BACKGROUND:Ischemic stroke (IS) remains a critical challenge in stroke management. Xiongzhi Tongluo formula (XZTLF), a traditional Chinese herbal prescription, has shown potential in treating ischemic stroke, yet its mechanisms remain elusive. METHODS:This integrated study combined clinical and in vivo approaches to investigate XZTLF. We first employed network node similarity algorithms, ultra-high performance liquid chromatography quadrupole-time-of-flight mass spectrometry (UPLC-Q-TOF/MS)-based phytochemical profiling, and network pharmacology to identify potential molecular targets for ischemic stroke (IS) intervention. The predicted hub genes were then validated through molecular docking and a multicenter randomized controlled trial in patients with acute IS. For in vivo validation, a middle cerebral artery occlusion (MCAO) rat model was used. Rats were treated with XZTLF via oral gavage at doses of 2.97 or 11.88 g/kg/day for 7 days, using edaravone dexborneol (10 mg/kg, i.p.) as a positive control. Key targets and mechanisms of action were further assessed through biochemical and histological analyses of rat brain tissue. RESULTS:XZTLF demonstrated significantly closer network-based proximity to IS targets compared to control prescriptions. Chemical systematic pharmacology analysis identified 173 bioactive constituents in XZTLF. Network pharmacology screening revealed eight core targets (NFKB1, BCL2L1, MAPK1, STAT1, CDKN2A, AR, RAF1, and MMP2), which were subsequently validated in IS patients through ELISA quantification. In MCAO rat models, XZTLF administration significantly reduced cerebral infarct volume and improved neurological function. Mechanistically, XZTLF attenuated neuroinflammation by downregulating pro-inflammatory mediators (including IL-6, TNF-α, and NF-κB), mitigated oxidative damage (MDA, SOD, CAT), and suppressed hyperactivation of the PI3K/AKT signaling pathway. CONCLUSION:XZTLF shows potential for treating IS through multimodal regulation of neuroinflammatory cascades, redox homeostasis, and autophagy pathways, based on integrated preclinical and preliminary clinical findings.

Inflammatory response and oxidative stress interact with each other and are involved in the pathogenesis of various chronic diseases. Senkyunolide A (SenA) is a phthalide compound isolated from the traditional Chinese medicine Chuanxiong Rhizoma (Ligusticum chuanxiong Hort.). At present, the anti‑inflammatory and anti‑oxidative stress effects of SenA remain unclear. In this study, we adopted an integrated strategy combining network pharmacology, bioinformatics analysis, molecular docking, molecular dynamics simulation, bio‑layer interferometry (BLI), and in vitro experiments to explore the anti‑inflammatory and anti‑oxidative stress effects and potential targets of SenA. Through network pharmacology and bioinformatics analysis, we identified four core target genes (Il1b, Ptgs2, Nos2, and Hmox1) of SenA against LPS‑induced inflammation in RAW264.7 cells. Direct binding of SenA to IL‑1β and PTGS2 was confirmed by molecular docking, molecular dynamics simulation, and BLI assays. In vitro experiments showed that SenA pretreatment effectively inhibited LPS‑induced inflammatory response and oxidative stress in RAW264.7 cells, as evidenced by reduced expression of pro‑inflammatory cytokines (TNF‑α, IL‑6, and IL‑1β), decreased levels of NO, ROS, and MDA, increased GSH levels, and alleviated cell swelling and mitochondrial damage. In addition, SenA pretreatment downregulated the mRNA expression levels of the core target genes Il1b, Ptgs2, Nos2, and Hmox1. In conclusion, our findings demonstrate that SenA exerts significant anti‑inflammatory and anti‑oxidative stress effects and may serve as a candidate compound for the treatment of inflammation‑related diseases.

Cardiovascular disease remains the leading cause of death and disability worldwide. The convergence of big data and artificial intelligence (AI) is reshaping precision cardiovascular medicine through multimodal integration of electronic health records (EHRs), imaging, omics, and wearable data across the care continuum, enabling predictive, diagnostic, therapeutic, and system-level optimization. However, translation into durable clinical benefit remains constrained by evidentiary gaps, implementation complexity, and fragmented governance architectures.

