Search Results (205)

Coronary artery disease is a leading cause of morbidity and mortality in modern medicine. In contrast, surgical myocardial revascularization via coronary artery bypass grafting (CABG) remains the gold standard of treatment for complex multivessel disease. The great saphenous vein remains the most frequently used conduit due to its availability and technical simplicity, but its long-term patency is significantly inferior to that of arterial grafts. The primary pathological process responsible for vein graft failure is intimal hyperplasia, which represents a complex response of the vascular wall to surgical trauma, vein arterialization, inflammation, and hemodynamic stress. This process is characterized by endothelial dysfunction, inflammatory cell activation, proliferation and migration of vascular smooth muscle cells, and extracellular matrix remodeling. Underpinning these alterations are numerous molecular pathways, including NF-κB, MAPK, PI3K/Akt, TGF-β, and mTOR signaling, as well as substantial contributions from oxidative stress, cytokines, growth factors, and microRNAs. Contemporary research indicates that the phenotypic transformation of vascular smooth muscle cells constitutes the central event in the development of intimal hyperplasia. Understanding the cellular and molecular mechanisms underlying this disease’s onset enables the development of novel therapeutic strategies to preserve long-term graft patency. This review paper aims to provide a systematic overview of current knowledge regarding the molecular and cellular mechanisms of intimal hyperplasia development in vein grafts following CABG. Full article

Background/Objectives: Proximal glue migration toward the saphenofemoral junction (SFJ) and endovenous glue-induced thrombosis are recognised concerns during cyanoacrylate ablation. This exploratory pilot study compared standard and modified ultrasound-guided compression protocols. Methods: Thirty patients with incompetent great saphenous veins (GSVs) were allocated non-randomly, in two sequential cohorts, to a standard (n = 15) or modified (n = 15) protocol. The modified protocol added a “release-and-check” duplex assessment after the initial 3 min compression, a 1 min recompression, and an extra minute for veins > 5.5 mm. The primary outcome was glue migration distance from the compression level, measured immediately postoperatively. Clinical and thromboembolic outcomes were not systematically ascertained; follow-up was one week. Results: Baseline variables were comparable (standardised differences ≤ 0.31). Mean migration distance was lower with the modified protocol (0.80 ± 0.34 vs. 1.97 ± 0.51 cm; mean difference −1.17 cm, 95% CI −1.50 to −0.85; p < 0.0001), persisting after covariate adjustment. Residual stump length was greater (4.41 ± 0.34 vs. 2.49 ± 1.27 cm; p < 0.001), although this SFJ-referenced measure is confounded by the unrecorded compression distance. Deep venous extension occurred in 3/15 standard and 0/15 modified limbs (p = 0.22); all three were asymptomatic Cho grade III events, resolved at one week. Immediate migration was recorded in 7/15 versus 0/15 limbs (p = 0.006). Conclusions: In this small, non-randomised exploratory cohort, a “release-and-check” modification was associated with shorter immediate glue migration. These hypothesis-generating findings rest on an unblinded surrogate endpoint with one-week follow-up and do not establish clinical safety, effectiveness or durability; adequately powered randomised trials with blinded assessment and adjudicated endpoints are required. Full article

