Conventional ultrafiltration (CUF) is employed during cardiopulmonary bypass to remove excess fluid and concentrate specific blood components. The study aimed to investigate the impact of CUF volume on postoperative cardiac surgery-associated acute kidney injury (CSA-AKI).

This single-center, retrospective study included adult patients undergoing on-pump cardiac surgery between 2018 and 2023. Patients were classified into four categories for comparative analysis: the none-CUF group and three groups according to tertiles of the weight-adjusted CUF volume (tertile 1, 0.1-15.2 mL/kg; tertile 2, 15.3-25.0 mL/kg; tertile 3, >25.0 mL/kg). The primary outcome was postoperative CSA-AKI according to the Kidney Disease Improving Global Outcomes (KDIGO) criteria, and secondary outcomes included perioperative blood transfusion, pulmonary complications, chest drainage volume, urine output, hospital and ICU lengths of stay, and in-hospital mortality. The association between weight-adjusted CUF volume and patient outcomes was assessed by multivariable logistic regression model.

A total of 22,403 patients were included and the incidence of CSA-AKI was 28.1%. Weight-adjusted CUF volume (per 10 mL/kg increase) was independently associated with higher risk of any-stage CSA-AKI (adjusted odds ratio [aOR], 1.25; 95% confidence interval [CI], 1.14-1.38; p < 0.001) and stage 2/3 CSA-AKI (aOR, 1.42; 95% CI, 1.22-1.66; p < 0.001). The restricted cubic splines model illustrated a nonlinear relationship between weight-adjusted CUF volume and any-stage CSA-AKI (p for nonlinearity 0.025), while a J-shaped relationship for stage 2/3 CSA-AKI (p for nonlinearity < 0.001). A higher CUF volume was associated with increased odds of prolonged mechanical ventilation (aOR, 1.38; 95% CI, 1.18-1.64; p < 0.001) and perioperative red blood cell (RBC) transfusion (aOR, 1.13; 95% CI, 1.03-1.25; p = 0.011).

Excess weight-adjusted CUF volume was significantly associated with increasing incidence of CSA-AKI and prolonged mechanical ventilation, but did not reduce the requirement for perioperative RBC transfusion. These findings highlight the cautious application of CUF in fluid management during cardiac surgery.

Although large randomized control trials have established the renal benefits of sodium-glucose cotransporter-2 inhibitors (SGLT2is) in chronic kidney disease (CKD), real-world evidence in Chinese CKD populations remains scarce. Here we report a multicenter real-world retrospective cohort study of SGLT2i use in hospitalized CKD patients in China.

We enrolled 155,053 adults with CKD from the China Renal Data System (CRDS) databases (January 2002-January 2023). We included patients treated with SGLT2i for at least 3 months. SGLT2i users and nonusers were matched (1:2) using propensity score matching (PSM). The main outcomes included renal, safety, and clinical outcomes. Renal outcomes included the first occurrence of CKD progression, end-stage kidney disease (ESKD), or composite outcomes. Multivariable Cox regression models and cumulative incidence were estimated post-PSM.

Overall, the core analysis included 1,477 SGLT2i users and 2,674 nonusers. The progression of CKD (HR 0.81, 95% confidence interval [CI] 0.69-0.95, p < 0.01), incidence of ESKD (HR 0.26, 95% CI 0.18-0.37, p < 0.001), and composite renal outcome (HR 0.68, 95% CI 0.59-0.77, p < 0.001) were significantly lower in the SGLT2i group compared to the non-SGLT2i group. Additionally, the SGLT2i group experienced lower rates of heart failure, stroke, transient ischemic attack, and severe hypoglycemia but a higher risk of acute pancreatitis compared to the non-SGLT2i group. Additionally, eGFR remains better preserved over 3 years in CKD patients treated with SGLT2i.

These findings suggest that SGLT2i offers substantial renal and cardiovascular benefits for Chinese CKD patients.

The impact of cardiometabolic multimorbidity (CMM), defined as the coexistence of multiple cardiometabolic diseases (CMD), on acute pulmonary embolism (PE) outcomes remains understudied. We investigated the burden of CMM and its association with short-term outcomes, treatment patterns, and potential mediators in PE.

We analyzed 7284 patients with acute PE from a nationwide multicenter prospective registry. CMM was defined as the presence of ≥2 CMDs (hypertension, diabetes, dyslipidemia, pre-existing cardiovascular disease, or stroke). The primary objective was to evaluate the association between CMM and 30-day all-cause death and bleeding events. Cox regression models were used to estimate hazard ratios (HR). Sensitivity and subgroup analyses confirmed the robustness of findings, while causal mediation analysis explored underlying pathways.