ObjectiveIn this study, we aimed to develop and validate an easy-to-use model for screening type 2 myocardial infarction (T2MI) in geriatric patients with acute coronary syndrome (ACS).MethodFrom January 2017 to December 2022, 891 geriatric patients who were clinically diagnosed with ACS and who underwent coronary angiography visited the Chest Pain Center of the Emergency Department at Jiading District Central Hospital affiliated Shanghai University of Medicine & Health Sciences were included. Univariate and multivariate logistic regression analyses were then performed to identify risk factors for T2MI among ACS patients. Subsequently, these factors were used to establish a scoring system, from which a nomogram was developed using R software.ResultThis study included 891 geriatric patients diagnosed with ACS who underwent coronary angiography and met the criteria. Among these patients, 21.3% (190/891) were diagnosed with T2MI. Univariate analysis identified 10 factors significantly associated with T2MI occurrence in geriatric ACS patients (P < 0.05). Multivariate logistic regression analysis revealed atrial fibrillation, COPD, anemia, chronic heart failure, presence of atypical symptoms, and non-ST-segment elevation as independent risk factors for T2MI in geriatric ACS patients. The nomogram model, constructed using troponin and the six identified risk factors, demonstrated a AUC of training set of 0.803 [95% confidence interval (CI): 0.765–0.841], indicating good discrimination. Moreover, calibration and clinical decision curve analyses further confirmed the reliability and clinical value of the proposed model.ConclusionThe predictive nomogram model, based on clinical features of geriatric ACS patients in the emergency department, enables emergency physicians to quickly screen T2MI. Consequently, early identification guides personalized treatment.

Cardiovascular diseases (CVDs) constitute a global health crisis, responsible for approximately 31% of all-cause mortality, and increasingly manifest as multisystem disorders involving cardio-cerebral, cardio-hepatic, and cardio-renal comorbidities, conceptualized as the cardiovascular-renal-hepatic-cerebral paradigm. This review synthesizes evidence demonstrating that circadian disruption (CD) serves as a pivotal underlying mechanism for these inter-organ interactions. The suprachiasmatic nucleus master clock synchronizes peripheral oscillators across organs, coordinating transcriptomic and physiological rhythms; however, misalignment due to sleep disorders, irregular meal timing, or shift work leads to internal desynchrony. This disruption propagates through shared pathways, including autonomic nervous system imbalance, hormonal fluctuations, metabolic dyshomeostasis, systemic inflammation, and gut microbiota dysbiosis. For instance, CD exacerbates morning surges in blood pressure and thrombosis risk in cardio-cerebral comorbidity, impairs lipid metabolism and insulin sensitivity in cardio-hepatic links, and dysregulates electrolyte handling and blood pressure in cardio-renal syndrome within the cardiovascular-kidney-metabolic framework. The review highlights the bidirectional nature of these relationships, where end-organ damage further perturbs circadian rhythms. Importantly, chronotherapeutic strategies, such as time-restricted eating to align nutrient intake with active phases or bedtime administration of antihypertensives, show promise in re-entraining circadian rhythms and mitigating multi-organ dysfunction. This chronobiological perspective underscores the need to integrate temporal dimensions into CVDs management, moving beyond organ-centric views to a network-based approach that targets circadian synchronization for personalized medicine.

BACKGROUND:Although basic research and observational clinical studies have shown an association between vascular calcification (VC) and heart failure (HF), the low level of evidence cannot directly indicate a causal relationship, and no Mendelian randomization (MR) study has been conducted to explore the relationship between VC and HF. METHODS:This study used bidirectional, multivariable, and mediation MR to comprehensively analyze the associations between different VC subtypes and HF as well as its subtypes from multiple perspectives. Accessible genome-wide association study (GWAS) data of VC were included, covering coronary artery calcification (CAC), abdominal aortic calcification (AAC), and calcific aortic valve stenosis (CAVS). Accessible public GWAS data of HF were also included, covering overall heart failure (HFall), ischemic heart failure (IHF), non-ischemic heart failure (ni-HF) recently published in Nature Genetics, and GWAS data of ni-HF with reduced ejection fraction (ni-HFrEF) and ni-HF with preserved ejection fraction (ni-HFpEF) which were classified based on ejection fraction. RESULTS:After sensitivity analysis and multiple correction, the following findings were obtained: (1) VC significantly increases the risk of HF. Specifically, CAC, AAC, and CAVS all significantly increase the risks of HFall and IHF; only CAVS is associated with an increased risk of ni-HF, while CAC and AAC have no impact on ni-HF; VC has no impact on ni-HFrEF or ni-HFpEF. (2) HF also promotes the progression of VC, indicating a bidirectional causal relationship between the two. Specifically, HFall and IHF significantly increase the risks of CAC and AAC; IHF increases the risk of CAVS; no reverse causal relationship is found between ni-HF (including its subtypes) and VC. (3) After two-step MR and multivariable MR correction, atrial fibrillation (AF) is found to partially mediate the causal effect of CAVS on HFall, with a mediation proportion of 21.65%. CONCLUSION:This study reveals a bidirectional causal relationship between VC and HF through two-sample bidirectional MR, suggesting that early detection and management of VC are conducive to the prevention and treatment of HF, especially in high-risk populations such as those with ischemic heart disease. Controlling HF also helps delay the progression of VC and improve vascular status, which is the cornerstone of the prognosis of various cardiovascular diseases. Mediation analysis identifies AF as an important mediating factor, suggesting that screening and intervention of AF may be the key link to block the "VC → AF → HF" pathway, providing new genetic evidence for the prevention and treatment of HF.

