Coronary Vein Graft Research Articles

The effectiveness of alternative vessel grafts for meso-rex bypass in the treatment of extrahepatic portal vein obstruction in children.

This study aims to evaluate the effectiveness of alternative autologous vessel grafts in creating a Meso-Rex bypass (MRB) compared to the distal splenorenal shunt (DSRS) in resolving symptoms of portal hypertension in children. All children with EHPVO evaluated for surgery at Siriraj Hospital from January 2011 to December 2023 were reviewed. Alternative autologous vessel grafts were used in all cases where MRB was feasible. DSRS was performed in patients for whom MRB was not possible. Baseline characteristics and outcomes were compared between the two groups. Eight children underwent successful MRB with alternative autologous vessel grafts, while six required DSRS. Children in the modified MRB group were significantly younger, with upper gastrointestinal bleeding the most common presenting symptom. In contrast, children in the DSRS group had significantly lower preoperative ammonia levels and platelet counts, with hypersplenism being the most common presenting symptom. All patients experienced complete relief of variceal bleeding and hypersplenism post-surgery. Complicated shunt thrombosis occurred after MRB using the gastric coronary vein graft. A significant decrease in ammonia levels was observed after MRB, whereas levels increased after DSRS. Alternative autologous vessel grafts are effective for constructing the MRB to resolve portal hypertension compared to DSRS.

Spatial Transcriptomic Profiling of Human Saphenous Vein Exposed to Ex Vivo Arterial Haemodynamics-Implications for Coronary Artery Bypass Graft Patency and Vein Graft Disease.

Vein graft disease is the process by which saphenous vein grafts, utilised for revascularisation during coronary artery bypass graft surgery, undergo an inflammation-driven intimal hyperplasia and accelerated atherosclerosis process in subsequent years after implantation. The role of the arterial circulation, particularly the haemodynamic properties' impact on graft patency, have been investigated but have not to date been explored in depth at the transcriptomic level. We have undertaken the first-in-man spatial transcriptomic analysis of the long saphenous vein in response to ex vivo acute arterial haemodynamic stimulation, utilising a combination of a custom 3D-printed perfusion bioreactor and the 10X Genomics Visium Spatial Gene Expression technology. We identify a total of 413 significant genes (372 upregulated and 41 downregulated) differentially expressed in response to arterial haemodynamic conditions. These genes were associated with pathways including NFkB, TNF, MAPK, and PI3K/Akt, among others. These are established pathways involved in the initiation of an early pro-inflammatory response, leukocyte activation and adhesion signalling, tissue remodelling, and cellular differentiation. Utilising unsupervised clustering analysis, we have been able to classify subsets of the expression based on cell type and with spatial resolution. These findings allow for further characterisation of the early saphenous vein graft transcriptional landscape during the earliest stage of implantation that contributes to vein graft disease, in particular validation of pathways and druggable targets that could contribute towards the therapeutic inhibition of processes underpinning vein graft disease.

FGL2/FcγRIIB Signalling Mediates Arterial Shear Stress-Mediated Endothelial Cell Apoptosis: Implications for Coronary Artery Bypass Vein Graft Pathogenesis.