Overall, 54.2% of patients had ≥1 CMD, and 24.8% had CMM. After multivariable adjustment, CMM was independently associated with increased risks of 30-day all-cause death (HR = 1.28, 95% CI 1.02-1.65) and bleeding (HR = 1.45, 95% CI 1.04-2.01), with mortality rising stepwise with increasing CMD burden. In intermediate-high risk PE, the presence of CMM was linked to lower use of reperfusion therapy. Mediation analysis identified body mass index, blood glucose, and renal function markers as partial drivers of these associations.

CMM is prevalent in PE and not only independently increases the risk of 30-day all-cause death and bleeding but also may influence reperfusion treatment choices. Future studies should test adding CMM to risk assessment to improve stratification and decision-making.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with atherosclerotic cardiovascular disease (ASCVD), yet the magnitude of cardiovascular risk across various disease labels and the clinical utility of readily available risk-associated markers remains unclear.

We searched PubMed, Embase, Web of Science, and the Cochrane Library from 1 January 2000 to 30 September 2025. Observational studies, as well as randomized trials contributing baseline cross-sectional observational data, were included. We pooled relative effects for (i) 10-year ASCVD high-risk classification as defined by established risk engines and (ii) incident major adverse cardiovascular events (MACE). Heterogeneity (I² and τ²), small-study effects (funnel plots and Egger's tests), and leave-one-out sensitivity analyses were assessed. Risk of bias was evaluated using customized Newcastle-Ottawa Scales.

Fifty-two studies were included. Compared with non-steatotic comparators, steatotic liver disease was associated with a higher overall cardiovascular burden (pooled relative effect 2.02, 95 % CI 1.90-2.14). When stratified by outcome, pooled effects were 1.91 (95 % CI 1.60-2.29) for predicted 10-year ASCVD high-risk classification and 1.74 (95 % CI 1.43-2.12) for incident MACE. Associations were consistent across disease labels, including nonalcoholic fatty liver disease (NAFLD; 1.98, 95 % CI 1.81-2.16), with higher but less precise estimates observed for nonalcoholic steatohepatitis (NASH; 3.60, 95 % CI 1.16-6.04). Readily available biomarkers may help complement established ASCVD risk scores by refining cardiovascular risk stratification in individuals with MASLD. Several readily available markers were informative for cardiovascular risk: Fatty Liver Index (FLI) ≥60 (hazard ratio [HR] 1.61, 95 % CI 1.12-2.11) and ≥30 (HR 1.39, 95 % CI 1.11-1.66); Fibrosis-4 index (FIB-4) ≥1.30 (HR 2.25, 95 % CI 1.84-2.65); blood pressure ≥130/85 mmHg (HR 2.16, 95 % CI 1.81-2.51); triglyceride-glucose index (TyG) >8.716 (HR 1.40, 95 % CI 1.26-1.54); and type IV collagen 7S ≥5 ng/mL (HR 2.37, 95 % CI 1.45-4.29). Compared with controls, MASLD was also associated with an adverse biomarker profile, including higher high-sensitivity C-reactive protein (hs-CRP) (+1.06 mg/L), homeostasis model assessment of insulin resistance (HOMA-IR) (+1.65), alanine aminotransferase (ALT) (+8.89 U/L), aspartate aminotransferase (AST) (+6.10 U/L), gamma-glutamyl transferase (GGT) (+13.23 U/L), total cholesterol (TC) (+9.05 mg/dL), triglycerides (TG) (+48.33 mg/dL), low-density lipoprotein cholesterol (LDL-C) (+8.46 mg/dL), glycated hemoglobin (HbA1c) (+0.43 %), and lower high-density lipoprotein cholesterol (HDL-C) (-8.41 mg/dL).

MASLD is associated with an approximate twofold increased risk of cardiovascular events, but this association varies based on population and clinical context. A concise and pragmatic panel-FIB-4, FLI, blood pressure, and triglyceride-glucose index, with type IV collagen 7S where available (and NAFLD-LFS in selected settings)-may complement established ASCVD risk assessment and support earlier, risk-guided prevention in routine MASLD care.

Severe aortic stenosis (AS) management increasingly requires multidisciplinary coordination across diagnostic, interventional, and rehabilitation stages. Integrated care pathways (ICPs) supported by structured data systems may improve safety and outcomes, but real-world evidence in AS remains limited. We aimed to characterize a contemporary cohort of patients with severe AS managed within an ICP at a tertiary hospital, comparing profiles and outcomes by treatment strategy, and to describe diagnostic procedures and the implementation of cardiac rehabilitation (CR) interventions embedded in the pathway.

