Vein Graft

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Deepak L Bhatt - One of the best experts on this subject based on the ideXlab platform.

  • randomized trial of endoscopic or open Vein Graft harvesting for coronary artery bypass
    The New England Journal of Medicine, 2019
    Co-Authors: Marco A Zenati, Deepak L Bhatt, Faisal G Bakaeen, Eileen M Stock, Kousick Biswas, Michael J Gaziano, Rosemary F Kelly, Elaine E Tseng, Jerene M Bitondo, Jacquelyn A Quin
    Abstract:

    Abstract Background The saphenous-Vein Graft is the most common conduit for coronary-artery bypass Grafting (CABG). The influence of the Vein-Graft harvesting technique on long-term clinical outcomes has not been well characterized. Methods We randomly assigned patients undergoing CABG at 16 Veterans Affairs cardiac surgery centers to either open or endoscopic Vein-Graft harvesting. The primary outcome was a composite of major adverse cardiac events, including death from any cause, nonfatal myocardial infarction, and repeat revascularization. Leg-wound complications were also evaluated. Results A total of 1150 patients underwent randomization. Over a median follow-up of 2.78 years, the primary outcome occurred in 89 patients (15.5%) in the open-harvest group and 80 patients (13.9%) in the endoscopic-harvest group (hazard ratio, 1.12; 95% confidence interval [CI], 0.83 to 1.51; P=0.47). A total of 46 patients (8.0%) in the open-harvest group and 37 patients (6.4%) in the endoscopic-harvest group died (haza...

  • drug eluting stents versus bare metal stents in saphenous Vein Graft intervention
    Circulation-cardiovascular Interventions, 2018
    Co-Authors: Nileshkumar Patel, George Dangas, Chirag Bavishi, Varunsiri Atti, Avnish Tripathi, Nikhil Nalluri, Mauricio G Cohen, Annapoorna Kini, Samin K Sharma, Deepak L Bhatt
    Abstract:

    Background Percutaneous coronary intervention with drug-eluting stents (DES) has been increasingly used for revascularization of saphenous Vein Graft stenosis without strong clinical evidence favor...

  • drug eluting stents versus bare metal stents in saphenous Vein Graft intervention
    Circulation-cardiovascular Interventions, 2018
    Co-Authors: Nileshkumar J Patel, George Dangas, Chirag Bavishi, Varunsiri Atti, Avnish Tripathi, Nikhil Nalluri, Mauricio G Cohen, Annapoorna Kini, Samin K Sharma, Deepak L Bhatt
    Abstract:

    Background Percutaneous coronary intervention with drug-eluting stents (DES) has been increasingly used for revascularization of saphenous Vein Graft stenosis without strong clinical evidence favoring their use. Randomized controlled trials comparing DES versus bare-metal stents (BMS) in saphenous Vein Graft-percutaneous coronary intervention have been inconclusive. Methods and Results We performed a comprehensive literature search through May 15, 2018, for all eligible studies comparing DES versus BMS in patients with saphenous Vein Graft stenosis in PubMed, EMBASE, SCOPUS, Google Scholar, and ClinicalTrials.gov. Clinical outcomes included all-cause mortality, cardiovascular mortality, major adverse cardiovascular events, myocardial infarction, stent thrombosis, and target vessel revascularization. Six randomized controlled trials were eligible and included 1582 patients, of whom 797 received DES and 785 received BMS. The follow-up period ranged from 18 months to 60 months. There was no statistically significant difference between DES and BMS for all-cause mortality (risk ratio [RR],1.11; 95% CI, 0.0.77-1.62; P=0.57), cardiovascular mortality (RR, 1.00; 95% CI, 0.64-1.57; P=0.99), major adverse cardiovascular events (RR, 0.83; 95% CI, 0.63-1.10; P=20), target vessel revascularization (RR, 0.73; 95% CI, 0.48-1.11; P=0.14), myocardial infarction (RR, 0.74; 95% CI, 0.48-1.16; P=0.19), or stent thrombosis (RR, 1.06; 95% CI, 0.42-2.65; P=0.90). Conclusions In patients undergoing percutaneous coronary intervention for saphenous Vein Graft lesions, our results showed that there was no significant difference between DES and BMS for mortality, major adverse cardiovascular events, target vessel revascularization, myocardial infarction, or stent thrombosis.

