modified Fisher Score (mFS), World Federation of Neurosurgical Societies (WFNS) score, and 3-month modified Rankin Scale (mRS). Associations with complications, including delayed cerebral ischemia (DCI) and infection, were also assessed. Results: CLDN3 and CLDN5 levels were significantly elevated in aSAH patients compared to controls (p <0.01 and p <0.0001, respectively), with CLDN5 levels consistently higher than CLDN3 at all time points (p <0.0001). CLDN5 levels were consistently higher than CLDN3 at all measured time points, and neither CLDN3 nor CLDN5 showed significant temporal variation between days 1, 5, and 9. Both markers showed significant positive correlation with mFS, with higher levels observed in mFS3 and mFS4 groups (p <0.05 to p <0.0001). No association was found between CLDN3 and 5 levels and WFNS score, 3-month mRS, age, sex, comorbidities, inflammatory markers, or DCI. Conclusion: Elevated serum CLDN3 and especially CLDN5 levels reflect hemorrhage extent and potential BBB disruption in aSAH. Their strong correlation with mFS suggests utility in grading imageological hemorrhagic severity, though not in predicting long-term functional outcomes. CLDN5 emerges as a promising biomarker for early assessment of BBB integrity in neurovascular injury.

Background: Subarachnoid hemorrhage is a serious condition caused by ruptured intracranial aneurysms, resulting in severe disability mainly in young adults. Cerebral vasospasm is one of the most common complication of subarachnoid hemorrhage; thus, active prevention is key to improve the prognosis. The glycosylation of proteins is a critical quality attribute which is reportedly altered in patients diagnosed with acute ischemic stroke. In this study, we examined the N-glycosylation profile of serum glycoproteins in patients with subarachnoid hemorrhage without vasospasm compared to patients with vasospasm. Methods: The serum N-glycans were released by PNGase F (Peptide: N-glycosidase F) digestion and subsequently labeled by procainamide via reductive amination. The samples were analyzed by hydrophilic-interaction liquid chromatography after solid-phase extraction-based sample purification. Results: Besides the glycosylation pattern, we also investigated the biomarkers following subarachnoid hemorrhage. Multiple statistical analyses were performed in order to find significant differences and identify potential prediction factors of cerebral vasospasm. Significant differences were identified such as higher sialylation on bi-, tri-, and tetra-antennary structures in patients with subarachnoid hemorrhage and cerebral vasospasm. Conclusions: Our results suggest that glycosylation analysis can improve the identification of patients with cerebral vasospasm in combination with laboratory parameters.

Background: Gut microbiome composition may influence the risk of intracranial aneurysm rupture. Methods: This study analyzed the gut microbiota of 48 patients-24 with ruptured aneurysms (RA) and 24 with unruptured intracranial aneurysms (UIA)-using next-generation sequencing. Results: While alpha diversity was similar between groups, beta diversity revealed significant taxonomic differences (Bray-Curtis: p = 0.02; unweighted UniFrac: p = 0.0291). Both groups were dominated by the phyla Bacillota, Bacteroidota, and Proteobacteria, but genus- and family-level differences were observed. RA patients showed higher abundances of Anaerotruncus, Coprobacillus, Sellimonas, Hungatella, and Ruthenibacterium, whereas UIA patients exhibited greater levels of Faecalibacterium, Brotolimicola, Clostridiaceae, Roseburia, and Agathobaculum. Linear discriminant analysis identified one class, 10 genera, and 17 species that differed significantly between groups. Notably, Faecalibacterium prausnitzii and Agathobaculum butyriciproducens-bacteria known for their anti-inflammatory and neuroprotective properties-were enriched in UIA patients. Conclusions: These findings suggest that gut microbiota, particularly short-chain fatty acid-producing bacteria, may contribute to vascular protection and aneurysm pathophysiology. Microbiome-based therapeutic strategies could offer new avenues for the prevention of cerebrovascular disease.

Aneurysmal subarachnoid hemorrhage (aSAH) is a serious condition complicated by delayed cerebral ischemia (DCI), where inflammation plays a key role. Although altered gut permeability is noted in other conditions, its significance in aSAH remains unclear. Fatty acid-binding protein (FABP-I), lipopolysaccharide-binding protein (LBP), and soluble CD-14 (sCD-14) are established markers of barrier dysfunction. This study investigates gut permeability marker changes in early and late aSAH phases. The study included 177 aSAH patients and 100 controls. Serum samples were collected on days 1 (D1) and 9 (D9) after ictus. FABP-I, LBP, and sCD-14 levels were measured via ELISA, and clinical data were recorded. Outcomes were assessed using the 90-day modified Rankin scale (mRS 0-3 = favorable outcome). Serum FABP-I was significantly lower in aSAH patients (p < 0.05), while LBP and sCD-14 were higher (p < 0.001) compared to controls. FABP-I did not differ between outcome groups, but LBP and sCD-14 were significantly elevated in unfavorable outcomes (p < 0.001). These markers differed in patients without in-hospital infection, with higher levels noted in DCI patients during the later phase (p < 0.05). In aSAH patients without infection, differences in LBP and sCD-14 levels between outcome groups suggest potential endotoxin release from microbial systems, contributing to neuroinflammation and influencing outcomes.