The sudden exposure of venous endothelial cells (vECs) to arterial fluid shear stress (FSS) is thought to be a major contributor to coronary artery bypass vein graft failure (VGF). However, the effects of arterial FSS on the vEC secretome are poorly characterised. We propose that analysis of the vEC secretome may reveal potential therapeutic approaches to suppress VGF. Human umbilical vein endothelial cells (HUVECs) pre-conditioned to venous FSS (18 h; 1.5 dynes/cm2) were exposed to venous or arterial FSS (15 dynes/cm2) for 24 h. Tandem Mass Tagging proteomic analysis of the vEC secretome identified significantly increased fibroleukin (FGL2) in conditioned media from HUVECs exposed to arterial FSS. This increase was validated by Western blotting. Application of the NFκB inhibitor BAY 11-7085 (1 µM) following pre-conditioning reduced FGL2 release from vECs exposed to arterial FSS. Exposure of vECs to arterial FSS increased apoptosis, measured by active cleaved caspase-3 (CC3) immunocytochemistry, which was likewise elevated in HUVECs treated with recombinant FGL2 (20 ng/mL) for 24 h under static conditions. To determine the mechanism of FGL2-induced apoptosis, HUVECs were pre-treated with a blocking antibody to FcγRIIB, a receptor FGL2 is proposed to interact with, which reduced CC3 levels. In conclusion, our findings indicate that the exposure of vECs to arterial FSS results in increased release of FGL2 via NFκB signalling, which promotes endothelial apoptosis via FcγRIIB signalling. Therefore, the inhibition of FGL2/FcγRIIB signalling may provide a novel approach to reduce arterial FSS-induced vEC apoptosis in vein grafts and suppress VGF.

The role of FGL2 in vascular smooth muscle cell dysfunction in coronary artery bypass vein graft failure

Abstract Funding Acknowledgements Type of funding sources: Other. Main funding source(s): British Heart Foundation Rationale The sudden exposure of venous endothelial cells (vECs) to arterial fluid shear stress (FSS) is thought to be a major contributor to coronary artery bypass vein graft failure (VGF). However, the acute effects of arterial FSS on the vEC secretome and the corresponding effects on underlying vascular smooth muscle cells (VSMCs) remains poorly characterised. Methods & Results Human umbilical vein endothelial cells (HUVECs; n=6) pre-conditioned to venous FSS (18h; 1.5 dynes/cm2) were further exposed to venous or arterial FSS (24h; 15 dynes/cm2) using an Ibidi pump system. Analysis of the EC secretome using Tandem Mass Tagging proteomics detected significantly increased fibroleukin (FGL2) in conditioned media from ECs exposed to arterial FSS compared to venous FSS (fold-change 1.97±0.72; P=0.0078). In addition, RT-qPCR analysis of FGL2 production showed a significant increase in vECs exposed to arterial FSS (2.11±0.27 vs. 0.05±0.04 log(copy number/mg); P=0.0312). Subsequently, pooled human saphenous vein VSMCs (3 donors per pool) were treated with conditioned media from ECs exposed to arterial FSS (n=6) which showed a significant increase in apoptosis, measured by active cleaved caspase-3 (CC3) immunocytochemistry (27±1% vs 22±1%; P=0.0391), and a significant decrease in the contractile markers smoothelin and desmin quantified by Western blotting (fold-change 0.76±0.06 and 0.44±0.11; P=0.004 and P=0.0421, respectively), in comparison to VSMCs treated with conditioned media from ECs exposed to venous FSS. Treatment of VSMCs (n=6) with recombinant FGL2 (20 ng/mL) for 72h likewise resulted in increased apoptosis (27±4% vs. 16±3%; P=0.0169) and decreased desmin and smoothelin (fold-change 0.68±0.03 and 0.61±0.07; P=0.0322 and P=0.0479, respectively). Conclusions The exposure of vECs to arterial FSS results in increased production and release of FGL2 which induced VSMC apoptosis and de-differentiation and therefore potentially contributes to VGF. Consequently, targeting FGL2 production or release may provide a therapeutic target to improve vein graft patency.

Kinked coronary saphenous vein graft after aortic dissection surgery: An unusual differential diagnosis of cardiac tamponade

A 73-year-old female patient presented with cardiac tamponade following Stanford type A aortic dissection required immediate pericardiocentesis and followed by root replacement with coronary artery bypass grafting. The patient's postoperative course was eventful and coronary graft kinking contributed to myocardial ischemia, but the presentation was confused with cardiac tamponade.