Margreet R. De Vries - One of the best experts on this subject based on the ideXlab platform.

  • Inflammation in Vein Graft Disease
    Frontiers Media S.A., 2018
    Co-Authors: Margreet R. De Vries, Paul H A Quax
    Abstract:

    Bypass surgery is one of the most frequently used strategies to revascularize tissues downstream occlusive atherosclerotic lesions. For venous bypass surgery the great saphenous Vein is the most commonly used vessel. Unfortunately, Graft efficacy is low due to the development of vascular inflammation, intimal hyperplasia and accelerated atherosclerosis. Moreover, failure of Grafts leads to significant adverse outcomes and even mortality. The last couple of decades not much has changed in the treatment of Vein Graft disease (VGD). However, insight is the cellular and molecular mechanisms of VGD has increased. In this review, we discuss the latest insights on VGD and the role of inflammation in this. We discuss Vein Graft pathophysiology including hemodynamic changes, the role of vessel wall constitutions and vascular remodeling. We show that profound systemic and local inflammatory responses, including inflammation of the perivascular fat, involve both the innate and adaptive immune system

  • abstract 303 increased endogenous hydrogen sulfide protects against Vein Graft disease
    Arteriosclerosis Thrombosis and Vascular Biology, 2017
    Co-Authors: Kaspar Trocha, Ming Tao, Michael R Macarthur, Alban Longchamp, James R Mitchell, Keith C Ozaki, Margreet R. De Vries
    Abstract:

    Objective: Vein Graft failure secondary to intimal hyperplasia remains a challenge. Hydrogen sulfide (H 2 S) is produced endogenously by cystathionine γ-lyase (CGL) in endothelial cells, and as a gasotransmitter holds numerous beneficial vascular effects. We thus hypothesized that increased endogenous H 2 S would attenuate the vascular response to injury. Here, we leveraged a CGL transgenic overexpressing mouse model to test the potential of increased endogenous H 2 S to attenuate the vascular response to injury in a Vein Graft model. Approach and Results: A murine carotid-interposition cuff technique Vein Graft model was employed, including an artificial bacterial chromosome-based CGL transgenic (Tg) strain with an extra copy of the CGL gene locus randomly inserted in the genome. CGL Tg mice were fed a high-fat/high-cholesterol diet, implanted with a Vein Graft from CGL Tg donors (n=8), and compared to wild-type (WT) controls (n=7; WT/ WT conduits); all on C57BL/6 background. Grafts were imaged in vivo with ultrasound biomicropscopy and harvested after 28 days. CGL Tg mice demonstrated an approximate two-fold increase in serum H 2 S production capacity (lead acetate assay) compared to controls. The CGL Tg mice exhibited a significant decrease in their intimal thickness (p= In vivo biomicroscopy was supportive: CGL tg mice had a larger mean luminal diameter relative to WT controls (p= Conclusion: Elevated endogenous H 2 S production reduces the fibroproliferative response to Vein Graft arterialization. Manipulation of this gasotransmitter’s biology stands as a novel approach to impact the durability of vascular reconstructions.

  • Vein Graft failure: from pathophysiology to clinical outcomes.
    Nature reviews. Cardiology, 2016
    Co-Authors: Margreet R. De Vries, Karin H. Simons, J. Wouter Jukema, Jerry Braun, Paul H A Quax
    Abstract:

    Veins are the most commonly used conduits for surgical revascularization; however, they are associated with a high failure rate. In this Review, de Vries and colleagues discuss the pathophysiological mechanisms underlying the development of Vein Graft failure, and summarize the current and developing therapies used to prevent Graft failure.

