We tested the hypothesis that oxidized low-density lipoprotein (oxLDL)-induced inactivation of Akt within endothelial progenitor cells (EPCs) is mediated at the level of Phosphoinositide 3-kinase (PI3K), specifically by nitrosylation of the p85 subunit of PI3K, and that this action is critical in provoking oxLDL-induced EPC apoptosis. Hypercholesterolemic ApoE null mice had a significant reduction of the phosphorylated Akt (p-Akt)/Akt ratio in EPCs, as well as a greater percentage of apoptosis in these cells than EPCs isolated from wild-type (WT) C57Bl/6 mice. EPCs were isolated from WT spleen and exposed to oxLDL in vitro. oxLDL increased O₂^– and H₂O₂ in these cells and induced a dose- and time-dependent reduction in the p-Akt/Akt ratio and increase in EPC apoptosis. These effects were significantly reduced by the antioxidants superoxide dismutase, L-NAME, epicatechin and FeTPPs. oxLDL also induced nitrosylation of the p85 subunit of PI3K and subsequent dissociation of the p85 and p110 subunits, an effect significantly reduced by all the antioxidant agents tested. EPC transfection with a constitutively active Akt isoform (Ad-myrAkt) significantly reduced oxLDL-induced apoptosis of WT EPCs. The present findings indicate that oxLDL disrupts the PI3K/Akt signaling pathway at the level of p85 in EPCs. This dysfunction can be reversed by ex vivo antioxidant therapy.

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We present the case report of a Staphylococcus hominis carotid artery plaque infection, without mycotic aneurysm formation, that provided the nidus for septic embolization. The patient presented with transient neurologic symptoms, with no clinical signs or symptoms of sepsis. Multiple preoperative imaging modalities revealed critical carotid stenosis but no indication of an infection. Secondary carotid infection was discovered incidentally intraoperatively, and carotid reconstruction was completed with autogenous tissue. The patient transiently manifested sepsis only after the carotid reconstruction and recovered with the institution of parenteral antibiotics.

aneurysm was present in 20 patients (67%), ranging in size from 2.6-9.6 cm. The most common repair was resection of aortic coarctation with interposition graft replacement (n ϭ 26). Other repairs included bypass from proximal descending thoracic aorta to the infrarenal aorta (n ϭ 2); and ascending, arch, and proximal descending aortic replacement via median sternotomy (n ϭ 2). Complications occurred in 7 patients (23%), including chylous effusion (n ϭ 2), recurrent laryngeal nerve injury (n ϭ 1), acute renal failure (n ϭ 1), respiratory failure (n ϭ 1), atrial fibrillation (n ϭ 1), and urinary tract infection (n ϭ 1). In-hospital mortality was 0%. There were no cases of immediate or delayed neurologic deficit. Death occurred in 3 patients during follow-up (mean 19 months, range 1-231); none were related to coarctation repair. One patient (3%) required reoperation 6 years later due to aneurysm formation distal to the initial repair.Conclusions: Open repair of adult aortic coarctation has acceptable morbidity, low mortality, and excellent durability.