Carotid artery stenting with single-layer stents carries a risk of periprocedural cerebral embolization compared to carotid endarterectomy. Dual-layer micromesh stents were designed for improved plaque coverage and sustained embolic protection. This analysis aimed to confirm the Roadsaver dual-layer micromesh stent safety in a real-world carotid artery stenting cohort. ROADSAVER was a prospective, single-arm, multicenter, observational study. Patients with carotid artery stenosis, eligible for elective stenting, were enrolled at 52 sites across 13 European countries. All procedures followed standard practice. The primary outcome was the 30-day major adverse event rate, defined as the cumulative incidence of any death or stroke. All deaths, strokes, and carotid artery revascularizations were independently adjudicated. In total, 1965 patients were analysed (mean age 70.6 ± 8.8 years). Cerebral ischaemia symptoms were present in 49.4% of participants. Radial/ulnar access was used in 26.3% of cases and embolic protection in 63.8%. The 30-day major adverse event incidence was 2.2% (1.6% in asymptomatic and 2.8% in symptomatic patients), with any stroke at 1.9%, any death at 0.8%, and stroke-related death at 0.5%. Predictors of higher 30-day major adverse event risk, identified through multivariable modelling, included residual stenosis ≥ 30%, thromboembolic venous disease, previous myocardial infarction, age ≥ 75 years, family history of atherosclerosis, non-insulin-dependent diabetes mellitus, symptomatic carotid stenosis, and stent length. Dual-layer micromesh carotid artery stenting is safe, with a low 30-day major adverse event incidence in real-world asymptomatic and symptomatic patients, supporting the sustained embolic protection design concept. Level 2, observational study (with dramatic effect).

Introduction Aneurysmal subarachnoid hemorrhage (aSAH) is a disease associated with high mortality, caused by the rupture of a cerebral aneurysm. Decision-support scoring systems used for managing unruptured aneurysms (UIAs) include only radiological parameters related to the size and configuration of the aneurysm, without incorporating blood-based markers. Our aim is to identify a serum marker that shows a correlation with aneurysm size in patients with ruptured aneurysms. Methods Arterial blood samples were collected from patients who experienced aSAH within 24 hours of the ictus, and serum desmosine levels were determined using ELISA. The morphological parameters of the aneurysms were assessed during 3D DSA. A favorable outcome was defined as a 3-month mRS score of 0–3. Results The study included 135 aSAH patients and 25 controls. (i) The desmosine level in serum collected within 24 hours after aneurysm rupture in patients with aSAH was significantly higher compared to the serum level in the control group (aSAH: 0.737 ng/mL [IQR: 0.401–1.214], vs. control: 0.365 ng/mL [IQR: 0.251–0.531], p < 0.001), (ii) examining the size of ruptured aneurysms, patients with aneurysms larger than 7 mm had significantly higher serum desmosine levels than those with aneurysms smaller than 7 mm, (iii) in the group with aneurysms smaller than 7 mm, serum desmosine levels correlated with the aneurysm neck width and the size ratio. Conclusion Serum desmosine shows a strong correlation with the size of ruptured aneurysms in aSAH patients.

The COVID-19 pandemic, caused by the SARS-CoV-2 virus, has introduced the medical community to the phenomenon of long COVID, a condition characterized by persistent symptoms following the resolution of the acute phase of infection. Among the myriad of symptoms reported by long COVID sufferers, chronic fatigue, cognitive disturbances, and exercise intolerance are predominant, suggesting systemic alterations beyond the initial viral pathology. Emerging evidence has pointed to mitochondrial dysfunction as a potential underpinning mechanism contributing to the persistence and diversity of long COVID symptoms. This review aims to synthesize current findings related to mitochondrial dysfunction in long COVID, exploring its implications for cellular energy deficits, oxidative stress, immune dysregulation, metabolic disturbances, and endothelial dysfunction. Through a comprehensive analysis of the literature, we highlight the significance of mitochondrial health in the pathophysiology of long COVID, drawing parallels with similar clinical syndromes linked to post-infectious states in other diseases where mitochondrial impairment has been implicated. We discuss potential therapeutic strategies targeting mitochondrial function, including pharmacological interventions, lifestyle modifications, exercise, and dietary approaches, and emphasize the need for further research and collaborative efforts to advance our understanding and management of long COVID. This review underscores the critical role of mitochondrial dysfunction in long COVID and calls for a multidisciplinary approach to address the gaps in our knowledge and treatment options for those affected by this condition.

We aimed to investigate the characteristics of serum metabolomics in aneurysmal subarachnoid hemorrhage patients (aSAH) with different 3-month outcomes (good = modified Rankin score: 0–3 vs. poor = mRS 4–6). We collected serum samples from 46 aSAH patients at 24 (D1) and 168 (D7) hours after injury for analysis by liquid chromatography-mass spectrometry. Ninety-six different metabolites were identified. Groups were compared using multivariate (orthogonal partial least squares discriminant analysis), univariate, and receiving operator characteristic (ROC) methods. We observed a marked decrease in serum homocysteine levels at the late phase (D7) compared to the early phase (D1). At both D1 and D7, mannose and sorbose levels were notably higher, alongside elevated levels of kynurenine (D1) and increased 2-hydroxybutyrate, methyl-galactoside, creatine, xanthosine, p-hydroxyphenylacetate, N-acetylalanine, and N-acetylmethionine (all D7) in the poor outcome group. Conversely, levels of guanidinoacetate (D7) and several amino acids (both D1 and D7) were significantly lower in patients with poor outcomes. Our results indicate significant changes in energy metabolism, shifting towards ketosis and alternative energy sources, both in the early and late phases, even with adequate enteral nutrition, particularly in patients with poor outcomes. The early activation of the kynurenine pathway may also play a role in this process.