  • abstract 370 interferon regulatory factors 3 and 7 regulate Vein Graft remodeling and vascular inflammation
    Arteriosclerosis Thrombosis and Vascular Biology, 2014
    Co-Authors: Margreet R. De Vries, Jacco C Karper, Erna Peters, Tineke C Van Der Pouw Kraan, Rob C De Jong, Jaap F Hamming, A J G Horrevoets
    Abstract:

    Introduction: Type I interferons (IFN) are implicated in the development of vascular proliferative diseases. Pathway analysis by gene set enrichment analysis of hypercholesterolemic ApoE3*Leiden murine Vein Grafts revealed that the type I IFN pathway belonged to the top 15 of significant regulated pathways. The transcriptional regulators of type I IFN and type I IFN responsive genes are the interferon regulatory factors (IRF). Activation of TLR3 results in activation of type I IFN in a IRF3 and IRF7 dependent manner. TLR3 has been shown to be protective in vascular remodeling. The aim of this study was to investigate the role of IRF3 and IRF7 on Vein Graft remodeling. Methods and Results: The importance of IRFs in Vein Graft remodeling is illustrated by the increase in Vein Graft thickening in Irf3-/- and Irf7-/- mice in comparison to control mice (n=9/group, Irf3-/- ; 39%, p=0.185, Irf7-/- ; 68% p=0.003). Also an increase in outward remodeling ( Irf3-/- ; 26%, p=0.081, Irf7-/- ; 42%, p=0.049) was observed comparable to that of Tlr3-/- (n=8, 52%, p<0.001) Immunohistochemical analysis revealed that both Irf3-/- and Irf7-/- mice showed a significant higher influx of macrophages in the vessel wall than the control mice whereas the Irf7-/- mice also showed a significant decrease in collagen content. RNA levels of typical type I IFN responsive genes such as Mx1, Ifit1-3 and Oas2 were down regulated in the knockout Vein Grafts in comparison to control Vein Grafts. Activation of both Irf3-/- and Irf7-/- bone marrow derived macrophages with LPS and poly:(IC) resulted in a significant increase in TNFα production. Conclusions: IRFs regulates Vein Graft remodeling since Irf3-/- and especially Irf7-/- Vein Grafts show increased vessel wall thickening and outward remodeling. This increased remodeling is the result of a pro-inflammatory response as reflected by the increase in macrophages in the Vein Graft wall.

  • complement factor c5a as mast cell activator mediates vascular remodelling in Vein Graft disease
    Cardiovascular Research, 2013
    Co-Authors: Margreet R. De Vries, Abbey Schepers, Jaap F Hamming, Anouk Wezel, Peter J Van Santbrink, Trent M Woodruff, Hans W M Niessen, Johan Kuiper, Ilze Bot
    Abstract:

    AIMS: Failure of Vein Graft conduits due to Vein Graft thickening, accelerated atherosclerosis, and subsequent plaque rupture is applicable to 50% of all Vein Grafts within 10 years. New potential therapeutic targets to treat Vein Graft disease may be found in components of the innate immune system, such as mast cells and complement factors, which are known to be involved in atherosclerosis and plaque destabilization. Interestingly, mast cells can be activated by complement factor C5a and, therefore, a direct role for C5a-mediated mast cell activation in Vein Graft disease is anticipated. We hypothesize that C5a-mediated mast cell activation is involved in the development and destabilization of Vein Graft lesions. METHODS AND RESULTS: Mast cells accumulated in time in murine Vein Graft lesions, and C5a and C5a-receptor (CD88) expression was up-regulated during Vein Graft disease in apolipoprotein E-deficient mice. Mast cell activation with dinitrophenyl resulted in a profound increase in Vein Graft thickening and in the number of plaque disruptions. C5a application enhanced Vein Graft lesion formation, while treatment with a C5a-receptor antagonist resulted in decreased Vein Graft disease. C5a most likely exerts its function via mast cell activation since the mast cell inhibitor cromolyn totally blocked C5a-enhanced Vein Graft disease. CONCLUSION: These data provide evidence that complement factor C5a-induced mast cell activation is highly involved in Vein Graft disease, which identifies new targets to prevent Vein Graft disease.

