The role of vein grafts in coronary surgery

Schachner, Thomas; Laufer, Günther; Bonatti, Johannes

doi:10.1007/s10353-007-0316-6

Cited by 4 publications

(3 citation statements)

References 19 publications

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“…Despite advances in the field of venous allografts and vascular xenografts, venous autografts are at present undoubtedly superior [1]. Intimal hyperplasia is the first significant pathophysiological change in arterialized veins and it is thought to ease the consecutive process of vein graft atherosclerosis that leads to stenosis and graft occlusion [2][3][4]. Different strategies have been proposed as adjuncts to a careful surgical technique, most of them in experimental settings.…”

Section: Introductionmentioning

confidence: 99%

Paclitaxel treatment reduces neointimal hyperplasia in cultured human saphenous veins☆

Schachner

Steger

Heiss

et al. 2007

European Journal of Cardio-Thoracic Surgery

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Section: Introductionmentioning

confidence: 99%

Paclitaxel treatment reduces neointimal hyperplasia in cultured human saphenous veins☆

Schachner

Steger

Heiss

et al. 2007

European Journal of Cardio-Thoracic Surgery

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“… 2 However, these arteries have limited availability; hence, saphenous vein grafts are more frequently used in CABG than arterial grafts (e.g. in 2004 at our institution, saphenous veins were used in 51% of bypass grafts 3 ). Clinical optimization like graft handling (e.g.…”

Section: Introductionmentioning

confidence: 99%

“…‘no touch techniques’) and aggressive lipid-lowering therapy has impressively increased the patency rates of saphenous vein conduits; the current rates are ∼60% 10 years after CABG. 3 – 5 The major reasons for a loss of patency at earlier time points are thromboses, neointima formation, and intimal hyperplasia, with 10–20% loss of patency occurring after the first year; loss at later periods are due to development of graft atherosclerosis. 4 , 6 , 7 …”

Section: Introductionmentioning

confidence: 99%

Leoligin, the major lignan from Edelweiss, inhibits intimal hyperplasia of venous bypass grafts

Reisinger

Schwaiger

Zeller

et al. 2009

Cardiovascular Research

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AimsDespite the lower patency of venous compared with arterial coronary artery bypass grafts, ∼50% of grafts used are saphenous vein conduits because of their easier accessibility. In a search for ways to increase venous graft patency, we applied the results of a previous pharmacological study screening for non-toxic compounds that inhibit intimal hyperplasia of saphenous vein conduits in organ cultures. Here we analyse the effects and mechanism of action of leoligin [(2S,3R,4R)-4-(3,4-dimethoxybenzyl)-2-(3,4-dimethoxyphenyl)tetrahydrofuran-3-yl]methyl (2Z)-2-methylbut-2-enoat, the major lignan from Edelweiss (Leontopodium alpinum Cass.).Methods and resultsWe found that leoligin potently inhibits vascular smooth muscle cell (SMC) proliferation by inducing cell cycle arrest in the G1-phase. Leoligin induced cell death neither in SMCs nor, more importantly, in endothelial cells. In a human saphenous vein organ culture model for graft disease, leoligin potently inhibited intimal hyperplasia, and even reversed graft disease in pre-damaged vessels. Furthermore, in an in vivo mouse model for venous bypass graft disease, leoligin potently inhibited intimal hyperplasia.ConclusionOur data suggest that leoligin might represent a novel non-toxic, non-thrombogenic, endothelial integrity preserving candidate drug for the treatment of vein graft disease.

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Perivascular administration of drugs and genes as a means of reducing vein graft failure

Wiedemann¹,

Kocher²,

Bonaros³

et al. 2012

Current Opinion in Pharmacology

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The role of vein grafts in coronary surgery

Cited by 4 publications

References 19 publications

Paclitaxel treatment reduces neointimal hyperplasia in cultured human saphenous veins☆

Paclitaxel treatment reduces neointimal hyperplasia in cultured human saphenous veins☆

Leoligin, the major lignan from Edelweiss, inhibits intimal hyperplasia of venous bypass grafts

Perivascular administration of drugs and genes as a means of reducing vein graft failure

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