Background:Osteoarthritis (OA), low back pain (LBP), and gout contribute substantially to global disability. Although high body mass index (BMI) is an important modifiable risk factor for these conditions, its attributable burden, temporal patterns, and genetically supported associations have not been comprehensively evaluated at the global level. Methods:Using Global Burden of Disease (GBD) 2021 data, we analyzed age-standardized years lived with disability (YLD) rates attributable primarily to high BMI, with kidney dysfunction additionally assessed for gout across sex, age, region, and SDI levels. Joinpoint regression assessed temporal trends. Two-sample Mendelian randomization (MR) evaluated the association between genetically predicted BMI and OA, LBP, and gout. Forecasts to 2040 were generated using a Bayesian age-period-cohort model. Results:From 1990 to 2021, global musculoskeletal disability attributable predominantly to high BMI increased across all three disorders, with kidney dysfunction additionally contributing to gout. Women bore a consistently higher absolute burden, whereas men showed a faster temporal increase (AAPC 1.21% vs 1.05%). The burden was highest in high-SDI regions but increased fastest in low- to middle-SDI settings. For each 1-SD increase in genetically predicted BMI, the ORs were 1.99 (95% CI, 1.79-2.21) for OA, 1.67 (95% CI, 1.37-2.03) for gout, and 1.31 (95% CI, 1.19-1.45) for LBP. Sensitivity analyses showed heterogeneity but no directional pleiotropy. Model-based projections indicated that global YLDs attributable to these selected risks (high BMI, with kidney dysfunction additionally contributing to gout) would increase from 14.10 million in 2022 to 23.88 million by 2040, representing an increase of approximately 69%, with age-standardized rates rising from 158.45 to 200.73 per 100,000. Conclusion:High BMI was a major contributor to the growing global MSK burden, with Mendelian randomization findings supporting an adverse association with OA, gout, and LBP. These findings support the integration of weight management into MSK prevention and management strategies to reduce future disability.

Tongue examination has been used in Traditional Chinese Medicine to assess overall health status from observable tongue phenotypes. With the in-depth integration of microbiome profiling and digital imaging technology, tongue coating, an important colonization interface for oral microorganisms, has provided a new perspective for the early risk detection of major diseases through the quantitative analysis of the microbiome and image features. This study proposes "tongue age” as an indicator reflecting the degree of biological aging of the body, evaluated by integrating tongue-coating microbiome profiling and tongue imaging phenotypes, which are distinct from chronological age. We outlined the definition and quantitative evaluation framework for tongue age, discussed its potential utility for cardiovascular disease risk stratification and longitudinal monitoring, and summarized the key challenges and future directions for standardization, validation, and clinical translation.

Diabetic nephropathy (DN) is characterized by significant endothelial barrier impairment, which leads to increased vascular permeability, albuminuria, and progressive renal dysfunction. Apelin-12, an endogenous bioactive peptide, has attracted attention for its potential protective roles in various cardiovascular and metabolic diseases, owing to its antioxidative and anti-inflammatory properties. This research investigated the renoprotective capacity of Apelin-12 against diabetic nephropathy (DN) by modulating oxidative stress and endothelial barrier dysfunction in both db/db mice and human renal glomerular endothelial cells (HRGECs). In diabetic mice, Apelin-12 treatment significantly ameliorated glomerular oxidative stress, restored JAM-A expression, and improved renal function, as evidenced by reduced albuminuria and serum creatinine levels. Histopathological analysis confirmed reduced glomerular damage. Apelin-12 also preserved endothelial marker expression and reduced inflammation without affecting blood pressure or glucose tolerance. In HRGECs, Apelin-12 attenuated high glucose-induced endothelial barrier disruption, restored JAM-A expression, activated the Nrf2/HO-1 antioxidant pathway, and suppressed p53 upregulation. Notably, p53 overexpression abolished Apelin-12's protective effects on JAM-A expression and endothelial integrity, suggesting that p53 is a critical mediator in this pathway. These findings indicate that Apelin-12 alleviates DN progression through counteracting oxidative stress and p53-dependent endothelial dysfunction, supporting its candidacy as a therapeutic agent. The study further establishes the mechanistic link between JAM-A and p53 in diabetic renal injury, providing new insights into DN pathogenesis.

