Search Results (18,066)

Patients with left ventricular dysfunction undergoing cardiac surgery face a heightened risk of perioperative complications, including postcardiotomy shock (PCS). Conventional management with inotropes and vasopressors can exacerbate end-organ dysfunction, underscoring the need for alternative strategies. The planned use of mechanical circulatory support (MCS) devices, such as the Impella, offers a proactive approach to mitigating PCS in high-risk patients. This study presents our early experience at Johns Hopkins with planned Impella utilization in high-risk cardiac surgery. We detail our risk stratification methodology, patient selection criteria, and perioperative management strategies. Our proposed risk stratification scoring system incorporates surgical intent, preoperative myocardial function, anticipated postoperative course, and exit strategy to identify optimal candidates for perioperative MCS. We describe the intraoperative central placement technique for the Impella 5.5, perioperative management protocols—including anticoagulation strategies and weaning protocols—and postoperative device extraction. A retrospective review of our first 11 consecutive patients with severely reduced left ventricular ejection fraction (<30%) who underwent Impella-assisted cardiac surgery demonstrated favorable outcomes, with no postoperative mortality and a two-year follow-up. Our findings suggest that planned Impella use in high-risk cardiac surgery is both feasible and beneficial. However, further studies are necessary to validate these results, assess long-term outcomes, and evaluate cost-effectiveness. Full article

Early-onset infection caused by Streptococcus agalactiae (Group B Streptococcus, GBS) may occur during gestation or delivery and can lead to severe neonatal sepsis, meningitis, or pneumonia. Discordant GBS infections in twin gestations are rare. We report a fatal case of early-onset GBS infection in dichorionic–diamniotic twins conceived via IVF and delivered by caesarean section at 32 weeks’ gestation due to discordant fetal growth and abnormal Doppler indices in Twin A (Umbilical Artery PI = 1.4; Middle Cerebral Artery PI = 1.5). Twin A had Apgar scores of 3, 5, and 5 and rapidly developed tachycardia, respiratory distress, and systemic infection, while Twin B, with Apgar scores of 7, 8, and 9, remained clinically stable. Both infants were admitted to the NICU and underwent routine blood, urine, and cerebrospinal fluid testing. Despite the prompt initiation of parenteral ceftriaxone and respiratory support, Twin A deteriorated rapidly and died within 28 h. GBS was isolated from Twin A’s blood culture, and maternal placental tissue and high vaginal samples collected before antibiotic administration also grew GBS, with all isolates demonstrating identical antimicrobial resistance profiles. Molecular analysis revealed matching rib1 and alp2/3 gene patterns in isolates from the mother and Twin A. Maternal anovaginal immunochromatography at delivery was positive, whereas screening cultures obtained at 29 weeks’ gestation were negative. This case highlights the limitations of culture-based GBS screening in high-risk pregnancies and preterm deliveries and underscores the potential value of molecular assays and point-of-care testing to improve detection of S. agalactiae throughout pregnancy and the peripartum period. Emerging preventive strategies, including modulation of the genital microbiome and maternal vaccination aligned with WHO recommendations, may further reduce the burden of neonatal GBS disease. Full article

Neuronal ferroptosis is a key contributor to secondary brain injury following cerebral ischemia, yet the metabolic mechanisms governing this process remain poorly understood. Enriched environment (EE) is a housing paradigm that provides enhanced sensory, cognitive, and social stimulation through complex physical surroundings and increased opportunities for voluntary activity. Our preliminary data indicate that EE confers cerebroprotection against ischemia-induced ferroptosis; however, whether this effect is associated with glycogen metabolic regulation and the underlying molecular pathways has not been elucidated. This study aimed to determine whether EE may influence ferroptosis-associated pathways, potentially via Sirtuin 1 (SIRT1)/protein kinase B (AKT)/glycogen synthase kinase-3β (GSK3β)-related mechanisms of glycogen metabolism. Using a mouse model of middle cerebral artery occlusion (MCAO) and an oxygen–glucose deprivation/reoxygenation (OGD/R) cellular model, we performed behavioral assessments, molecular and biochemical analyses, and pharmacological interventions to elucidate mechanistic pathways. EE was associated with improved neurological outcomes and reduced infarct volume after ischemia. Mechanistically, EE appeared to activate the SIRT1/AKT pathway and increase the inhibitory phosphorylation of GSK3β and relieving its suppressive effect on glycogen synthase, which may underlie the observed increase in glycogen levels within ischemic brain tissue. Pharmacological inhibition of SIRT1 largely diminished these metabolic and neuroprotective benefits. Consistently, at the cellular level, SIRT1 overexpression contributed to the restoration of glycogen metabolism and robustly attenuated ferroptosis under ischemic conditions. Collectively, these findings suggest that EE may attenuate ferroptosis-related pathways possibly involving SIRT1/AKT/GSK3β-dependent glycogen metabolic remodeling, providing a novel metabolic perspective on EE-induced cerebroprotection and highlighting SIRT1-centered regulation of glycogen metabolism as a potential therapeutic target for ischemic stroke. Full article

