Saphenous Vein Grafts Display Poor Endothelium-Dependent and Endothelium-Independent Dilation—Implications for the Pathogenesis of Vein Graft Atherosclerosis

Objective As endothelial dysfunction has been implicated in the pathogenesis of late failure of saphenous vein grafts (SVG), we assessed endothelium-dependent and endothelium-independent vascular responses of SVG in humans. Methods Subjects undergoing angiography after bypass grafting had selective...

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Veröffentlicht in:Heart, lung & circulation lung & circulation, 2008-04, Vol.17 (2), p.96-99
Hauptverfasser: Kilian, Jens G., MBBS, Thanyasiri, P., PhD, Celermajer, David S., PhD, Adams, Mark R., PhD
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Sprache:eng
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Zusammenfassung:Objective As endothelial dysfunction has been implicated in the pathogenesis of late failure of saphenous vein grafts (SVG), we assessed endothelium-dependent and endothelium-independent vascular responses of SVG in humans. Methods Subjects undergoing angiography after bypass grafting had selective infusions of acetylcholine (ACh, an endothelium-dependent dilator) and sodium-nitroprusside (SNP, an endothelium-independent dilator) into a non-obstructed vein graft. SVG diameters were measured by quantitative coronary angiography. Two matched groups of control subjects, with or without coronary artery disease (CAD), were studied after similar infusions into their femoral arteries. Results We assessed 10 subjects with SVG, 8 controls with and 8 without CAD. SVG dilatation to high-dose ACh was 5 ± 3%, similar to the femoral arteries of subjects with CAD (10 ± 5%), but significantly less than the ACh-related arterial dilatation in the non-CAD group (16 ± 2%, p = 0.02). Similarly, dilatation of SVG after SNP infusion was 9 ± 3%, which was not significantly different from the nitrate responses of femoral arteries in the CAD group (21 ± 5%), but significantly poorer than in the non-CAD subjects (27 ± 5%, p = 0.02). Conclusion Saphenous vein bypass grafts display poor endothelium-dependent and endothelium-independent vascular responses in vivo , compared with healthy systemic arteries. This may contribute to the pathogenesis of accelerated atherosclerosis seen in SVG.
ISSN:1443-9506
1444-2892
DOI:10.1016/j.hlc.2007.07.001