Despite intensive glycemic control, diabetic cardiomyopathy (DCM) often progresses due to hyperglycemic memory (HGM), yet the specific cardiac cells perpetuating this injury remain unknown. To address this, we performed single-nucleus RNA sequencing (snRNA-seq) on hearts from an HGM rat model. Our analysis of 86,120 nuclei revealed HGM-specific inflammatory and epigenetic reprogramming signatures. Fibroblasts emerged as potential mediators, appearing to drive extracellular matrix remodeling via upregulated LAMININ and COLLAGEN signaling. We uncovered a distinct HGM-specific fibroblast subpopulation characterized by oxidative stress and H3K27 demethylation. Integrative analysis prioritized Fmo2 as a key pathogenic candidate, which was further supported via Mendelian randomization and clinical data as a putative causal gene. This study suggests that a pathogenic Fmo2+ fibroblast subpopulation may act as a pathological “memory carrier,” providing novel mechanistic insights and proposing exploratory therapeutic avenues for HGM-induced cardiac damage beyond glycemic control.

BackgroundMyocardial ischemia-reperfusion injury (MIRI) remains a major complication. Fusobacterium nucleatum (F. nucleatum), an oral pathobiont associated with cardiometabolic disease, may influence host physiology by reshaping gut microbial function through an oral-gut axis. Whether such microbial interactions contribute to MIRI remains unclear.MethodsAn oral F. nucleatum gavage mouse model and cohorts were established to investigate the effect of oral F. nucleatum on MIRI, gut microbial histidine metabolism including imidazole propionate (ImP) production, the association of ImP with coronary heart disease (CHD), and its microbial sources. MIRI was induced with or without antibiotic-mediated microbiota depletion and/or ImP administration, and p62 dependence was examined by knockdown approaches in vitro and in vivo. Plasma metabolites, cardiac injury, ultrastructure, and p62/mTOR signaling were assessed.ResultsF. nucleatum aggravated MIRI despite the absence of persistent colonic colonization. Instead, F. nucleatum altered gut microbial composition, including Lactobacillus abundance, and was associated with elevated circulating ImP. Antibiotic-mediated microbiota depletion reduced ImP and attenuated myocardial injury. Plasma ImP was elevated in patients with CHD, and ImP-producing capacity was supported primarily by gut microbiota urocanate reductase (UAR)-associated functions. In H9c2 cells, ImP exacerbated hypoxia/reoxygenation injury, and increased the autophagy adaptor p62 together with downstream mTOR/S6K1 signaling. p62 knockdown attenuated the mTOR/S6K1 response and injury-associated changes, whereas IRS1 suppression persisted.ConclusionsF. nucleatum reshapes gut microbial metabolism, thereby amplifying MIRI via ImP. ImP emerges as a functional mediator linking oral dysbiosis to MIRI, and reducing microbiota-derived ImP may represent a more mechanistically grounded strategy to mitigate MIRI.