Background: the pathophysiological mechanisms underlying spontaneous coronary artery dissection (SCAD) remain incompletely understood. Inflammation may play a pivotal role by promoting vascular susceptibility to SCAD. This study aimed to evaluate pericoronary adipose tissue (PCAT) attenuation, a recognized imaging marker of vascular inflammation, in patients with SCAD. Methods: patients with SCAD who underwent coronary computed tomography angiography (CCTA) within 48 h of the index event and with an identifiable trigger were included. Patients were classified according to the trigger preceding the event (emotional vs. physical). PCAT attenuation was measured in culprit and non-culprit vessels in all patients. Results: A total of 25 SCAD patients were included (mean age 55 ± 11 years, 80.0% female). Emotional triggers were reported in 17 patients (68.0%), while 8 (32.0%) experienced a physical trigger. Type 2 dissections were more common in the emotional trigger group (64.7% vs. 25.0%, p = 0.040). Patients with emotional triggers exhibited higher PCAT attenuation compared with those with physical triggers in the SCAD-related vessel (−62.35 ± 6.46 HU vs. −70.86 ± 8.45 HU; p = 0.028) and in non-culprit vessels (−61.39 ± 7.24 HU vs. −71.16 ± 5.28 HU; p = 0.001). Conclusions: patients with SCAD demonstrated elevated PCAT attenuation, particularly in those with emotional triggers, in both culprit and non-culprit vessels. These findings suggest that vascular inflammation may represent a predisposing factor for SCAD and a target for preventive and therapeutic strategies. Full article

Background: Extracorporeal membrane oxygenation (ECMO) is lifesaving in pediatric patients with respiratory and/or cardiovascular failure. Cardiac catheterization is an important diagnostic and therapeutic tool in patients with congenital heart disease supported by ECMO, allowing the assessment of residual lesions, hemodynamically significant anatomical abnormalities, and unexplained indications for ongoing ECMO support. The timing and clinical contribution of cardiac catheterization in these patients are still debated. Objective: This study aimed to evaluate the indications, safety, and impact of cardiac catheterization on clinical management in pediatric patients receiving postoperative ECMO support. Methods: This single-center, retrospective study examined 39 pediatric patients under the age of 18 who underwent postoperative cardiac catheterization with ECMO support between January 2022 and December 2025. Demographic data, procedure characteristics, and clinical outcomes were analyzed. Results: Of the 190 patients under postoperative ECMO support, 39 underwent catheterization. The median age of the patients was 2.5 months (range, 6 days–180 months) and median weight was 4.2 kg (range, 2.8–57 kg). The most frequent diagnoses were ventricular septal defect-pulmonary atresia (VSD-PA) in 20.5% (n = 8) and transposition of the great arteries (TGA) in 15.3% (n = 6). The indication for catheterization was to investigate the reason for ECMO placement in 26 patients (66.6%). Most patients underwent catheterization within the first 24 h after ECMO initiation. Patients who underwent catheterization represented a higher-risk subgroup, with a greater proportion of STAT 4-5 procedures (59% vs. 40%) compared with the overall ECMO cohort. Cardiac catheterization resulted in a change in clinical management in 25.6% of patients through catheter-based intervention or surgical revision. Survival in the catheterized subgroup was 12.8%, reflecting the high-risk nature of this population. Conclusions: Cardiac catheterization in pediatric patients on postoperative ECMO support can be performed with a low complication rate and can significantly alter clinical management. Cardiac catheterization should be considered an important diagnostic and therapeutic modality, particularly in the presence of suspected residual lesions or unexplained hemodynamic instability. Additionally, we recommend that cardiac catheterization be performed promptly within the first 24–48 h in this patient group on ECMO support. Full article