Computerized tomographic angiography in patients having external stent supported coronary saphenous vein grafts

Computerized tomographic angiography in patients having external stent supported coronary saphenous vein grafts

Rapidly expanding saphenous vein graft myoctic aneurysm causing ST-elevation myocardial infarction: a case report.

Background Mycotic aneurysms of coronary vein grafts are rare and associated with high mortality. They are most commonly a result of surgical or percutaneous intervention, and present with complications including myocardial infarction (MI), infective endocarditis. A recent literature review identified 97 cases of mycotic coronary aneurysms in total.Case summaryA 49-year-old man with a history of coronary artery bypass grafting and septic arthrithis presented with chest pain and fevers and ST elevation on electrocardiogram. Urgent angiogram showed an aneurysmal saphenous vein graft from the PL branch to PDA—no acute intervention was performed due to concern about bacteraemia. Methicillin-sensitive Staphylococcus aureus was grown in urine and blood but no focus of infection was identified. Despite treatment with antibiotics and antiplatelets, the patient returned with evidence of expansion of the SVG aneurysm requiring surgical resection.Discussion This case highlights the difficulty in treating acute coronary syndromes involving mycotic aneurysms. Multimodal imaging approaches are useful to identify suspected infection, but false negatives occur. Due to high risk of rupture or haemorrhage, there are limited options for urgent reperfusion in cases of MI with mycotic aneurysm, demonstrating the need for an individualized approach and close follow-up.

Non-pharmaco, non-invasive management of coronary no-reflow phenomenon.

IntroductionNo-reflow is an infrequent but dreaded complication of percutaneous coronary intervention (PCI), where the culprit is obstruction of the downstream microvascular bed. The aim of this study was to evaluate the efficacy and safety of forceful injection of blood (autologous blood transfusion – ABT) in reversing no-reflow during PCI because data regarding its effectiveness is not available.Material and methods100–120 ml of blood was withdrawn through guiding catheter over 3 to 5 min using a 10 ml syringe and re-infused by forceful injection over 3 min through it, and its efficacy was assessed at 10 min using TIMI flow grade and quantitative corrected TIMI frame count.ResultsIn total 93 patients received ABT following no-reflow. Their clinical presentation was ST-elevation myocardial infarction (STEMI) (n = 61; 65.6%), non-ST-elevation myocardial infarction (NSTEMI) (n = 23; 24.7%), and unstable angina (n = 9; 9.6%). It was observed among patients undergoing primary PCI (n = 18; 19.3%), pharmaco-invasive PCI (n = 27; 29%), rescue PCI (n = 11; 11.8%), and PCI for cardiogenic shock (n = 5; 5.3%). A mean volume of 108 ±4 ml blood was transfused. Commonest culprit vessel was left anterior descending artery (n = 51; 54.8%) followed by right coronary (n = 29; 31.2%), left circumflex (n = 19; 10.8%), and saphenous vein grafts (n = 3; 3.2%). Following ABT, TIMI 3 flow was successfully restored in 77 (82.7%) patients. TIMI flow grade improved from 1.02 to 2.52 and cTIMI frame count decreased from 60.6 ±12 to 16.1 ±6 (p < 0.001). ABT was well tolerated except transient hypotension (n = 17; 18.3%). Overall mortality was reported in 10 (10.7%) patients at 1 year.ConclusionsIn this largest and only study to date, ABT is a safe and highly effective approach to reverse no-reflow by raising driving pressure across the capillary bed.

Percutaneous Management of Acquired Right Ventricular Outflow Tract Obstruction due to Giant Coronary Vein Graft Aneurysm

A 56-year-old fireman previously revascularized by coronary artery bypass presented unable to work 9 years following index surgery. Investigations revealed extrinsic compression of the right ventri...