Eric J. Topol - One of the best experts on this subject based on the ideXlab platform.

  • aortocoronary saphenous Vein Graft disease pathogenesis predisposition and prevention
    Circulation, 1998
    Co-Authors: Joseph G Motwani, Eric J. Topol
    Abstract:

    Abstract—Aortocoronary saphenous Vein Graft disease, with its increasing clinical sequelae, presents an important and unresolved dilemma in cardiological practice. During the 1st month after bypass surgery, Vein Graft attrition results from thrombotic occlusion, while later the dominant process is atherosclerotic obstruction occurring on a foundation of neointimal hyperplasia. Although the risk factors predisposing to Vein Graft atherosclerosis are broadly similar to those recognized for native coronary disease, the pathogenic effects of these risk factors are amplified by inherent deficiencies of the Vein as a conduit when transposed into the coronary arterial circulation. A multifaceted strategy aimed at prevention of Vein Graft disease is emerging, elements of which include: continued improvements in surgical technique; more effective antiplatelet drugs; increasingly intensive risk factor modification, in particular early and aggressive lipid-lowering drug therapy; and a number of evolving therapies, s...

  • aortocoronary saphenous Vein Graft disease pathogenesis predisposition and prevention
    Circulation, 1998
    Co-Authors: Joseph G Motwani, Eric J. Topol
    Abstract:

    Aortocoronary saphenous Vein Graft disease, with its increasing clinical sequelae, presents an important and unresolved dilemma in cardiological practice. During the 1st month after bypass surgery, Vein Graft attrition results from thrombotic occlusion, while later the dominant process is atherosclerotic obstruction occurring on a foundation of neointimal hyperplasia. Although the risk factors predisposing to Vein Graft atherosclerosis are broadly similar to those recognized for native coronary disease, the pathogenic effects of these risk factors are amplified by inherent deficiencies of the Vein as a conduit when transposed into the coronary arterial circulation. A multifaceted strategy aimed at prevention of Vein Graft disease is emerging, elements of which include: continued improvements in surgical technique; more effective antiplatelet drugs; increasingly intensive risk factor modification, in particular early and aggressive lipid-lowering drug therapy; and a number of evolving therapies, such as gene transfer and nitric oxide donor administration, which target Vein Graft disease at an early and fundamental level. At present, a key measure is to circumvent the problem of Vein Graft disease by preferential selection of arterial conduits, in particular the internal mammary arteries, for coronary bypass surgery whenever possible.

Paul H A Quax - One of the best experts on this subject based on the ideXlab platform.

  • Inflammation in Vein Graft Disease
    Frontiers Media S.A., 2018
    Co-Authors: Margreet R. De Vries, Paul H A Quax
    Abstract:

    Bypass surgery is one of the most frequently used strategies to revascularize tissues downstream occlusive atherosclerotic lesions. For venous bypass surgery the great saphenous Vein is the most commonly used vessel. Unfortunately, Graft efficacy is low due to the development of vascular inflammation, intimal hyperplasia and accelerated atherosclerosis. Moreover, failure of Grafts leads to significant adverse outcomes and even mortality. The last couple of decades not much has changed in the treatment of Vein Graft disease (VGD). However, insight is the cellular and molecular mechanisms of VGD has increased. In this review, we discuss the latest insights on VGD and the role of inflammation in this. We discuss Vein Graft pathophysiology including hemodynamic changes, the role of vessel wall constitutions and vascular remodeling. We show that profound systemic and local inflammatory responses, including inflammation of the perivascular fat, involve both the innate and adaptive immune system

  • Vein Graft failure: from pathophysiology to clinical outcomes.
    Nature reviews. Cardiology, 2016
    Co-Authors: Margreet R. De Vries, Karin H. Simons, J. Wouter Jukema, Jerry Braun, Paul H A Quax
    Abstract:

    Veins are the most commonly used conduits for surgical revascularization; however, they are associated with a high failure rate. In this Review, de Vries and colleagues discuss the pathophysiological mechanisms underlying the development of Vein Graft failure, and summarize the current and developing therapies used to prevent Graft failure.