Prospective observational study of all consecutive patients with AS evaluated by a multidisciplinary heart team between 2018 and 2022. Baseline characteristics and frailty, diagnostic tests, CR interventions, procedural details, and outcomes were collected via an interoperable data management platform and compared across treatment groups: surgical (SAVR) or transcatheter (TAVR) valve replacement, or conservative management. Early survival was assessed using Kaplan-Meier analysis with log-rank testing.

Among 984 patients (median age 78 years, 42% women), 43.9% underwent SAVR, 49.8% TAVR, and 6.3% were managed conservatively. TAVR and conservative groups were older, frailer, and had higher comorbidity. Device success at 30 days was high (≈91%), with periprocedural death at 2.5% for interventions, vs. 9.7% early mortality for conservative management (p < 0.001). Early survival differed significantly (log-rank p = 0.004). TAVR had higher permanent pacemaker implantation (21.7% vs. 7.4% for SAVR, p < 0.001) and major vascular complications (4.1% vs. 0.2%, p < 0.001), while SAVR had more reoperations (8.3% vs. 0.2%, p < 0.001) and atrial fibrillation (18.9% vs. 10.1%, p = 0.001). Prehabilitation was implemented in 64.6% of candidates, while postprocedural CR remained underutilized (11.3%).

Integrated care for a cohort of patients with AS, supported by structured data management, enabled comprehensive profiling, systematic outcome monitoring, and identification of improvement areas. Both SAVR and TAVR achieved high success with low early mortality, while conservative management had poor survival.

Traumatic Brain Injury (TBI) triggers an acute systemic inflammatory response, which may impact outcomes. This response may interact with pre-existing factors linked to inflammation, such as age, to influence outcomes. Previous studies have typically measured few cytokines, but high-dimensional proteomic approaches can sensitively detect a broad range of inflammatory markers, to better characterise post-TBI inflammation. We analysed plasma from BIO-AX-TBI study participants (n = 37 acute moderate-severe TBI (Mayo Criteria), n = 22 acute non-TBI trauma (NTT), n = 28 non-injured controls (CON)) using the Alamar NULISA™ panel (>200 inflammatory markers). The NTT group enabled differentiation of TBI-specific versus general injury-related responses. Inflammatory markers were correlated with plasma NFL, GFAP, total tau, UCH-L1 (Simoa®), S100B (Millipore), and subacute (10 days-6 weeks) 3T MRI measures of lesion volume and white matter injury. Differential expression analysis identified four markers elevated specifically in TBI (VSNL1, IL1RN/IL-1Ra, GFAP, IKBKG), while other derangements reflected non-specific injury responses. Higher VSNL1 correlated with greater lesion volume (r_s = 0.53) and higher IL1RN/IL-1Ra with greater white matter injury (r_s = -0.66, both FDR-adjusted p < 0.05). IL33, part of the non-specific injury response was higher in participants with good (GOS-E 5-8) versus poor (GOS-E 1-4) outcomes (W = 47, FDR-adjusted p = 0.0024). Using an Elastic Net model trained on healthy controls, we show that "inflammation age" exceeded chronological age in TBI, particularly in younger participants. In summary, acute post-TBI inflammation includes both TBI-specific and non-specific components, linked to structural brain injury and functional outcome. Age modulates the inflammatory response. VSNL1, IL1RN/IL-1Ra, and IL33 are potential mediators of post-TBI pathophysiology.

The human plasma virome is dominated by anelloviruses which are increasingly associated with several clinical conditions including among others HIV-1, COVID-19, autoimmune diseases, and cardiovascular and metabolic diseases. Due to their high genetic divergence, most studies investigated human anellome at broad family or genus level. These approaches obscure the contributions of specific anellovirus species to clinical conditions. We conducted plasma metagenomics in 218 individuals from young (0-16 years) and old (63-100 years) cohorts to resolve the anellome at the species level and examine its patterns across age, sex, and associations with cytokines and cardiometabolic outcomes. Older adults exhibited near-universal anellovirus detection and significantly higher abundance compared with youth. Species-specific analysis revealed that Alphatorquevirus_homin1 and Alphatorquevirus_homin13 were markedly enriched in diseased older adults. Predictive modeling based on machine learning algorithms distinguished disease status in the young cohort with high accuracy (AUC = 0.86), but performance was limited in the elderly (AUC = 0.58), suggesting a lack of diagnostic value in advanced age. Specific species abundances and diversity were associated with stroke and coronary heart disease, while cytokine correlations revealed module-specific immune signatures: Gammatorquevirus-dominated modules associated positively with pro-inflammatory cytokines and growth factors (e.g., IL-1β, IL-15, VEGF), whereas Beta- and some Alphatorquevirus-dominated modules showed predominantly negative correlations with several inflammatory and regulatory mediators (e.g., IL-6, TNF-α, IL-10). These findings demonstrate that the anellome is influenced by age and immune status and shows associations with cardiometabolic health, although these relationships do not guarentee diagnostic or causal significance. Additonally, we found no significant differences of Human endogenous retrovirus K Env expression between disease and healthy controls. This work underscores the importance of resolving human anollome to species level in future longitudinal studies to strengthen their clinical significance and biomarker potential.