Casein kinase-2 (CK2) inhibition by TBCA attenuates VSMC and fibroblast proliferation without adverse effects on endothelial cell behaviour or inflammation

Aim: Intimal thickening within human saphenous vein (HSV) grafts leads to unacceptably high failure rates of coronary artery vein grafts. Treatments to reduce intimal thickening need to attenuate vascular smooth muscle cell (VSMC) and fibroblast proliferation without detrimental effects on endothelial cells (ECs). In this study we compared the effect of four CK2 inhibitors on VSMC, fibroblast and EC behaviour to determine their potential use in retarding intimal thickening.

Vitamin D deficiency and periprocedural myocardial infarction in patients undergoing percutaneous coronary interventions.

Vitamin D deficiency has been implicated in the progression of atherosclerosis and acute thrombotic events. We aimed at evaluating the impact of vitamin D deficiency on periprocedural myocardial infarction (PMI) in patients undergoing percutaneous coronary interventions (PCI). We included 934 patients undergoing non-urgent PCI. Assessment of myocardial biomarkers was performed from 6 to 48 h after PCI. PMI was defined as Creatine Kinase-MB increase by 3 times the Upper Limit Normal or by 50% of an elevated baseline value, periprocedural myocardial damage as Troponin I increase by 3 × ULN or 50% of baseline. Patients were divided according to vitamin D tertiles values (<10.2 ng/ml; 10.2-18.7 ng/ml; ≥18.8 ng/ml). Lower tertiles values of vitamin D were associated with age (p = 0.04), female gender, (p = 0.001), and a higher cardiovascular risk profile. Lower vitamin D levels related with PCI of descending anterior coronary artery or bypass vein grafts (p = 0.03), treatment of bifurcations (p = 0.05) and side branch loss (p = 0.05) and inversely with direct stenting (p = 0.002). However, lower vitamin D levels did not influence the risk of PMI (adjusted OR [95% CI] = 0.81[0.65,1.18], p = 0.09) or periprocedural myocardial damage (adjusted OR [95% CI] = 0.93[0.77,1.13], p = 0.48). Similar results were achieved when considering the severity of vitamin D deficiency. Therefore, in patients undergoing PCI, no association was observed between vitamin D deficiency and the risk of periprocedural MI and myocardial damage.

A Rabbit Model for Testing Helper-Dependent Adenovirus-Mediated Gene Therapy for Vein Graft Atherosclerosis

Coronary artery bypass vein grafts are a mainstay of therapy for human atherosclerosis. Unfortunately, the long-term patency of vein grafts is limited by accelerated atherosclerosis. Gene therapy, directed at the vein graft wall, is a promising approach for preventing vein graft atherosclerosis. Because helper-dependent adenovirus (HDAd) efficiently transduces grafted veins and confers long-term transgene expression, HDAd is an excellent candidate for delivery of vein graft-targeted gene therapy. We developed a model of vein graft atherosclerosis in fat-fed rabbits and demonstrated long-term (≥20 weeks) persistence of HDAd genomes after graft transduction. This model enables quantitation of vein graft hemodynamics, wall structure, lipid accumulation, cellularity, vector persistence, and inflammatory markers on a single graft. Time-course experiments identified 12 weeks after transduction as an optimal time to measure efficacy of gene therapy on the critical variables of lipid and macrophage accumulation. We also used chow-fed rabbits to test whether HDAd infusion in vein grafts promotes intimal growth and inflammation. HDAd did not increase intimal growth, but had moderate—yet significant—pro-inflammatory effects. The vein graft atherosclerosis model will be useful for testing HDAd-mediated gene therapy; however, pro-inflammatory effects of HdAd remain a concern in developing HDAd as a therapy for vein graft disease.

Role of PVAT in coronary atherosclerosis and vein graft patency: friend or foe?

This article is part of a themed section on Molecular Mechanisms Regulating Perivascular Adipose Tissue - Potential Pharmacological Targets? To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.20/issuetoc.

Sealing Intermediate Nonobstructive Coronary Saphenous Vein Graft Lesions With Drug-Eluting Stents as a New Approach to Reducing Cardiac Events: A Randomized Controlled Trial.

