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Aortocoronary saphenous vein graft disease : Pathogenesis, predisposition, and prevention
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 atheroscle...
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Published in: | Circulation (New York, N.Y.) N.Y.), 1998-03, Vol.97 (9), p.916-931 |
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container_title | Circulation (New York, N.Y.) |
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creator | MOTWANI, J. G TOPOL, E. J |
description | 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. |
doi_str_mv | 10.1161/01.CIR.97.9.916 |
format | article |
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G ; TOPOL, E. J</creator><creatorcontrib>MOTWANI, J. G ; TOPOL, E. J</creatorcontrib><description>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.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.97.9.916</identifier><identifier>PMID: 9521341</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Arteriosclerosis - etiology ; Arteriosclerosis - prevention & control ; Biological and medical sciences ; Coronary Artery Bypass ; Humans ; Hyperplasia - etiology ; Hyperplasia - prevention & control ; Hypolipidemic Agents - therapeutic use ; Medical sciences ; Platelet Aggregation Inhibitors - therapeutic use ; Risk Factors ; Saphenous Vein - pathology ; Saphenous Vein - transplantation ; Smoking Cessation ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Surgery of the heart ; Thrombosis - etiology ; Thrombosis - prevention & control</subject><ispartof>Circulation (New York, N.Y.), 1998-03, Vol.97 (9), p.916-931</ispartof><rights>1998 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. 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J</creatorcontrib><title>Aortocoronary saphenous vein graft disease : Pathogenesis, predisposition, and prevention</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>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.</description><subject>Arteriosclerosis - etiology</subject><subject>Arteriosclerosis - prevention & control</subject><subject>Biological and medical sciences</subject><subject>Coronary Artery Bypass</subject><subject>Humans</subject><subject>Hyperplasia - etiology</subject><subject>Hyperplasia - prevention & control</subject><subject>Hypolipidemic Agents - therapeutic use</subject><subject>Medical sciences</subject><subject>Platelet Aggregation Inhibitors - therapeutic use</subject><subject>Risk Factors</subject><subject>Saphenous Vein - pathology</subject><subject>Saphenous Vein - transplantation</subject><subject>Smoking Cessation</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</subject><subject>Surgery of the heart</subject><subject>Thrombosis - etiology</subject><subject>Thrombosis - prevention & control</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><recordid>eNpdkM1LxDAQxYMouq6ePQlFxJOtmaRtGm_L4seCoIgePIWYTncr3aQmreB_bxYXD56GN-83w8wj5ARoBlDCFYVsvnjOpMhkJqHcIRMoWJ7mBZe7ZEIplangjB2QwxA-oiy5KPbJviwY8Bwm5G3m_OCM885q_50E3a_QujEkX9jaZOl1MyR1G1AHTK6TJz2s3BIthjZcJr3HaPUutEPr7GWibb3pfaHd6COy1-gu4PG2Tsnr7c3L_D59eLxbzGcPqeFVNaSspowK5FRiPA_rqCVI3rxro4scGkFrBCN4aXI0lPMmOlDwRtcVA8EqPiUXv3t77z5HDINat8Fg12mL8RElpCiozEUEz_6BH270Nt6mGDDBaQUsQle_kPEuBI-N6n27jtEooGqTuKKgYuJKCiVVTDxOnG7Xju9rrP_4bcTRP9_6OhjdNV5b04Y_LD4hIsd_AN7aiOw</recordid><startdate>19980310</startdate><enddate>19980310</enddate><creator>MOTWANI, J. G</creator><creator>TOPOL, E. 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J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c388t-2d0207e309e000ed2d09193fbaca541f70de1c736c4ec033ffba153fad8217283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Arteriosclerosis - etiology</topic><topic>Arteriosclerosis - prevention & control</topic><topic>Biological and medical sciences</topic><topic>Coronary Artery Bypass</topic><topic>Humans</topic><topic>Hyperplasia - etiology</topic><topic>Hyperplasia - prevention & control</topic><topic>Hypolipidemic Agents - therapeutic use</topic><topic>Medical sciences</topic><topic>Platelet Aggregation Inhibitors - therapeutic use</topic><topic>Risk Factors</topic><topic>Saphenous Vein - pathology</topic><topic>Saphenous Vein - transplantation</topic><topic>Smoking Cessation</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Surgery of the heart</topic><topic>Thrombosis - etiology</topic><topic>Thrombosis - prevention & control</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MOTWANI, J. G</creatorcontrib><creatorcontrib>TOPOL, E. J</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MOTWANI, J. G</au><au>TOPOL, E. J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aortocoronary saphenous vein graft disease : Pathogenesis, predisposition, and prevention</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1998-03-10</date><risdate>1998</risdate><volume>97</volume><issue>9</issue><spage>916</spage><epage>931</epage><pages>916-931</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><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.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>9521341</pmid><doi>10.1161/01.CIR.97.9.916</doi><tpages>16</tpages></addata></record> |
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subjects | Arteriosclerosis - etiology Arteriosclerosis - prevention & control Biological and medical sciences Coronary Artery Bypass Humans Hyperplasia - etiology Hyperplasia - prevention & control Hypolipidemic Agents - therapeutic use Medical sciences Platelet Aggregation Inhibitors - therapeutic use Risk Factors Saphenous Vein - pathology Saphenous Vein - transplantation Smoking Cessation Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Surgery of the heart Thrombosis - etiology Thrombosis - prevention & control |
title | Aortocoronary saphenous vein graft disease : Pathogenesis, predisposition, and prevention |
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