While glucose-driven mitochondrial dysfunction has been proposed to promote vascular dysfunction responsible for saphenous vein graft failure (VGF) following bypass surgery, the impact of type 2 diabetes mellitus (T2DM) on mitochondrial function in human saphenous vein smooth muscle cells (HSVSMCs) responsible for maladaptive remodelling is unknown. Our aim was to identify signalling pathways that mediate any mitochondrial dysfunction in HSVSMCs in vitro and assess the impact of T2DM. HSVSMCs explanted from surplus HSV tissues from consenting T2DM and non-diabetic patients undergoing coronary artery bypass graft surgery were treated with known activators and inhibitors of the JAK/STAT and MAPK/ERK pathways. Following this, real-time oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) measures of mitochondrial function were then determined. Our findings revealed that both IL-6/sIL-6Rα trans-signalling complexes and platelet-derived growth factor-BB (PDGF-BB) significantly increased OCR in HSVSMCs from T2DM patients but not non-diabetic controls. Meanwhile, only PDGF-BB increased ECAR in HSVSMCs from T2DM patients but not in non-diabetic controls. The observed increases in OCR and ECAR were abolished by JAK1/2-selective inhibitor ruxolitinib. Furthermore, thrombin caused a significant increase in OCR, specifically in HSVSMCs from T2DM patients, and this effect was abolished by the MEK1/2-selective inhibitor trametinib. Both ruxolitinib and trametinib significantly reduced basal OCR and ECAR in HSVSMCs from both T2DM and non-diabetic patients. Together, these findings demonstrate a JAK/STAT- and MAPK/ERK-mediated regulation of mitochondrial function in HSVSMCs. As such, they represent potential targets for regulation of HSVSMC function that can be explored for drug development to limit saphenous VGF in T2DM. Full article

Background/Objectives: Chronic venous insufficiency (CVI) is a progressive vascular disorder characterized by sustained venous hypertension leading to structural and functional alterations of the venous wall. Despite its clinical significance, the molecular mechanisms driving venous remodeling remain incompletely understood. The Wnt signaling pathway has emerged as an important regulator of vascular homeostasis and remodeling; however, the expression and coordination of its core components in chronic venous insufficiency (CVI)-affected tissue have not been directly investigated. This study aimed to analyze mRNA expression of FZD2, DVL2, and AXIN1 in great saphenous vein specimens. In addition to gene expression analysis at the individual level, an investigation of co-regulatory networks was also performed to provide insight into Wnt cascade regulation in the varicose and healthy vein tissues. Methods: This single-center, retrospective observational study was conducted on 60 great saphenous vein specimens (32 CVI patients and 28 healthy controls) using re-al-time quantitative PCR. Results: The findings indicate that individual mRNA expression levels of FZD2, DVL2, and AXIN1 remained stable between varicose vein and healthy control tissues, but there were significant changes in transcriptional coordination among these genes in varicose vein tissues, especially enhanced co-expression between AXIN1 and DVL2. All three co-regulated genes exhibited moderate and generally comparable positive correlations in healthy controls: FZD2 with DVL2 (r = 0.526, p-value = 0.0069), DVL2 with AXIN1 (r = 0.486, p-value = 0.0161), and AXIN1 with FZD2 (r = 0.593, p-value = 0.0014). While in varicose vein tissues, DVL2-AXIN1 showed the highest correlation (r = 0.722, p-value < 0.0001), FZD2-DVL2 (r = 0.517, p-value = 0.0096) and AXIN1-FZD2 (r = 0.480, p-value = 0.0084) remained comparable to the healthy tissues. Conclusions: This finding indicates that the involvement of FZD2, DVL2, and AXIN1 in CVI may be driven by altered transcriptional coordination rather than by differential individual gene expression, which may contribute to the molecular pathology of chronic venous insufficiency. Full article

Background and Objectives: Ultrasound-guided sciatic and saphenous nerve blocks are widely used as analgesic alternatives for multimodal analgesia. However, how to objectively quantify the opioid- and anaesthetic-sparing effects of an additional peripheral nerve block in patients undergoing ankle fracture surgery under general anaesthesia remains unclear. This study aimed to evaluate their efficacy in managing postoperative pain and opioid-sparing effects following ankle fracture surgery. Materials and Methods: Patients scheduled for ankle fracture surgery were randomly assigned to the nerve block (n = 30) or control group (n = 30). The primary outcome was the postoperative numeric rating scale (NRS) score. The secondary outcomes included the total doses of remifentanil and propofol, Quality of Recovery-40 Korean (QoR-40K) scores, and self-reported patient satisfaction. Results: The NRS score immediately after surgery was significantly lower in the nerve block group compared with that in the control group (2.6 ± 2.5 vs. 6.2 ± 2.6; p < 0.001). The total remifentanil dose required during surgery was also significantly lower in the nerve block group than in the control group (1148.1 ± 391.8 vs. 1487.4 ± 798.8; p = 0.041). However, the patient satisfaction scale (3 [IQR, 2–4] vs. 3 [IQR, 2–4]; p = 0.206) and QoR-40K score 24 h after surgery (169 [IQR, 155–184] vs. 175 [IQR, 154–165]; p = 0.324) did not differ significantly between the two groups. Conclusions: Ultrasound-guided sciatic and saphenous nerve blocks significantly reduced immediate postoperative pain and intraoperative remifentanil consumption under qNOX (quantitative nociception index)-guided general anaesthesia during ankle fracture surgery. Full article

