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Replacement of the abdominal aorta, whether by autogenous or prosthetic conduit, has been an a priori requisite in the vascular surgeon's armamentarium since its technical feasibility was described in the early 1950s. The Achilles' heel of this operation, in spite of the progress made over the last half century, is still, however, aortic graft infection. Though survival and limb salvage rates have improved over time-commensurate with advances in surgical technique, critical care, and antimicrobial agents-the prevention and treatment of aortic graft infection remains a formidable challenge to the vascular surgeon. The authors herein review the current literature on this topic with an emphasis on the surgical management options available and suggest an individualized operative strategy based on patient as well as microbial factors to attain the best possible outcome.

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Myointimal hyperplasia (MIH) after vascular intervention is a major problem. Recent reports describing elimination of within-stent restenosis by means of rapamycin-eluting stents prompted us to examine the effect of systemic oral rapamycin on MIH induced by arterial trauma. We studied the effect of oral rapamycin on MIH after rabbit aorta balloon injury. Thirty-five New Zealand white rabbits (2.5-3 kg) had aortic injury and were given either no rapamycin (control), 0.1 (low dose) rapamycin mg/kg/day, or 0.4 mg/kg/day (high dose). Rapamycin was started 1 week before injury and continued for 3 (4 weeks total) or 6 weeks (7 weeks total) post-injury. Sections were analyzed to measure aortic intima/media area ratios (I:M) at either 3 or 6 weeks. At 3 weeks, the I:M (mean ± SD) for controls was 0.53 ± 0.1; for low dose, 0.17 ± 0.13; and for high dose, 0.24 ± 0.07 (p < 0.001 vs. control). At 6 weeks, the I:M for controls was 0.52 ± 0.12; for low dose-4 weeks, 0.29 ± 0.15; low dose-7 weeks, 0.33 ± 0.07; and high dose-4 weeks, 0.47 ± 0.16. At 6 weeks only the difference between the low dose-4 weeks and control I:M ratios was significant (p = 0.018). The results confirm earlier studies showing that systemic rapamycin inhibits MIH after arterial injury when drug therapy is started before injury. Therapy for 3 or 6 weeks after injury yields similar inhibition, indicating that exposure to the drug early in the response to injury is more important than prolonged exposure. We observed a paradoxical relation between dose and degree of MIH inhibition, with the low dose being more effective than the high dose at both time intervals studied. Overall, the results suggest that oral rapamycin therapy might be a useful adjunct to clinical interventions at risk for development of MIH.