—Intimal hyperplasia after vascular injury is usually studied in animal models with healthy, normocholesterolemic animals. Here, we assess the effect of diet-induced hypercholesterolemia on the induction of intimal hyperplasia in ApoE*3Leiden mice. A nonconstrictive polyethylene cuff was placed around the femoral artery of ApoE3*Leiden mice fed a highly cholesterol-rich diet, a mildly cholesterol-rich diet, or a chow diet for 4 weeks. Diets were continued after cuff placement until euthanization. At several time points (1 to 14 days), mice were euthanized and the intimal hyperplasia in the cuffed arteries was analyzed. In mice fed a chow diet, a 2- to 4-cell-layer–thick intima, predominantly consisting of α smooth muscle cell actin–positive cells, was observed after 14 days. A mildly cholesterol-rich diet (mean plasma-cholesterol level, 10.5 mmol/L) resulted in a 2.7-fold increase of total intimal area, and a highly cholesterol-rich diet (mean plasma cholesterol level 28.6 mmol/L), in a 7.8-fold increase. In the high-cholesterol group, the intima consisted predominantly of lipid-loaded foam cells and α smooth muscle cell actin–positive cells. Foam cell accumulation could be observed by as early as 3 days, resulting in a near-total occlusion of the lumen after 14 days. Hypercholesterolemia resulted in a rapid, cholesterol-dependent induction of foam cell–rich intimal hyperplasia in cuffed femoral arteries of ApoE*3Leiden mice. In conclusion, the present data show that the combination of a local (cuff placement) and a systemic (hypercholesterolemic) risk factor of atherosclerosis results in a rapid induction (within 14 days) of atherosclerotic-like lesions in ApoE*3Leiden mice.

Abstract-Therapeutic angiogenesis using vascular endothelial growth factor (

Initial and short-term results of FEVAR using the fenestrated Anaconda endograft are promising, with acceptable technical success and short-term complication rates. Growing experience and long-term results are needed to support these findings.

Abstract-Vein grafts fail due to development of intimal hyperplasia and accelerated atherosclerosis. Many murine genetic models in which genes are overexpressed, deleted, or mutated have been introduced recently. Therefore, mouse models are very well suited to dissect the relative contribution of different genes in the development of accelerated atherosclerosis. In the present study, we evaluated whether accelerated atherosclerosis in human vein grafts could be mimicked in hypercholesterolemic APOE*3 Leiden transgenic mice. Venous bypass grafting was performed in the carotid artery in APOE*3 Leiden mice fed either a standard chow diet or a high cholesterol-rich diet for 4 weeks. At several time points (0 hour to 28 days), mice were euthanized and the morphology of the vein grafts was analyzed. In normocholesterolemic mice, vein graft thickening up to 10-fold original thickness, predominantly consisting of ␣-smooth muscle cell actin-positive cells, was observed after 28 days. In hypercholesterolemic mice, accelerated atherosclerosis with accumulation of lipid-loaded foam cells was observed within 7 days after surgery. This accelerated atherosclerosis progressed in time and resulted in significant increase in vein graft thickening up to 50 times original thickness with foam cell-rich lesions and calcification within 28 days after surgery.

Objective-Vein grafts fail because of the development of intimal hyperplasia and accelerated atherosclerosis. Placement of an external stent around vein grafts resulted in an inhibition of intimal hyperplasia in several animal studies. Here, we assess the effects of external stenting on accelerated atherosclerosis in early vein grafts in carotid arteries in hypercholesterolemic apolipoprotein E*3-Leiden transgenic mice. Methods and Results-Venous interposition grafting was performed in apolipoprotein E*3-Leiden mice fed standard chow or a highly cholesterol-rich diet for 4 weeks. After engraftment, external stents with different inner diameters (0.4 or 0.8 mm) were placed. In unstented vein grafts in hypercholesterolemic mice, thickening up to 50 times the original thickness, with foam cell-rich lesions, calcification, and necrosis, was observed within 28 days. Key Words: atherosclerosis Ⅲ vein grafting Ⅲ external stent Ⅲ transgenic mice V ein bypass grafting remains the most common method of vascular reconstruction for bypassing obstructive arterial lesions. 1 However, aorta-coronary and peripheral vein grafts are known to have a high failure rate: 10% to 40% after 1 year and 50% to 60% after 10 years. 2 These vein grafts undergo early intimal thickening and accelerated atherosclerosis, 3-6 both of which may contribute to eventual graft failure.In patients with angiographic evidence of occlusive disease after vein grafting, atherosclerotic lesions within the graft have been demonstrated as early as 6 to 12 months after surgery. 3,4,6,7 Vein graft atherosclerotic lesions are more diffuse, concentric, and friable with a poorly developed or absent fibrous cap, whereas native vessel atheroma are proximal, focally eccentric, and nonfriable with a welldeveloped fibrous cap. 8,9 Also, compared with native atherosclerotic lesions, accelerated atherosclerotic lesions in vein grafts contain more foam cells with varying degrees of lipid accumulation and macrophage/mononuclear and inflammatory cell infiltration. 10 Compared with atherosclerosis in native arteries, this accelerated atherosclerosis in vein grafts progresses more rapidly. 11,12 Recently, Dietrich et al 13 described the fast initiation of accelerated atherosclerosis in vein grafts in hypercholesterolemic transgenic mice with the use of the very elegant, recently described technique of placing a venous interposition in the mouse carotid artery. 14 The atherosclerotic lesions observed in these murine grafts show high morphological resemblance to lesions observed in human vein grafts.A reduction of vein graft thickening or, more precisely, a reduction of neointimal thickening in vein grafts in various animal models was achieved by external stenting of grafted veins, 15-18 yielding decreased smooth muscle cell (SMC) proliferation. However, in none of these studies was the effect of external stenting on accelerated atherosclerosis in grafts determined.In the present study, we investigate the effect of external stenting on accelerated atherosclerosis, monitored as a...

Nonambulatory patients suffer from extensive comorbid conditions. They are accompanied with an increased occurrence of AEs, unplanned reinterventions, and poor long-term survival rates. Successful LEAR did not improve their functional status after 6 years. This emphasizes that attempts for limb salvage must be carefully considered in these patients.

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The new protocol outlined in a bimonthly multidisciplinary meeting for vascular access surgery of AVFs/AVGs for hemodialysis resulted in more effective logistics according to preoperative diagnostics and operation. More importantly, a significant increase in endovascular balloon angioplasties and a significant decrease in surgical revisions was observed, resulting in less patient morbidity. Also, higher primary and secondary patency was achieved after the introduction of the new optimized care protocol.