Truncal vein insufficiency can be treated with endovenous thermal ablation (EVTA), non-thermal non-tumescent techniques, ultrasound-guided foam or microfoam sclerotherapy, and high ligation with stripping. However, the optimal management of large-diameter truncal veins remains unclear. This structured review summarizes treatment outcomes in large-diameter incompetent truncal veins and compares available modalities according to vein diameter, anatomical success, recurrence, reintervention, and complications. A PubMed/MEDLINE search was performed for studies published between January 2000 and June 2026. Studies were eligible if they specifically evaluated incompetent great saphenous veins, small saphenous veins, or accessory saphenous veins described as large-diameter, large-caliber, very large, enlarged, or wide-diameter truncal veins. Twenty-three primary studies met the inclusion criteria. Definitions of large-diameter veins varied widely, ranging from >8 mm to >20 mm. EVTA represented the largest evidence base and generally showed high anatomical success, with most studies reporting occlusion, recurrence-free, or recanalization-free rates above 90%. Foam-based treatment, cyanoacrylate closure, and mechanochemical ablation were supported by fewer large-vein-specific studies, and durability in larger veins remains less certain. High ligation and stripping showed low recurrence or residual stump rates in selected comparative studies, but outcome definitions differed from endovenous occlusion endpoints. Current evidence supports individualized treatment selection based on vein diameter, anatomy, tortuosity, reflux pattern, and expected durability. Dedicated randomized trials using standardized diameter definitions and outcome reporting are needed. Full article

Background: Endovascular repair with covered stent is an established minimally invasive treatment for popliteal artery lesions, particularly in elderly or high-risk patients. Infectious complications are exceptionally rare but may result in arterial destruction, limb loss, and death. Salmonella species demonstrate a well-recognized affinity for diseased arterial walls and prosthetic vascular material. Case Presentation: An 82-year-old man with stage G4 chronic kidney disease and previous nephrectomy for renal cell carcinoma, complicated by Salmonella Enteritidis septic shock 20 years earlier, presented with acute left lower limb ischemia caused by a post-traumatic popliteal artery pseudoaneurysm. Urgent endovascular repair was performed using a 6 × 100 mm covered stent (Viabahn) with adjunctive angioplasty of the anterior tibial artery. Two weeks later, he was readmitted with fever, severe popliteal pain, local erythema, and elevated inflammatory markers. Imaging demonstrated early stent occlusion with a large peri-graft abscess and contained arterial rupture. Emergency open conversion included radical debridement, complete graft explantation, and popliteal-to-posterior tibial bypass using an autologous great saphenous vein. Cultures grew Salmonella Enteritidis. Retrospective history revealed a previously undocumented episode of Salmonella Enteritidis bacteremia approximately 20 years earlier. At 2-year follow-up, the patient remained free of recurrent infection with a patent vein graft and preserved ambulatory function. Conclusions: Early Salmonella Enteritidis infection of a popliteal covered stent is an exceptionally rare but life-threatening complication. This case suggests that remote Salmonella bacteremia may represent a potential, hypothesis-generating risk factor for prosthetic graft infection. Prompt graft explantation followed by radical debridement and autologous venous reconstruction remain essential for durable limb salvage. Full article