The objective of this study was to assess the efficacy of sealing intermediate nonobstructive coronary saphenous vein graft (SVG) lesions with drug-eluting stents (DES; paclitaxel- or everolimus-eluting stents) for reducing major adverse cardiac events (MACE). This was a randomized controlled multicenter clinical trial that enrolled patients with a previous coronary artery bypass graft who had developed at least 1 intermediate nonobstructive SVG lesion (30%-60% diameter stenosis by visual estimation). Patients were randomized (1:1) to DES implantation (SVG-DES) or medical treatment (SVG-MT) of the target SVG lesion. The primary efficacy outcome was the first occurrence of MACE defined as the composite of cardiac death, myocardial infarction, or coronary revascularization related to the target SVG during the duration of follow-up (minimum of 2 years). Secondary efficacy outcomes included MACE related to the target SVG lesion and overall MACE. A total of 125 patients (mean age 70±9 years, 87% men) were included, with a mean time from coronary artery bypass graft of 12±5 years. Sixty and 65 patients were allocated to the SVG-DES and SVG-MT groups, respectively. There were no events related to the target SVG at 30 days. After a median follow-up of 3.4 (interquartile range: 2.8-3.9) years, the MACE rate related to the target SVG was not significantly different in the 2 groups (SVG-DES: 15.0%, SVG-MT: 20.0%; hazard ratio, 0.65; 95% confidence interval, 0.23-1.53; P=0.33). There were no significant differences between groups in MACE related to the target SVG lesion (SVG-DES: 10.0%, SVG-MT: 16.9%; hazard ratio, 0.53; 95% confidence interval, 0.20-1.43; P=0.21) or global MACE (SVG-DES: 36.7%, SVG-MT: 44.6%; hazard ratio, 0.73; 95% confidence interval, 0.42-1.27; P=0.26). Sealing intermediate nonobstructive SVG lesions with DES was safe but was not associated with a significant reduction of cardiac events at 3-year follow-up. URL: http://www.clinicaltrials.gov. Unique identifier: NCT01223443.

Limitation of Infarct Size and the Open Artery Hypothesis: A Conversation With Eugene Braunwald, MD.

Eugene Braunwald received an MD from the New York University School of Medicine. He completed an internal medicine residency at Johns Hopkins Hospital and cardiology fellowships at Mount Sinai Hospital, Columbia University, and the National Heart Institute. He served as chief of cardiology and subsequently clinical director of the institute. From 1968 to 1972, he was the founding chair of medicine at the University of California, San Diego. From 1972 to 1996, he served as chair of medicine at the Brigham and Women’s Hospital. In 1975, he was elected to the National Academy of Sciences. He is now the Distinguished Hersey Professor of Medicine at Harvard Medical School and a senior investigator of the TIMI Study Group, which he founded in 1984. Dr Braunwald replies: I became aware of the importance of AMI in 1951 during an elective in cardiology during my senior year at the New York University School of Medicine. At the time, AMI was by far the most common cause of death in adults in the United States. Of the patients who survived to be admitted to hospitals (no one knew how many AMI patients failed to reach hospital emergency departments), about one third died before discharge, either suddenly, presumably from an arrhythmia, or secondary to pump failure. Of the patients who were discharged alive, about one quarter died within a year, most frequently as a consequence of heart failure or recurrent MI. Pathologists had taught that AMI was usually associated with coronary thrombosis. Indeed, during my cardiology elective, Herrick’s classic article describing AMI was required reading. Its title, “Clinical Features of Sudden Obstruction of the Coronary Arteries,” showed how these 2 conditions (coronary occlusion and AMI) were intertwined.1 My direct involvement in the care of several patients who did not survive the acute event left …

Standard Surgical Skin Markers Should Be Avoided for Intraoperative Vein Graft Marking during Cardiac and Peripheral Bypass Operations.