Carpal tunnel syndrome (CTS) is the most common entrapment neuropathy of the upper extremity and results from compression of the median nerve within the fibro-osseous carpal tunnel. Anatomical variants such as a bifid median nerve (BMN) and a persistent median artery (PMA) may increase tunnel occupancy and complicate both diagnosis and treatment. High-resolution musculoskeletal ultrasound enables detailed evaluation of these anatomical variations and facilitates image-guided interventions. Ultrasound-guided hydrodissection has emerged as a minimally invasive technique capable of mechanically releasing perineural adhesions and restoring nerve mobility. Alpha-2 macroglobulin (A2M), an autologous plasma protease inhibitor with anti-inflammatory and cytokine-binding properties, has recently been explored as a biologic adjunct in musculoskeletal conditions. We report the case of a 60-year-old right-handed woman who presented with a one-year history of numbness, paresthesia, and pain within the median nerve distribution of her dominant hand. Ultrasound examination demonstrated a bifid median nerve accompanied by a persistent median artery and perineural edema within the proximal carpal tunnel. The patient underwent three weekly sessions of ultrasound-guided hydrodissection using autologous A2M prepared through the APEX filtration system. The patient reported progressive clinical improvement following treatment. Grip strength increased from 12 kg at baseline to 22 kg at week twelve. Follow-up ultrasound performed ten months after treatment showed restoration of median nerve fascicular architecture and normalization of nerve morphology, findings consistent with interval structural improvement. This case highlights the role of ultrasound in the integrated evaluation and management of CTS with anatomical variants, including diagnosis, procedural guidance, and longitudinal assessment. Ultrasound-guided hydrodissection with A2M may represent a feasible minimally invasive approach in selected patients; however, further prospective studies are required to determine its safety and therapeutic efficacy. Full article

Background/Objectives: Reconstruction of complex lower extremity soft tissue defects remains challenging, particularly in the proximal and middle tibial regions, including the knee, where suitable recipient vessels are often limited due to prior trauma, infection, or surgical intervention. This study aimed to evaluate the feasibility and clinical applicability of anterior tibial vessel turnover as an alternative recipient vessel strategy in free flap reconstruction. Methods: A retrospective review was conducted of seven patients who underwent free flap reconstruction using anterior tibial vessel turnover as the recipient vessel between 2019 and 2024. Preoperative imaging was performed to assess vascular status and collateral circulation. Clinical data, including patient demographics, defect characteristics, flap parameters, and postoperative outcomes, were analyzed. Results: The mean patient age was 62.7 years (range, 38–86 years). Defects were primarily located in the proximal and middle tibial regions and were associated with trauma, postoperative infection, chronic osteomyelitis, or burn injury. The mean flap size was 137.4 cm² (range, 49.5–280 cm²). All flaps survived, resulting in a flap survival rate of 100%, with no cases of total flap loss or re-exploration due to vascular compromise. One patient experienced partial flap loss, while no other flap-related complications were observed. Most patients achieved stable wound coverage and favorable functional recovery. Conclusions: Anterior tibial vessel turnover may serve as an alternative recipient vessel strategy for selected cases of complex lower extremity free flap reconstruction. This technique enables microvascular anastomosis in a more superficial and accessible field and expands reconstructive options in cases with compromised recipient vessels. Full article

Background: The Circle of Willis (CoW) is a key collateral pathway that enables communication between the anterior and posterior cerebral circulations. However, anatomical variations in the A1 segment of the anterior cerebral artery, such as hypoplasia or aplasia, can alter hemodynamics and may compromise this collateral function. While incomplete CoW configurations have been linked to aneurysm formation and altered patterns of hemorrhage, their role in the distribution of cerebral infarctions remains controversial. We aimed to explore the association between A1 segment hypoplasia/aplasia and infarct laterality across different etiological subtypes. Methods: We retrospectively analyzed patients with unilateral anterior circulation infarction admitted between April 2017 and March 2023. The CoW was assessed by magnetic resonance angiography (MRA). A1 segment hypoplasia was defined as a segment diameter <1 mm, and A1 aplasia was defined as non-visualization on MRA. The side with hypoplasia or aplasia was defined as the minor side, and the contralateral side as dominant. We assessed whether infarction occurred on the minor or dominant side. Results: Among 198 patients with unilateral anterior circulation infarction classified as lacunar, cardioembolic stroke (CES), or embolic stroke of undetermined source (ESUS), 30% had A1 hypoplasia or aplasia, with similar prevalence across subtypes. Infarcts occurred on the A1 dominant side in 53% of lacunar, 55% of ESUS, and 75% of CES cases. Although this difference did not reach statistical significance (p = 0.43), it should be interpreted with caution given the limited sample size. Conclusions: The rates of A1 hypoplasia and aplasia were similar across stroke types. No statistically significant association was identified. The findings remain inconclusive given the limited sample size. These results should be considered exploratory and hypothesis-generating. Full article

