Type I endoleaks represent a persistent risk of aneurysm rupture and should be treated promptly by endovascular means. Type II leaks are less dangerous and more difficult to treat, but coil embolization of feeding arteries may be warranted when leakage is associated with aneurysm enlargement.

Antioxidants have been proposed to be anti-atherosclerotic agents; however, the mechanisms underlying their beneficial effects are poorly understood. We have examined the effect of a-tocopherol (a-tcp) on one cellular event in atherosclerotic plaque development, monocyte adhesion to stimulated endothelial cells (ECs). Human umbilical vein ECs were pretreated with a-tcp before stimulation with known agonists of monocyte adhesion: IL-1 (10 ng/ml), LPS (10 ng/ ml), thrombin (30 U/ml), or PMA (10 nM). Agonist-induced monocytic cell adhesion, but not basal adhesion, was inhibited in a time-and concentration-dependent manner by atcp. The IC50 of a-tcp on an IL-i-induced response was 45 jpM. The inhibition correlated with a decrease in steady state levels of E-selectin mRNA and cell surface expression of E-selectin which is consistent with the ability of a monoclonal antibody to E-selectin to inhibit monocytic cell adhesion in this system. Probucol (50 ,uM) and N-acetylcysteine (20 mM) also inhibited agonist-induced monocytic cell adhesion; whereas, several other antioxidants had no significant effect. Protein kinase C (PKC) does not appear to play a role in the a-tcp effect since no suppression of phosphorylation of PKC substrates was observed. Activation of the transcription factor NF-cB is reported to be necessary but not sufficient for E-selectin expression in EC. Electrophoretic mobility shift assays failed to show an cr-tcp-induced decrease in activation of this transcription factor after cytokine stimulation. It has been hypothesized that ca-tcp acts as an anti-atherosclerotic molecule by inhibiting generation of oxidized LDL-a putative triggering molecule in the atherosclerotic process. Our results point to a novel alternative mechanism of action of a-tcp. (J. Clin. Invest. 1994. 94:592-600.)

Endovascular aneurysm repair is safe and effective in patients at high risk, for whom it may be the preferred method of treatment.

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The use of a fenestrated stent-graft is feasible, but the type of fenestration in this case has limited applicability owing to the rarity of patients with suitable anatomy.