One cause of early graft failure following coronary and peripheral vein grafting is kinking or mechanical twisting of the conduit. The blind tunneling necessitated in peripheral bypasses can lead to this consequence (1). In coronary artery bypass grafting (CABG), grafts to the posterior branches of the right or circumflex coronary arteries are placed to the back of the heart and are generally the longest aortocoronary grafts. These grafts are particularly prone to twisting and kinking. Additionally, single vein grafts to two or more coronary branches (“sequential vein grafts”) present special challenges with respect to maintenance of proper alignment (2, 3). The coronary vein graft failure rate at 1 year in the PRoject of Ex vivo Vein graft ENgineering via Transfection IV (PREVENT IV) cohort was 25%, suggesting that early graft failure is a significant problem (4, 5). The incidence of vein graft failure due to twisting or kinking is not well studied, though some reports estimate that obstructing lesions, including but not limited to twisting or kinking, account for 15–25% of early (<1 year) graft failures (6–8). Preparation and preservation techniques have advanced the field of solid organ allotransplantation, but vein graft failure rates suggest room for improvement in the handling of saphenous vein (SV) harvested for autotransplantation. Interventions for ex vivo graft treatment, including appropriate choice of preservation solution and minimization of manual pressure distension via chemical vasodilators such as papaverine, have been proposed (9–12). Additionally, the “no-touch” technique has emerged as a method of minimizing detrimental handling of graft during harvest with adventitial preservation (4, 13–15). Marking of the SV graft using a surgical skin marker in an “off-label” fashion represents another such preparation technique and is the most commonly employed method of preventing graft torsion (16). This marking allows for the maintenance of continuous alignment along the length of the vein in the same longitudinal plane. These lines provide a visible guide for surgeons to use during conduit routing and tunneling to avoid mechanical obstructions related to vein alignment (17). While operating rooms have adapted less traumatic methods of vein harvest, preservation, and distension, surgical skin marker use remains ubiquitous as the primary method to maintain graft orientation. The use of surgical skin markers during graft preparation is toxic to the tissue and impairs physiologic function (16). We argue that the data support avoidance of standard surgical skin markers for marking on vascular tissue; We further contend that brilliant blue FCF (for coloring food) may represent a viable alternative dye for intraoperative graft marking.

A Closer Look at Fractional Flow Reserve in Complex Anatomic Subsets: Left Main Disease, Bifurcation Lesions, and Saphenous Vein Grafts.

Fractional flow reserve (FFR) is a well-validated tool for determining the functional significance of a coronary artery stenosis, facilitating clinical decisions regarding the need for revascularization. FFR-guided revascularization improves clinical and economic outcomes. However, its application remains challenging in certain complex anatomic subsets, including left main coronary artery stenosis, bifurcation disease, and saphenous vein graft disease. This article reviews recent data supporting the use of FFR in these complex anatomic subsets.