Background and Objectives: Residual coronary anatomical complexity following culprit-lesion-only percutaneous coronary intervention (PCI) remains a major determinant of clinical outcomes in patients with multivessel coronary artery disease (CAD). Platelet distribution width (PDW), a marker of platelet heterogeneity and activation, has been associated with adverse cardiovascular outcomes; however, its relationship with post-procedural residual disease burden remains unclear. This study aimed to evaluate the association between PDW and residual SYNTAX (Synergy between Percutaneous Coronary Intervention with Taxus and Cardiac Surgery) score and to determine its incremental predictive value beyond established clinical variables. Materials and Methods: In this retrospective, single-center study, 140 patients with multivessel CAD undergoing culprit-lesion-only PCI followed by planned staged revascularization were included. Clinical presentation was categorized as chronic coronary syndrome (CCS), non-ST-elevation myocardial infarction (NSTEMI), or ST-elevation myocardial infarction (STEMI). Residual SYNTAX score was calculated after the index procedure, and patients were stratified into low (≤22) and high (≥23) groups. Associations between PDW and residual SYNTAX score were assessed using correlation and regression analyses. Model discrimination and incremental predictive value were evaluated using ROC analysis, hierarchical logistic regression, and reclassification metrics. Nonlinear relationships were explored using restricted cubic spline analysis, and clinical utility was assessed by decision curve analysis. Results: PDW was significantly correlated with residual SYNTAX score (Spearman ρ = 0.503, p < 0.001) and increased progressively across SYNTAX severity strata and clinical presentation groups. In multivariable analysis, PDW remained independently associated with high residual SYNTAX score (OR 1.38, 95% CI 1.07–1.82, p = 0.016). The addition of PDW to a hierarchical clinical model significantly improved model performance (ΔR² = 0.049, p = 0.012). Although the improvement in area under the curve (AUC) was modest, reclassification analyses demonstrated significant net reclassification and discrimination improvements. Spline analysis revealed a nonlinear relationship, with a marked increase in risk beyond PDW levels of approximately 13 fL. Decision curve analysis confirmed the clinical utility of PDW across a range of threshold probabilities. Conclusions: PDW is independently associated with post-procedural coronary anatomical complexity and provides incremental predictive value beyond established clinical variables. However, PDW should be interpreted as a biomarker reflecting platelet heterogeneity within a thromboinflammatory context, without the ability to distinguish between acute and chronic components. Full article

Background/Objectives: Severe hemorrhagic shock progressing to clinical death remains a major cause of mortality and long-term neurological morbidity despite advances in trauma care. While current resuscitation strategies restore circulation, their ability to preserve brain structure and function following global ischemia–reperfusion injury remains limited. Hemorrhagic shock induces widespread neuronal vulnerability, particularly within the hippocampus and prefrontal cortex, contributing to persistent cognitive and behavioral deficits among survivors. Methods: Using a rat model of hemorrhagic shock-induced clinical death, we evaluated whether resuscitation with VBI-1, a phospholipid nanoparticle-based colloid, supports neurological recovery compared with whole blood-based resuscitation. Animals underwent controlled exsanguination to the point of clinical death, followed by rapid intra-arterial reanimation with either shed whole blood or VBI-1. Two phases of study were performed: histological evaluation of tissues 12 h after resuscitation and, in a separate cohort of animals, longitudinal behavioral recovery over 30 days. Histology focused on evaluating neuronal integrity in the hippocampal CA1 region and prefrontal cortex, neuronal functional status, and microglial responses. Sex was analyzed as a biological variable. Results: Resuscitation with VBI-1 is associated with sustained behavioral recovery, with pronounced sex-dependent effects favoring females during the subacute-to-chronic recovery phase. VBI-1 preserved neuronal density, laminar organization, and neuronal functional integrity in ischemia-vulnerable brain regions. This, and neuronal preservation, correlated with hippocampal-dependent working memory performance. Importantly, resuscitation with VBI-1 did not increase microglial density, coverage, or spatial organization, exacerbating the neuroinflammatory burden. Conclusions: These findings demonstrate that phospholipid nanoparticle-based resuscitation confers meaningful neurological recovery following profound circulatory collapse, highlighting the importance of evaluating resuscitation agents based on long-term brain outcomes. Full article