ABSTRACT Background Pressure ulcers (PUs) remain a major clinical challenge, particularly among immobilized and critically ill patients. Accumulating evidence suggests that alterations in gut microbiota composition and diversity are associated with PUs. But until now, the causal association between them has been unclear. Aim We conducted a two‐sample Mendelian randomisation (MR) study to investigate the causal effect of gut microbiota on PUs. Study Design Gut microbiota summary statistics were obtained from the MiBioGen Consortium (18,340 individuals, 24 cohorts, 211 taxa), and PU data were derived from the FinnGen biobank (354,567 Europeans; 1479 PU cases, 353,088 controls). Causal estimates were calculated using inverse variance weighted (IVW), weighted median, simple mode, weighted mode and MR‐Egger methods, with sensitivity analyses including pleiotropy tests, Cochran's Q and leave‐one‐out analysis. MR Steiger's test was applied to infer directionality. Results IVW analysis indicated protective effects of Clostridiaceae 1 (odds ratio, OR = 0.668, 95% confidence intervals (CI) = 0.455–0.982, p = 0.040), genus Coprococcus2 (OR = 0.508, 95% CI = 0.344–0.751, p = 0.001) and genus Gordonibacter (OR = 0.812, 95% CI = 0.676–0.976, p = 0.027) against PUs. While genus Anaerotruncus (OR = 1.729, 95% CI = 1.189–2.513, p = 0.004) and genus Christensenellaceae R7 (OR = 1.953, 95% CI = 1.087–3.508, p = 0.025) increased PUs’ risk. Reverse MR suggested causal effects of PUs on five genera, including Butyrivibrio (OR = 0.887, 95% CI = 0.798–0.985, p = 0.026), Erysipelotrichaceae UCG003 (OR = 1.057, 95% CI = 1.004–1.113, p = 0.035), Eubacterium fissicatena group (OR = 0.898, 95% CI = 0.811–0.995, p = 0.040), Faecalibacterium (OR = 0.952, 95% CI = 0.908–0.999, p = 0.046) and Eubacterium oxidoreducens group (OR = 1.093, 95% CI = 1.001–1.194, p = 0.047). Sensitivity analysis supported the robustness of the findings, and Steiger's test confirmed directionality from gut microbiota to PUs. Conclusion This MR study provides genetic evidence for a causal role of gut microbiota in PU risk, supporting the potential of microbiota‐targeted interventions and offering new insights into PU pathogenesis and highlighting their particular relevance for prevention strategies in immobilized critical care patients. Relevance to Clinical Practice The study provides epidemiological evidence for a gut–skin link in PUs and suggests personalised microbiota‐based intervention strategies for critically bedridden patients.

Tea intake (TI) has been associated with a reduced risk of ischemic heart disease (IHD) through antioxidant, anti-inflammatory, and metabolic regulatory biological mechanisms, but a comprehensive global assessment of the IHD burden reduction potentially associated with TI is lacking. This study aimed to quantify the reductions in global IHD incidence and mortality associated with TI from 1990 to 2021, and explore heterogeneity in these associations across demographic subgroups and regions. We conducted a comparative risk assessment analysis integrating data from the Global Dietary Database (GDD), IHD burden estimates from the Global Burden of Disease (GBD) study, and BMI-stratified population distributions from the NCD Risk Factor Collaboration (NCD-RisC) across 180 countries and regions. TI distributions were modeled using gamma distributions, and BMI-stratified relative risks derived from dose-response meta-analyses were applied to estimate population attributable fractions. The analysis was stratified by sex, age, education level, and urbanicity. Proportional and absolute burden reductions (cases per million adults) were estimated, with uncertainty propagated through Monte Carlo simulation. Globally in 2021, approximately 28.66 million (95

Ischemic stroke remains a leading cause of mortality and disability worldwide. Current reperfusion therapies are limited by narrow therapeutic time windows and the risk of secondary reperfusion injury, underscoring the urgent need for novel translatable neuroprotective targets. Mitochondrial dysfunction serves as a central hub in the ischemic cascade, contributing to energy failure, oxidative stress, calcium dysregulation, and various forms of programmed cell death. Recently, intercellular mitochondrial transfer has emerged as a crucial form of metabolic communication within the neurovascular unit (NVU). In the context of ischemia-reperfusion, donor cells can transfer functional mitochondria to compromised cells, facilitating metabolic rescue and remodeling the local microenvironment. Extensive in vivo and in vitro studies have shown that astrocytes, mesenchymal stem cells (MSCs), and pericytes can deliver mitochondria to neurons or brain microvascular endothelial cells (BMECs) through mechanisms such as tunneling nanotubes (TNTs), extracellular vesicles (EVs), and gap junctions. This transfer helps maintain blood-brain barrier (BBB) integrity and promotes neurological recovery. The process is finely regulated by inflammatory signaling, metabolic reprogramming, and epigenetic modulation, all of which influence the directionality and functional outcomes of the transfer. As a result, pharmacotherapies, non-pharmacological interventions, and direct mitochondrial transplantation have demonstrated considerable neuroprotective potential in experimental models and early-stage clinical research. However, challenges related to transfer selectivity, the durability of effects, delivery efficiency, and immune safety still hinder clinical translation. Future efforts must prioritize elucidating the underlying mechanisms, standardizing protocols, and developing precise stratification strategies to advance mitochondrial transfer-based interventions from proof-of-concept to a controllable and evaluable therapeutic option for stroke treatment.