Background: The radial artery (RA) is widely used as a conduit in coronary artery bypass grafting. Its fascial layer provides mechanical stability but may reduce graft flexibility and promote kinking when routed over the margo acutus during right coronary artery bypass. This study investigated the impact of graft fascial orientation on RA patency and clinical outcomes. Methods: In this retrospective observational cohort study with prospective follow-up, 100 patients undergoing CABG with the RA grafted to the right coronary artery were included. Patients were assigned to a “prone” group (n = 50), with the fascial side oriented toward the sternum, or a “supine” group (n = 50), with the fascia facing the epicardium. Clinical follow-up was performed after a mean of 4.25 years. MDCT-based graft patency assessment was available in 89 patients. Results: Overall survival at follow-up was 100%, with no postoperative myocardial infarctions or reoperations. Overall RA patency was 94%, with patency rates of 91.5% in the supine group and 97.6% in the prone group (p = 0.37). Internal mammary artery and saphenous vein graft patency rates were 92.8% and 96.4%, respectively. Competitive flow showed a near-significant association with RA occlusion (p = 0.09). Conclusions: RA grafts demonstrated excellent mid-term patency. Fascial orientation of the pedicled RA graft was not significantly associated with graft patency. Full article

Adductor canal block (ACB) is widely used for perioperative analgesia in knee surgery because it provides effective pain control while preserving quadriceps muscle strength. With the increasing use of ultrasound-guided regional anesthesia, interest has expanded beyond conventional morphologic imaging toward quantitative assessment of peripheral nerve function and biomechanics. Shear wave elastography (SWE) is an emerging ultrasound-based technique that enables real-time quantification of tissue stiffness and has recently gained attention in peripheral nerve evaluation. Previous SWE studies have primarily focused on chronic neuropathic conditions, including entrapment neuropathy and diabetic neuropathy, in which increased nerve stiffness is commonly observed. However, emerging observations suggest that peripheral nerve stiffness may dynamically decrease following regional anesthesia procedures such as ACB. This finding raises the possibility that nerve stiffness reflects not only chronic structural pathology but also transient physiologic and biomechanical modulation. Potential mechanisms underlying reduced stiffness after ACB include perineural hydrodissection, decreased fascial compression, sympathetic blockade-induced vasodilation, altered intraneural pressure, and changes in surrounding muscle tension. Because the saphenous nerve within the adductor canal is superficial and consistently visualized under ultrasound guidance, ACB represents an attractive model for investigating dynamic changes in peripheral nerve biomechanics. This narrative review summarizes current evidence regarding SWE assessment of peripheral nerves and discusses the potential implications of dynamic stiffness changes after regional anesthesia. We review the biomechanical principles of SWE, factors affecting nerve stiffness, current evidence in neuropathic and perioperative settings, technical limitations, and future clinical applications. Understanding the dynamic behavior of peripheral nerve stiffness may expand the role of SWE from a diagnostic tool for neuropathy to a quantitative biomarker for regional anesthesia and perioperative nerve physiology. Full article

Coronary in-stent restenosis (ISR) remains a major contributor to repeat revascularisation despite advances in drug-eluting stent (DES) technology. Its persistence reflects a complex and heterogeneous interplay among mechanical, biological, and procedural factors, and understanding the dominant mechanism in each case is fundamental to effective treatment selection. This narrative review provides a contemporary, mechanism-guided approach to the practical management of coronary ISR. We summarise the definition, incidence, and classification of ISR—including the Mehran, Waksman, and SCAI 2023 time-based frameworks—and outline patient-related, procedural, anatomical, and stent-related risk factors. The pathophysiology of neointimal hyperplasia and neoatherosclerosis is discussed with reference to its clinical implications. Intracoronary imaging with intravascular ultrasound (IVUS) or optical coherence tomography (OCT) is central to ISR characterisation and treatment planning. Current international guidelines support imaging use in ISR management, though it is important to recognise that this recommendation is based largely on observational and surrogate-endpoint data rather than ISR-specific randomised trials demonstrating reductions in hard clinical outcomes, and practical barriers including cost, availability, and operator expertise must be acknowledged. Evidence-based treatment strategies—including drug-coated balloons (DCB), repeat DES implantation, lesion-modifying therapies, vascular brachytherapy, and coronary artery bypass grafting—are reviewed critically with reference to contemporary trial data and their specific clinical applicability. The choice between DCB and repeat DES is addressed with greater nuance, accounting for ISR type (BMS-ISR versus DES-ISR), lesion pattern, stent layering, and bleeding risk. Management considerations in complex subsets—chronic total occlusion ISR, left main ISR, saphenous vein graft ISR, and recurrent ISR—are also addressed. We propose a practical, substrate-driven management framework aligned with the 2024 ESC, 2021 ACC/AHA/SCAI, and 2018 JCS/JSCVS guidelines. Future research priorities include ISR-specific randomised trials with hard clinical endpoints, prospective validation of imaging-guided treatment algorithms, head-to-head comparisons of DCB platforms, and investigation of pharmacological strategies targeting neoatherosclerosis progression. Full article