Background: Melatonin has antioxidant and anti-inflammatory properties that may attenuate ischemia-reperfusion injury, but randomized cardiovascular trial data remain inconsistent. Objectives: This study sought to evaluate the association of melatonin supplementation with cardiovascular outcomes across randomized trials. Methods: We performed a systematic review and meta-analysis of randomized trials comparing melatonin with placebo, usual care, or no melatonin in patients with cardiovascular disease. PubMed, Embase, and CENTRAL were searched from inception to 1 January 2026. Random-effects models with Hartung–Knapp–Sidik–Jonkman confidence intervals were used. Prespecified outcomes included left ventricular ejection fraction (LVEF), change in LVEF, troponin, infarct size by cardiac magnetic resonance, heart failure outcomes, inflammatory and oxidative stress biomarkers, and adverse events. Results: A total of 14 randomized controlled trials involving 1027 participants were included. Melatonin significantly improved change in LVEF from baseline to follow-up (mean difference: 3.95 percentage points; 95% CI: 1.70–6.20; p < 0.001), with the most consistent signal in coronary artery bypass grafting studies (mean difference: 4.65 percentage points; 95% CI: 2.56–6.74). Final LVEF was numerically higher with melatonin but not statistically significant. Troponin reduction was not significant. Narrative synthesis suggested lower inflammatory and oxidative stress markers after coronary artery bypass grafting and improvement in heart failure symptoms and quality of life, whereas infarct size findings in ST-segment elevation myocardial infarction were mixed and timing-dependent. Conclusions: Melatonin was associated with improved LVEF change, particularly in coronary artery bypass grafting settings, but benefit was not consistently demonstrated across final LVEF, troponin, or infarct size outcomes. Full article

Fatty acids serve dual roles in cardiac physiology: as energy substrates and as precursors of bioactive lipid mediators (prostaglandins, leukotrienes, oxylipins) from n-3/n-6 PUFAs that regulate inflammation, thrombosis, and remodeling. Saturated, monounsaturated, and trans fatty acids modulate metabolism and membrane function, thereby shaping these pathways. Clinically, n-3 long-chain PUFAs (EPA and DHA) reduce cardiovascular mortality and aid postischemic remodeling; however, high doses increase the risk of atrial fibrillation. By contrast, trans and saturated fatty acids promote dyslipidemia, dysfunction, and higher rates of coronary artery disease and heart failure. Mechanistically, fatty acid uptake via FABPpm, CD36 (FAT), and FATPs, along with β-oxidation and PPAR signaling, regulates metabolism, while COX/LOX/CYP pathways generate eicosanoids and resolvins that influence inflammation and repair. This review synthesizes evidence on the roles of fatty acids and oxylipins in lipotoxicity, heart failure, ischemia–reperfusion, and arrhythmias, and evaluates dietary and supplemental interventions to optimize cardiac lipid metabolism, aligning with fatty acid signaling. Full article

Background/Objectives: Elevated lipoprotein(a) [Lp(a)] is an independent causal risk factor for atherosclerotic cardiovascular disease and may contribute to increased coronary complexity and adverse outcomes after acute myocardial infarction (AMI). Data regarding its prognostic significance in Southeastern Europe remains limited. This study aimed to evaluate the association between elevated Lp(a) levels, coronary artery disease severity, and major adverse cardiovascular events (MACE) at 1 and 6 months after AMI. Methods: This prospective study included 150 consecutive patients with STEMI and NSTEMI enrolled between December 2024 and August 2025. MACE was defined as a composite of overall cardiac death, recurrent myocardial infarction, cerebrovascular insult, heart failure with reduced ejection fraction occurrence, and new revascularization, either PCI or CABG. Results: Patients with elevated Lp(a) had significantly greater coronary disease burden, reflected by higher mean SYNTAX scores (17.3 ± 7.0 vs. 13.8 ± 7.0; p = 0.011) and a greater proportion of intermediate- and high-risk SYNTAX classifications (p = 0.016). Although the number of diseased vessels did not differ significantly, three-vessel disease was more frequent in the elevated Lp(a) group. At 1-month follow-up, overall MACE incidence was numerically higher but not statistically significant between groups. At 6 months, heart failure with reduced ejection fraction was significantly increased in patients with elevated Lp(a) (27.7% vs. 12.2%; p = 0.027). Binary logistic regression demonstrated that elevated Lp(a) independently predicted 6-month MACE (OR 2.768, p = 0.011, 95% CI 1.262–6.072), but not 1-month outcomes. Conclusions: Elevated Lp(a) is associated with increased coronary artery disease severity and higher mid-term MACE risk after AMI. Full article