  • a novel urokinase receptor targeted inhibitor for plasmin and matrix metalloproteinases suppresses Vein Graft disease
    Cardiovascular Research, 2010
    Co-Authors: Daniel Eefting, Jos M Grimbergen, Margreet R. De Vries, Leonard Seghers, Hetty C De Boer, J H P Lardenoye, Wouter J Jukema, Hajo J Van Bockel, Paul H A Quax
    Abstract:

    Aims Matrix metalloproteinases (MMP) and plasminogen activator (PA)/plasmin-mediated proteolysis, especially at the cell surface, play important roles in matrix degeneration and smooth muscle cell migration, which largely contributes to Vein Graft failure. In this study, a novel hybrid protein was designed to inhibit both protease systems simultaneously. MMP and plasmin activity were inhibited at the cell surface by this hybrid protein, consisting of the receptor-binding amino-terminal fragment (ATF) of urokinase-type PA, linked to both the tissue inhibitor of metalloproteinases (TIMP-1) and bovine pancreas trypsin inhibitor (BPTI), a potent protease inhibitor. The effect of overexpression of this protein on Vein Graft disease was studied. Methods and resultsA non-viral expression vector encoding the hybrid protein TIMP-1.ATF.BPTI was constructed and validated. Next, cultured segments of human Veins were transfected with this vector. Expressing TIMP-1.ATF.BPTI in Vein segments resulted in a mean 36 ± 14 reduction in neointima formation after 4 weeks. In vivo inhibition of Vein Graft disease by TIMP-1.ATF.BPTI is demonstrated in venous interpositions placed into carotid arteries of hypercholesterolaemic APOE*3Leiden mice. After 4 weeks, Vein Graft thickening was significantly inhibited in mice treated with the domains TIMP-1, ATF, or BPTI (36-49 reduction). In the TIMP-1.ATF.BPTI-treated mice, Vein Graft thickening was reduced by 67±4, which was also significantly stronger when compared with the individual components.Conclusion These data provide evidence that cell surface-bound inhibition of the PA and MMP system by the hybrid protein TIMP-1.ATF.BPTI, overexpressed in distant tissues after electroporation-mediated non-viral gene transfer, is a powerful approach to prevent Vein Graft disease. © 2010 The Author.

  • Local lentiviral short hairpin RNA silencing of CCR2 inhibits Vein Graft thickening in hypercholesterolemic apolipoprotein E3-Leiden mice
    Journal of vascular surgery, 2009
    Co-Authors: Daniel Eefting, Abbey Schepers, Ilze Bot, Margreet R. De Vries, J. Hajo Van Bockel, Theo J.c. Van Berkel, Erik A.l. Biessen, Paul H A Quax
    Abstract:

    Objective: Inflammatory responses to vascular injury are key events in Vein Graft disease and accelerated atherosclerosis, which may result in bypass failure. The monocyte chemoattractant protein-1 (MCP-1)/CC-chemokine receptor (CCR)-2 pathway is hypothesized to play a central role. A murine model for Vein Graft disease was used to study the effect of local application of lentiviral short hairpin RNA (shRNA) targeted against CCR2. Methods: A venous interposition was placed into the carotid artery of hypercholesterolemic apolipoprotein E3-Leiden (APOE*3-Leiden) mice to induce Vein Graft thickening with features of accelerated atherosclerosis. To demonstrate the efficacy of the lentiviral shRNA targeting murine CCR2 (shCCR2) in blocking Vein Graft disease in vivo, lentiviral shCCR2 or a control lentivirus was used to infect the Vein Graft locally (n = 8). Results: Vascular CCR2 and MCP-1 messenger RNA expression levels were significantly upregulated during lesion progression in the Vein Graft. Infection of smooth muscle cells (SMCs) with a lentiviral shRNA targeting shCCR2 completely abolished MCP-1-induced SMC migration and inhibited SMC proliferation in vitro (n = 3 per group). Morphometric analysis of sections of Grafts showed a significant 38% reduction in Vein Graft thickening in the shCCR2-treated mice 4 weeks after surgery (control, 0.42 ± 0.05 mm2; shCCR2, 0.26 ± 0.03 mm2; P = .007). Conclusion: Vascular CCR2 contributes to Vein Graft disease, and local application of shRNA against CCR2 to the vessel wall prevents Vein Graft thickening in hypercholesterolemic mice, suggesting that local overexpressing of shRNA using organ-targeted lentiviral gene delivery may be a promising therapeutic tool to improve Vein Graft disease in bypassed patients. © 2009 Society for Vascular Surgery.

  • inhibition of complement component c3 reduces Vein Graft atherosclerosis in apolipoprotein e3 leiden transgenic mice
    Circulation, 2006
    Co-Authors: Abbey Schepers, M R De Vries, C J Van Leuven, Jos M Grimbergen, J. Hajo Van Bockel, V. Michael Holers, Mohamed R. Daha, Paul H A Quax
    Abstract:

    BACKGROUND - Venous bypass Grafts may fail because of development of intimal hyperplasia and accelerated atherosclerosis. Inflammation plays a major role in these processes. Complement is an important part of the immune system and participates in the regulation of inflammation. The exact role of complement in the process of accelerated atherosclerosis of Vein Grafts has not yet been explored, however. METHODS AND RESULTS - To assess the role of complement in the development of Vein Graft atherosclerosis, a mouse model, in which a venous interposition was placed in the common carotid artery, was used. In this model, Vein Graft thickening appeared within 4 weeks. The expression of complement components was studied with the use of immunohistochemistry on sections of the thickened Vein Graft. C1q, C3, C9, and the regulatory proteins CD59 and complement receptor-related gene y could be detected in the lesions 4 weeks after surgery. Quantitative mRNA analysis for C1q, C3, CD59, and complement receptor-related gene y revealed expression of these molecules in the thickened Vein Graft, whereas C9 did not show local mRNA expression. Furthermore, interference with C3 activation with complement receptor-related gene y-Ig was associated with reduced Vein Graft thickening, reduced C3 and C9 deposition, and reduced inflammation as assessed by analysis of influx of inflammatory cells, such as leukocytes, T cells, and monocytes. In addition, changes in apoptosis and proliferation were observed. When C3 was inhibited by cobra venom factor, a similar reduction in Vein Graft thickening was observed. CONCLUSIONS - The complement cascade is involved in Vein Graft thickening and may be a target for therapy in Vein Graft failure disease. © 2006 American Heart Association, Inc. Chemicals / CAS: cobrotoxin, 12584-83-7, 8001-03-4; complement component C1q, 80295-33-6; complement component C3, 80295-41-6; apolipoprotein E3 (Leidein); Apolipoprotein E3; Complement C3

Renato D Lopes - One of the best experts on this subject based on the ideXlab platform.

  • saphenous Vein Graft failure after coronary artery bypass surgery pathophysiology management and future directions
    Annals of Surgery, 2013
    Co-Authors: Ralf E Harskamp, Renato D Lopes, Clinton E Baisden, Robbert J De Winter, John H Alexander
    Abstract:

    Objective:To review our current understanding of the epidemiology and pathogenesis of Vein Graft failure (VGF), give an overview of current preventive and interventional measures, and explore strategies that may improve Vein Graft patency.Background:VGF and progression of native coronary artery dise

  • association between endoscopic vs open Vein Graft harvesting and mortality wound complications and cardiovascular events in patients undergoing cabg surgery
    JAMA, 2012
    Co-Authors: Judson B Williams, Renato D Lopes, Eric D Peterson, John H Alexander, Matthew J Brennan, Art Sedrakyan, Dale R Tavris, Rachel S Dokholyan, Yue Zhao, Sean M Obrien
    Abstract:

    Context The safety and durability of endoscopic Vein Graft harvest in coronary artery bypass Graft (CABG) surgery has recently been called into question. Objective To compare the long-term outcomes of endoscopic vs open Vein-Graft harvesting for Medicare patients undergoing CABG surgery in the United States. Design, Setting, and Patients An observational study of 235 394 Medicare patients undergoing isolated CABG surgery between 2003 and 2008 at 934 surgical centers participating in the Society of Thoracic Surgeons (STS) national database. The STS records were linked to Medicare files to allow longitudinal assessment (median 3-year follow-up) through December 31, 2008. Main Outcome Measures All-cause mortality. Secondary outcome measures included wound complications and the composite of death, myocardial infarction, and revascularization. Results Based on Medicare Part B coding, 52% of patients received endoscopic Vein-Graft harvesting during CABG surgery. After propensity score adjustment for clinical characteristics, there were no significant differences between long-term mortality rates (13.2% [12 429 events] vs 13.4% [13 096 events]) and the composite of death, myocardial infarction, and revascularization (19.5% [18 419 events] vs 19.7% [19 232 events]). Time-to-event analysis for those patients receiving endoscopic vs open Vein-Graft harvesting revealed adjusted hazard ratios [HRs] of 1.00 (95% CI, 0.97-1.04) for mortality and 1.00 (95% CI, 0.98-1.05) for the composite outcome. Endoscopic Vein-Graft harvesting was associated with lower harvest site wound complications relative to open Vein-Graft harvesting (3.0% [3654/122 899 events] vs 3.6% [4047/112 495 events]; adjusted HR, 0.83; 95% CI, 0.77-0.89; P  Conclusion Among patients undergoing CABG surgery, the use of endoscopic Vein-Graft harvesting compared with open Vein-Graft harvesting was not associated with increased mortality.

  • association between endoscopic vs open Vein Graft harvesting and mortality wound complications and cardiovascular events in patients undergoing cabg surgery
    JAMA, 2012
    Co-Authors: Judson B Williams, Renato D Lopes, Eric D Peterson, John H Alexander, Matthew J Brennan, Art Sedrakyan, Dale R Tavris, Rachel S Dokholyan, Yue Zhao, Sean M Obrien
    Abstract:

    Context The safety and durability of endoscopic Vein Graft harvest in coronary artery bypass Graft (CABG) surgery has recently been called into question. Objective To compare the long-term outcomes of endoscopic vs open Vein-Graft harvesting for Medicare patients undergoing CABG surgery in the United States. Design, Setting, and Patients An observational study of 235 394 Medicare patients undergoing isolated CABG surgery between 2003 and 2008 at 934 surgical centers participating in the Society of Thoracic Surgeons (STS) national database. The STS records were linked to Medicare files to allow longitudinal assessment (median 3-year follow-up) through December 31, 2008. Main Outcome Measures All-cause mortality. Secondary outcome measures included wound complications and the composite of death, myocardial infarction, and revascularization. Results Based on Medicare Part B coding, 52% of patients received endoscopic Vein-Graft harvesting during CABG surgery. After propensity score adjustment for clinical characteristics, there were no significant differences between long-term mortality rates (13.2% [12 429 events] vs 13.4% [13 096 events]) and the composite of death, myocardial infarction, and revascularization (19.5% [18 419 events] vs 19.7% [19 232 events]). Time-to-event analysis for those patients receiving endoscopic vs open Vein-Graft harvesting revealed adjusted hazard ratios [HRs] of 1.00 (95% CI, 0.97-1.04) for mortality and 1.00 (95% CI, 0.98-1.05) for the composite outcome. Endoscopic Vein-Graft harvesting was associated with lower harvest site wound complications relative to open Vein-Graft harvesting (3.0% [3654/122 899 events] vs 3.6% [4047/112 495 events]; adjusted HR, 0.83; 95% CI, 0.77-0.89; P  Conclusion Among patients undergoing CABG surgery, the use of endoscopic Vein-Graft harvesting compared with open Vein-Graft harvesting was not associated with increased mortality.