Background: Although chronic venous insufficiency is often treated as a localized problem, it is a systemic condition that can negatively affect cardiac hemodynamics. This study investigates the associated effects of eliminating the pathologic venous reservoir on right ventricular (RV) functions, systolic pulmonary artery pressure (sPAP), and inferior vena cava (IVC) diameter in patients undergoing endovenous radiofrequency ablation (RFA) for severe great saphenous vein (GSV) insufficiency. Methods: This retrospective observational study included 154 patients who presented between September 2023 and May 2025 with GSV insufficiency (CEAP C3-C4b) and underwent endovenous RFA. Patients with major cardiopulmonary diseases were strictly excluded. Preoperative and 6-month postoperative transthoracic echocardiography records were analyzed to evaluate RV diastolic diameter, tricuspid annular plane systolic excursion (TAPSE), sPAP, the TAPSE/sPAP ratio, and IVC diameter. Results: At 6 months post-RFA, compared to preoperative values, a significant decrease was detected in the mean sPAP (14.7 ± 2.5 vs. 11.8 ± 1.8 mmHg, p < 0.001) and IVC diameter (2.1 ± 0.2 vs. 1.9 ± 0.2 cm, p < 0.001). Furthermore, significant improvements were observed in TAPSE (20.0 ± 2.0 vs. 21.5 ± 1.8 mm, p < 0.001) and the TAPSE/sPAP ratio (1.36 ± 0.15 vs. 1.82 ± 0.18 mm/mmHg, p < 0.001). Conclusions: Endovenous RFA is associated with favorable changes in right heart parameters. Eliminating pathologic extremity blood pooling may optimize venous return kinetics and subclinically improve right ventricular–pulmonary arterial coupling. Full article

The failure of saphenous vein grafts following coronary artery bypass grafting (CABG) remains a significant issue, as it limits the durability of vein-based surgical revascularisation compared to arterial conduits. Venous graft disease is a dynamic process that begins early in the perioperative period as a consequence of harvesting trauma, ex vivo preservation, and the sudden exposure of the conduit to the arterial haemodynamic environment. This narrative review summarises the available evidence on local graft protection strategies, focusing on intraoperative and perioperative approaches aimed at preserving endothelial integrity, attenuating initial inflammation, and limiting maladaptive remodelling. Specifically, the review analyses the role of endothelium-protective preservation solutions, external support devices, biodegradable drug-eluting biomaterials, and locally targeted RNA therapies. Preclinical and early clinical evidence suggests that local graft protection is biologically plausible and may reduce intimal hyperplasia, luminal irregularity and adverse graft remodelling. However, its impact on long-term clinical outcomes remains uncertain. An integrated approach combining harvest optimisation, conduit preservation, mechanical support, and local delivery of drugs or regulatory molecules may represent a promising framework for improving vein graft biology; however, its ability to translate into durable patency gains and improved clinical outcomes after CABG requires further clinical validation. Full article