Per- and polyfluoroalkyl substances (PFAS), such as PFHpA, PFOA, PFNA, and PFDA, are persistent environmental pollutants associated with multiple diseases. This study investigates the toxic mechanisms and pathways by which PFAS derivatives contribute to coronary artery disease (CAD) and renal arteriosclerosis. Using multiple databases, we identified toxic and disease-related targets and constructed a protein-protein interaction (PPI) network via the STRING database to analyze their interactions. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed to identify relevant disease pathways. GO and KEGG results indicated significant enrichment in lipid metabolism, arteriosclerosis, cell proliferation, apoptosis, and inflammation. Molecular docking and dynamics simulations were used to evaluate the binding affinity and stability of PFAS derivatives with key targets. Core regulatory targets within the toxicity network-STAT3, MMP9, NFκB1, CASP3, AKT1, and PPARG-were found to mediate cardiotoxicity and nephrotoxicity through multiple pathways. Docking studies confirmed strong binding affinity (<-5 kcal/mol) between PFAS derivatives and these targets. Molecular dynamics simulations suggested that PFDA binds more stably to MMP9 than to other proteins. These findings indicate that PFAS derivatives may exacerbate renal and coronary arteriosclerosis by modulating lipid and arteriosclerosis signaling pathways and affecting key genes including STAT3, MMP9, and NFκB1. This study highlights potential mechanisms underlying PFAS-induced cardiovascular and renal damage.

Since inflammation and oxidative stress are risk factors for cardiovascular diseases, so it seems that α-lipoic acid consumption as a potent antioxidant can improve vascular function and reduce the risk of vascular disease. The aim of this study is determine the impact of ALA supplementation on vascular function and inflammatory markers in patients who newly experienced stroke.

In this randomized double-blind, placebo-controlled clinical trial, 80 patients were randomly divided into two groups: α-lipoic acid (600 mg ALA daily for 12 weeks) and placebo groups. Serum concentration of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and high-sensitivity C-reactive protein (hs-CRP) were measured by the ELISA method, and carotid intima-media thickness (CIMT) and flow-mediated dilation (FMD) were assessed using the Doppler ultrasound method. All statistical analyses were conducted using SPSS-16 and P values <0.05 were considered statistically significant.

After 12 weeks' supplementation, CIMT, FMD and hs-CRP changed between the ALA and placebo groups, significantly but we observed no significant difference in TNF-α and IL-6 levels either within or between the groups.

The results showed that 600 mg ALA supplementation for 12 weeks improved CIMT, FMD and hs-CRP significantly so it seems that ALA supplementation may reduce the risk of cardiovascular disease.

Cardiovascular diseases, particularly myocardial infarction, remain a leading cause of mortality globally, primarily due to the adult heart's limited regenerative capacity. Recent discoveries have highlighted the epicardium, a mesothelial layer surrounding the heart, as a critical player in cardiac repair and regeneration. During development, the epicardium plays a central role in heart formation by providing progenitor cells, structural components, and paracrine signals. Emerging evidence indicates that this developmental potential can be reactivated in the adult heart following injury. Upon activation, epicardial cells undergo epithelial-to-mesenchymal transition, proliferate, and secrete a range of paracrine factors that influence angiogenesis, inflammation resolution, and extracellular matrix remodeling. This review explores the mechanisms underlying epicardial activation, its contributions to heart development and myocardial repair, and its therapeutic potential. We discuss small molecule modulators, gene therapy, cellular therapies, and biomaterial-based approaches that aim to harness the regenerative capacity of the epicardium. These approaches, which move beyond scar tissue formation to possible regeneration, have the potential to transform the landscape of cardiac regenerative medicine. Despite promising preclinical results, however, challenges such as interindividual variability, incomplete differentiation of epicardial-derived cells, and delivery constraints must be addressed. Advances in single-cell technologies, biomaterial engineering, and translational research are paving the way for personalized and effective epicardium-based therapies. By redefining the role of the epicardium in cardiac biology, epicardial activation offers a novel paradigm for treating ischemic heart disease and heart failure.