Neointimal hyperplasia, vein graft remodeling, and long-term patency

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Neointimal hyperplasia, vein graft remodeling, and long-term patency.

NEOINTIMAL HYPERPLASIA is generally considered as the major cause of vein graft stenosis and is the leading pathological sign of vein graft disease. Most research on this problem has focused on the inhibition of neointimal growth, based on the hypothesis that the inhibition of neointimal hyperplasia would improve long-term patency of the vein graft. However, the inhibition of cell proliferation...

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Perivascular mast cells regulate vein graft neointimal formation and remodeling

Objective. Emerging evidence suggests an important role for mast cells in vein graft failure. This study addressed the hypothesis that perivascular mast cells regulate in situ vascular inflammatory and proliferative responses and subsequent vein graft neointimal lesion formation, using an optimized local mast cell reconstitution method. Methods and Results. Neointimal hyperplasia was induced by...

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Understanding saphenous vein graft patency.

Saphenous vein was the conduit used in the first series of coronary surgery, and, with the exception of revascularization of the left anterior descending coronary artery, it remains the most commonly used conduit.1 There are several reasons for this. First, because of its relatively large diameter and wall characteristics, it is technically easy to use; second, it is plentiful, and therefore ca...

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Locally applied cilostazol suppresses neointimal hyperplasia and medial thickening in a vein graft model.

BACKGROUND Pathological changes in vein grafts begin immediately after arterial circulation is applied to the grafts. Chemical mediator stimulation and mechanical strain induce neointimal hyperplasia and medial thickening of the vein grafts, resulting in their failure. We investigated the inhibitory effect of locally applied cilostazol, an inhibitor of cyclic adenosine monophosphate phosphodies...

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ژورنال

عنوان ژورنال: American Journal of Physiology-Heart and Circulatory Physiology

سال: 2009

ISSN: 0363-6135,1522-1539

DOI: 10.1152/ajpheart.00703.2009