Micro- and nanoplastics (MNPs) have now been detected in human blood, placenta, and arterial tissue, yet the oral cavity has received strikingly little mechanistic attention despite serving as a primary portal of environmental exposure and a local site of polymer generation from dental and oral-care materials. This narrative review addresses that gap from an environmental microbiology perspective, synthesizing recent literature on periodontal disease, chronic low-grade inflammation, oral biofilms, dental materials, microbial–plastic interactions, and systemic chronic disease risk. Unlike prior reviews, we apply an explicit three-tier evidentiary framework (established, plausible, unproven) that distinguishes what is directly demonstrated from what is biologically plausible but unproven, and we situate the periodontal environment specifically as a particle-retention and inflammatory-amplification niche. The strongest direct oral evidence shows that human dental calculus harbors at least 26 microplastic types, dominated by polyamide (41.4%), polyethylene (32.7%), and polyurethane (7.0%). Polyethylene isolated from calculus induces cytotoxicity, apoptosis, impaired migration, NF-κB activation, and upregulation of IL-1β and IL-6 in human gingival fibroblasts. From a microbiological standpoint, oral organisms actively degrade methacrylate dental polymers, and the degradation products of these polymers reciprocally modulate oral bacterial virulence gene expression. Across experimental systems, MNPs activate oxidative stress, inflammasome signaling, macrophage polarization, and barrier dysfunction, pathways that overlap extensively with periodontal pathobiology. Adjacent environmental microbiology demonstrates that plastic-associated biofilms enhance extracellular polymeric substance production, quorum sensing, pathogen persistence, and antibiotic resistance gene transfer, supporting a plausible but not yet validated oral plastisphere within plaque and calculus. We argue that periodontitis should be reconceptualized as a chronically inflamed particle-processing interface that may increase local MNP retention, cellular reactivity, and systemic inflammatory spillover, with implications for cardiovascular, metabolic, and other chronic disease risk pathways. Current evidence does not yet prove that environmental MNP exposure causes human periodontitis, and that evidentiary boundary is maintained throughout. A priority research agenda is proposed, centered on contamination-controlled subgingival biomonitoring stratified by periodontal status, spatially resolved multi-species biofilm models, polymer source attribution, and longitudinal clinical studies linking oral plastic burden to inflammatory and systemic outcomes. Full article

Background/Objectives: Restenosis following coronary artery bypass grafting (CABG) remains a major long-term complication that adversely affects patient prognosis. Although prior studies have investigated clinical features, imaging parameters, and circulating biomarkers for restenosis risk stratification, the metabolic mechanisms underlying long-term restenosis—particularly those reflecting both the local cardiac microenvironment and systemic circulation—remain poorly defined. Therefore, this study aims to identify restenosis-associated metabolic alterations and develop a risk prediction model based on integrated targeted metabolomic profiling of pericardial fluid (PF) and serum in patients undergoing isolated CABG. Methods: Patients undergoing isolated CABG were prospectively enrolled. Paired PF and serum samples were collected during surgery or the perioperative period for targeted metabolomic analysis. Differential metabolite (DM) analysis was performed between patients with and without restenosis. Key metabolites were selected to construct a restenosis risk prediction model, which was subsequently evaluated in training and validation cohorts. Results: Compared with patients without restenosis, those who developed restenosis exhibited two key differential metabolites identified in PF and serum: 7α-Hydroxy-4-cholesten-3-one and Phenoxyacetic acid (PAA). A logistic regression-based prediction model incorporating these metabolites was developed and evaluated using receiver operating characteristic (ROC) analysis, integrated discrimination improvement (IDI), and decision curve analysis (DCA). The model demonstrated robust predictive performance in both training and validation cohorts. Kaplan–Meier survival analysis further revealed that higher model scores were significantly associated with an increased risk of long-term restenosis in the training cohort (HR = 1.44, p = 0.047) and validation cohort (HR = 1.83, p = 0.012). Conclusions: This study provides the first evidence that integrated metabolomic signatures derived from PF and serum are associated with long-term restenosis after CABG. By capturing complementary metabolic information from the local cardiac microenvironment and systemic circulation, this integrated approach enhances current understanding of restenosis biology and supports the potential clinical utility of targeted metabolomics for long-term restenosis risk prediction following CABG. Full article