Hypereosinophilic syndrome (HES) is a heterogeneous disorder characterised by persistent, abnormal eosinophil elevation in blood and tissues, with multisystem involvement. Cardiac manifestations are frequent in HES and significantly worsen prognosis. Recent evidence establishes a direct link between HES and myocardial infarction (MI), demonstrating that HES induces MI primarily via non-atherosclerotic mechanisms. Critically, HES-related MI is fundamentally distinct from atherosclerotic MI in pathogenesis, diagnosis and management. This paradigm shift redefines diagnostic frameworks for cardiovascular disease and provides targeted strategies for non-atherosclerotic MI. This review synthesises current knowledge on HES-associated MI, emphasising its unique epidemiology, pathophysiology, evidence-based diagnostic criteria and mechanism-specific therapies. Future research priorities are discussed to advance clinical translation.

Diabetes is associated with a higher burden and heterogeneous phenotypes of plaque calcification, which may influence plaque stability and cardiovascular risk. This review examines diabetic plaque calcification as a dynamic process driven by hyperglycemia and other metabolic disturbances through downstream mechanisms including inflammation, apoptosis, matrix vesicles, and osteogenic transdifferentiation. It highlights the importance of multidimensional imaging assessment beyond calcification burden and discusses current therapeutic limitations and future research directions.

The leaves of Crataegus pinnatifida Bge., a medicinal plant and a source of brewed tea, are often overlooked as a byproduct of fruit consumption. Despite this, these leaves have demonstrated significant cardiovascular protective and lipid-lowering properties. To further investigate their potential applications, nine novel compounds (1-9) and twelve known flavonoids were isolated from C. pinnatifida leaves. Their structures were elucidated through comprehensive spectroscopic analysis, including experimental and calculated electronic circular dichroism. The antioxidant capacities of these 21 compounds were assessed using DPPH˙ and ABTS˙+ assays. Notably, the newly identified biphenyl compounds 7 and 8 exhibited potent antioxidant activities, surpassing that of vitamin C in both assays. Additionally, the ABTS˙+ assay revealed that flavonoid O-glycosides generally possess stronger antioxidant activity compared to flavonoid C-glycosides. To evaluate their cytoprotective potential, compounds 12-14 and 18-20 were tested against H2O2-induced neurotoxicity in human neuroblastoma SH-SY5Y cells. At 100 μM, these compounds demonstrated significant protective effects. Furthermore, flavonoid C-glycosides exhibited stronger protective activity against alcohol-induced injury in BRL-3A hepatocytes than flavonoid O-glycosides. In conclusion, this study provides compelling evidence that C. pinnatifida leaves contain valuable bioactive compounds with potent antioxidant and cytoprotective properties. These findings further validate the traditional use of this plant and offer promising avenues for future research and potential therapeutic applications.

Background Aprotinin was suspended in cardiac surgery following prior research indicating an association with elevated adverse clinical event risks. Recently, debate and divergent opinions regarding its use have emerged. This study aimed to assess the safety and efficacy of aprotinin by comparing outcomes in patients undergoing ONCAB before and after its suspension. Methods A multicenter retrospective cohort study was conducted to evaluate the efficacy and safety of aprotinin in ONCAB surgery. The aprotinin group (n = 919) included patients who received aprotinin and met the inclusion criteria prior to December 19, 2007. The control group (n = 935) included patients who received neither aprotinin nor any anti-fibrinolytic agents and met the inclusion criteria subsequent to December 19, 2007. Postoperative outcomes were compared between the two groups. Results In the aprotinin group, a discernible reduction in bleeding volume was observed, accompanied by a lower transfusion rate and volume, and a decreased reoperation incidence. Additionally, no significant difference was found in the composite endpoints ( P > .05), which encompassed perioperative seizure, renal dysfunction, MI, stroke, DVT, PE, and all-cause mortality, when comparing the two groups. Notably, aprotinin use resulted in a marginal prolongation of hospital stay by 0.42 days ( P = .041). Findings from the univariate analysis were corroborated by multivariable logistic regression, adjusting for baseline characteristics, thus yielding consistent results. Conclusions Aprotinin use in ONCAB surgery significantly minimized bleeding volume, transfusion rate and volume, and reoperation incidence, without elevating the risk of adverse clinical events.