  • endoscopic versus open Vein Graft harvesting in coronary artery bypass surgery
    The New England Journal of Medicine, 2009
    Co-Authors: Renato D Lopes, Gail E Hafley, Keith B Allen, Bruce T Ferguson, Eric D Peterson, Robert A Harrington, Rajendra H Mehta, Michael C Gibson, Michael J Mack, Nicholas T Kouchoukos
    Abstract:

    BACKGROUND Vein-Graft harvesting with the use of endoscopy (endoscopic harvesting) is a technique that is widely used to reduce postoperative wound complications after coronary-artery bypass Grafting (CABG), but the long-term effects on the rate of Vein-Graft failure and on clinical outcomes are unknown. METHODS We studied the outcomes in patients who underwent endoscopic harvesting (1753 patients) as compared with those who underwent Graft harvesting under direct vision, termed open harvesting (1247 patients), in a secondary analysis of 3000 patients undergoing CABG. The method of Graft harvesting was determined by the surgeon. Vein-Graft failure was defined as stenosis of at least 75% of the diameter of the Graft on angiography 12 to 18 months after surgery (data were available in an angiographic subgroup of 1817 patients and 4290 Grafts). Clinical outcomes included death, myocardial infarction, and repeat revascularization. Generalized estimating equations were used to adjust for baseline covariates associated with Vein-Graft failure and to account for the potential correlation between Grafts within a patient. Cox proportional-hazards modeling was used to assess long-term clinical outcomes. RESULTS The baseline characteristics were similar between patients who underwent endoscopic harvesting and those who underwent open harvesting. Patients who underwent endoscopic harvesting had higher rates of Vein-Graft failure at 12 to 18 months than patients who underwent open harvesting (46.7% vs. 38.0%, P<0.001). At 3 years, endoscopic harvesting was also associated with higher rates of death, myocardial infarction, or repeat revascularization (20.2% vs. 17.4%; adjusted hazard ratio, 1.22; 95% confidence interval [CI], 1.01 to 1.47; P=0.04), death or myocardial infarction (9.3% vs. 7.6%; adjusted hazard ratio, 1.38; 95% CI, 1.07 to 1.77; P=0.01), and death (7.4% vs. 5.8%; adjusted hazard ratio, 1.52; 95% CI, 1.13 to 2.04; P=0.005). CONCLUSIONS Endoscopic Vein-Graft harvesting is independently associated with Vein-Graft failure and adverse clinical outcomes. Randomized clinical trials are needed to further evaluate the safety and effectiveness of this harvesting technique.

  • endoscopic versus open Vein Graft harvesting in coronary artery bypass surgery
    The New England Journal of Medicine, 2009
    Co-Authors: Renato D Lopes, Gail E Hafley, Keith B Allen
    Abstract:

    Background Vein-Graft harvesting with the use of endoscopy (endoscopic harvesting) is a technique that is widely used to reduce postoperative wound complications after coronary-artery bypass Grafting (CABG), but the long-term effects on the rate of Vein-Graft failure and on clinical outcomes are unknown. Methods We studied the outcomes in patients who underwent endoscopic harvesting (1753 patients) as compared with those who underwent Graft harvesting under direct vision, termed open harvesting (1247 patients), in a secondary analysis of 3000 patients undergoing CABG. The method of Graft harvesting was determined by the surgeon. Vein-Graft failure was defined as stenosis of at least 75% of the diameter of the Graft on angiography 12 to 18 months after surgery (data were available in an angiographic subgroup of 1817 patients and 4290 Grafts). Clinical outcomes included death, myocardial infarction, and repeat revascularization. Generalized estimating equations were used to adjust for baseline covariates as...