Sudden Thrombosis in Coronary Artery Bypass Grafting Surgery

Sudden Thrombosis in Coronary Artery Bypass Grafting Surgery

Bilateral Saphenous Vein Graft Aneurysms

SESSION TITLE: Procedures Case Report Posters SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 27, 2015 at 01:30 PM - 02:30 PM INTRODUCTION: More than 50 years have passed since CABG was first successfully performed in humans. Despite many improvements in surgical technique, complications of CABG continue to occur. Here, we present a rare case of bilateral saphenous vein graft aneurysm as a late complication of CABG. CASE PRESENTATION: 77 yo man with CAD status post CABG 12 years ago, presented for evaluation of chest pain and dyspnea. On examination, his vitals were stable and his exam was unremarkable. Basic labs, including cardiac enzymes, were unrevealing. A chest x-ray demonstrated fullness in the right hilum worrisome for a mass (1). CT of the chest with contrast confirmed two large anterior mediastinal masses as well as mediastinal lymphadenopathy. Percutaneous CT guided biopsy showed only blood and was complicated by a hemothorax. Further work up with bronchoscopy and biopsy was non diagnostic. Coronary CT angiography revealed aneurysms of two coronary bypass vein grafts (2). The right graft was patent to the RCA, but the left was occluded. Patient was offered surgical treatment, but he declined, opting for conservative management. He is doing well 1 year after initial diagnosis. DISCUSSION: Saphenous Vein Graft Aneurysm (SVGA) is a rare complication of CABG. The overall incidence is likely less than 0.5% of grafts. Proposed etiologies include exposure to arterial pressures, atherosclerotic changes, infection, and technical factors during harvest and transplant. Typical presentation is with chest pain, dyspnea, and MI, but a large number of patients are asymptomatic. Multiple studies have documented aneurysmal enlargement, however the rate of growth is variable. Large aneurysms have higher rates of mechanical complications, but increasing size has not been demonstrated to increase the risk of rupture or death. Treatment data is limited, with some case series advocating conservative management 1, and others suggesting surgical treatment 2. Recently, increasing percutaneous options are becoming available. CONCLUSIONS: Anterior mediastinal mass with a history of CABG should raise suspicion for SVGA. More data is needed to determine optimal treatment. Reference #1: Dieter, R. S., et al. (2003). “Conservative vs. invasive treatment of aortocoronary saphenous vein graft aneurysms: Treatment algorithm based upon a large series.” Cardiovasc Surg 11(6): 507-513. Reference #2: Sareyyupoglu, B., et al. (2009). “Surgical treatment of saphenous vein graft aneurysms after coronary artery revascularization.” Ann Thorac Surg 88(6): 1801-1805. DISCLOSURE: The following authors have nothing to disclose: Michael Tatusov No Product/Research Disclosure Information

Abstract 440: Increased Migration and Proliferation of Human Venous Valve Wall Smooth Muscle Cells are Mediated by FGF2

Introduction: Lesions causing coronary and peripheral vein graft failure often occur at valves. To test the hypothesis that intrinsic differences in cells of the valve wall contribute to graft failure we measured cell migration from tissue explants and migration and proliferation of cultured cells from valve and non-valve sections of human saphenous vein (HSV). Methods: After removal of endothelium, HSVs were dissected into an outer wall with adventitia and some media and an inner wall with intima and some media. Cell migration from explants and migration (microchemotaxis chambers) and proliferation of cultured cells at passage 6 were measured. Results: Cells migrated faster from valve compared to non-valve tissue of the inner wall (Figure A; P&lt;0.01, N=24 veins), but not the outer wall (not shown). PDGF-BB- or serum-mediated migration of valve inner wall smooth muscle cells (VSMC) was greater than with non-valve SMCs (NVSMC; P&lt;0.05, N=6 pairs, 6.5 ± 1.2 vs. 4.2 ± 0.8 fold of control for PDGF-BB and 4.7 ± 0.6 vs. 3.4 ± 0.4 for serum). VSMC also proliferated faster than NVSMC after stimulation with PDGF-BB plus 2% serum (P&lt;0.01, N=6 pairs, 3.3 ± 0.4 vs. 2.2 ± 0.2 fold of control). Finally, a blocking antibody to FGF2 had no effect on PDGF-mediated migration or proliferation of NVSMC (migration: IgG 2.2 ± 0.3 vs anti-FGF2 2.0 ± 0.4, N=6; proliferation: IgG 2.6 ± 0.1 vs anti-FGF2 2.5 ± 0.2, N=7), but largely blocked the enhanced migration and proliferation of VSMC (migration: Figure B; P&lt;0.01, N=6; proliferation: control IgG 3.4 ± 0.3 vs. Anti-FGF2 Ab 2.7 ± 0.3 fold; P&lt;0.01, N=7). Conclusion: The increased migration and proliferation of VSMC compared to NVSMC is largely mediated by FGF2.