Vein graft restenosis is a leading cause of long-term failure after coronary artery bypass grafting (CABG), driven by maladaptive vascular smooth muscle cell (VSMC) responses to arterialization-induced inflammation. The key molecular mediators of this pathological remodeling, however, remain incompletely defined. Here, we integrated multi-omics analyses of human and canine vein graft specimens with in vitro functional assays to identify tenascin-C (TNC)—a matricellular extracellular matrix protein—as a critical regulator of VSMC dysfunction. TNC was specifically enriched in a synthetic, pro-inflammatory VSMC subpopulation. Pro-inflammatory stimuli potently induced TNC expression, which was functionally linked to VSMC phenotypic modulation, hyperproliferation, and enhanced migration. Mechanistically, TNC acts upstream of NF-κB signaling; siRNA-mediated TNC knockdown significantly reduced nuclear p65 protein levels and attenuated inflammatory responses. Our integrated computational and experimental data suggest that TNC, NF-κB, and TNF-α function within a sequential pro-inflammatory signaling cascade that sustains vascular inflammation and promotes neointimal hyperplasia. These findings reposition TNC from a passive structural component to an active driver of vascular pathology and highlight the TNC–NF-κB axis as a candidate target for therapeutic intervention to improve vein graft patency. Full article

Background: Preoperative ultrasonographic mapping of the great saphenous vein (GSV) is a valuable tool for improving assessment of vein caliber during surgical planning. However, current data are insufficient to establish clear standards for optimal anatomical evaluation. The aim of this study was to investigate the effect of anesthetic induction on GSV caliber in patients undergoing CABG. Methods: In this retrospective study, the diameter of the GSV was measured using ultrasonography at predefined anatomical landmarks during the pre- and post-induction periods in patients undergoing CABG, and the obtained values were compared. Results: A total of 59 patients were included. A significant increase in the GSV diameter was observed after anesthetic induction in all segments (all p < 0.001). The median diameters increased from 1.9 to 2.7 mm in the distal segment, from 1.6 to 2.4 mm in the mid segment, and from 2.3 to 3.4 mm in the proximal segment. The percentage change in diameter after anesthetic induction was comparable across all measured segments (p = 0.888). The pre-induction diameter was strongly and negatively correlated with the percentage diameter change in all segments (all p < 0.001), and this association remained significant after controlling for the post-induction diameter (all p < 0.001). Conclusions: In this study, the ultrasonographic assessment timing was found to significantly influence GSV caliber evaluation in patients undergoing CABG. Anesthetic induction was associated with a significant and consistent increase in saphenous vein diameter across all measured segments, suggesting that anesthetic status may influence ultrasound-based vein mapping and conduit assessment. Further prospective studies incorporating clinical outcome measures and conduit suitability assessment are needed to better clarify the clinical implications of these findings. Full article

Coronary artery bypass grafting (CABG) using the autologous saphenous vein (SV) remains widely performed for obstructive atherosclerosis; however, vein graft disease drives recurrent ischaemia through early thrombosis and progressive intimal hyperplasia, and accelerated atherosclerosis developing within the grafts. Extracellular vesicles (EVs) are membrane-bound particles that transfer proteins, lipids, and microRNAs between cells. They modulate endothelial dysfunction, vascular smooth muscle cell phenotypic switching, inflammation, and coagulation, which are core processes in vein graft remodelling. Arterialisation exposes the vein to abrupt rises in shear stress, cyclic stretch, and intraluminal pressure. These forces increase EV release and reshape EV cargo in experimental systems, suggesting a potential mechanism for amplifying early graft injury which warrants direct investigation in vein tissue. This review synthesises current evidence for cell-specific EV contributions from ECs, vascular smooth muscle cells, platelets, and macrophages, and appraises EV-associated microRNAs with biomarker potential relevant to graft failure pathways. We also review therapeutic strategies that may modulate EV signalling including antiplatelet therapy, statins, KCa3.1 inhibition, and pro-reparative mesenchymal stromal cell-derived EVs. No published clinical studies evaluate EV-based biomarkers specifically for saphenous vein graft patency, and none prospectively predict saphenous graft failure. CABG provides a well-defined time zero event that enables longitudinal sampling and risk stratification. Prospective studies linking EV phenotypes and miRNA signatures to imaging-defined graft outcomes are needed to support clinical translation. Full article