Perioperative stroke and death with CEA + IPE are substantial and consistent across centers. It is strikingly different from isolated CEA or CEA added to open brachiocephalic reconstruction. Restenosis is frequent, and reintervention at either the proximal stent or bifurcation is common. This technical strategy should be used cautiously and selectively reserved for those who are symptomatic with hemodynamically relevant tandem lesions and unfit for open revascularization.

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Results: Rapamycin reduced AVF wall thickness at days 7 and 21 (P < .05; n ¼ 6) with no change in AVF diameter (P ¼ .5). Rapamycin decreased the proliferation rate of smooth muscle cells (SMCs) and macrophages (P < .05), with reduced M1 (inducible nitric oxide synthase, tumor necrosis factor a) and M2 (interleukin 10, CD206) macrophages at days 3 and 7 (P < .05). Rapamycin treatment was associated with diminished phosphorylation of Akt1 and the mTORC1 pathway members mTOR (Ser2481), 4EBP1, and p70S6K (P < .05; n ¼6) but not of the mTORC2 pathway members mTOR (Ser2448) and serum and glucocorticoid-regulated kinase 1 (P > .4). With rapamycin treatment, there was decreased p-Akt1 and p-mTORC1 intensity in SMCs and macrophages at days 3, 7, and 21 (P < .05). There was also reduced p-endothelial nitric oxide synthase intensity in SMCs but not in endothelial cells. After depletion of macrophages with clodronate liposomes, there was reduced wall thickness (P < .01, day 21), SMC proliferation, and p-mTORC1 intensity in SMCs (P ¼ .001); however, AVF patency was reduced (P < .05). Rapamycin improved AVF patency by day 42 (P ¼ .04; n ¼ 14); these AVFs showed less thickening (P < .05) and had similar p-Akt1 and p-mTORC1 intensity in macrophages compared with control (P > .5). However, rapamycin treatment initiated after day 21 did not improve patency (P ¼ .62). Conclusions: Rapamycin improves AVF patency by reducing early inflammation and wall thickening while attenuating the Akt1-mTORC1 signaling pathway in SMCs and macrophages. Macrophages are associated with AVF wall thickening, and M2-type macrophages may play a mechanistic role in AVF maturation. Rapamycin is a potential translational strategy to improve AVF patency. Objective: Current arteriovenous grafts (AVGs) have unacceptably high failure rates. This issue led to the development of tissue-engineered vascular grafts in an attempt to mimic a native blood vessel. We hypothesized that a novel synthetic vascular graft could be developed using electrospinning technology that functions as scaffolding for cell ingrowth, thereby providing the added natural protection of native cells against thrombosis and infection. The resulting graft would also maintain e44 Abstracts

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