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A postoperative superior mesenteric artery pseudoaneurysm that communicates with a pancreatic pseudocyst after aortic surgery is a difficult management problem. Untreated, this condition can lead to exsanguination. Traditional surgical treatment has many potential complications. Endovascular repair has the potential for avoidance of surgical complications. We present the first superior mesenteric artery pseudoaneurysm successfully treated with A polytetrafluorethylene covered stent.

Endoleaks were detected with helical computed tomographic (CT) angiography in five patients after placement of an aortobiliac stent-graft. The leaks were subsequently evaluated with duplex ultrasonography (US) and, in four patients, with conventional aortography as well. CT angiography revealed a total of seven endoleaks, all of which were prospectively classified as reconstitution (type II) leaks. Duplex US demonstrated six of the seven endoleaks. At duplex US, two of the leaks were characterized as attachment-site (type I) leaks; these two diagnoses were confirmed during subsequent angiography and profoundly altered clinical care. As an adjunct to CT angiography in evaluating endoleaks, duplex US provides hemodynamic information that enables further characterization of the type of endoleak and facilitates appropriate clinical care.

The objectives of the present study were to determine whether serum hypercholesterolemia (HC) promotes the development of spontaneous and angioplasty-induced lesions and whether amlodipine inhibits these lesions and cellular processes underlying their genesis. Rabbits were fed normal, 0.5%, or 2% cholesterol diets for 9 wk, which resulted in the development of increasing HC. After week one, balloon dilation of the abdominal aorta was performed while the thoracic aorta was not disturbed and monitored for the development of spontaneous lesions. Lesion size increased with the degree of HC and was accompanied by increased collagen synthesis and smooth muscle cell (SMC) proliferation at each site. Amlodipine (5 mg/kg p.o.) inhibited lesion size by 50% (P < 0.01) at both sites in cholesterol-fed animals but not at angioplasty sites in animals on a normal diet. Local collagen synthesis was inhibited at both sites by amlodipine in the diet animals. The increase in HC was accompanied by a 1.7-fold increase in basal Ca2+ uptake in SMCs in the thoracic aorta, which was not altered by amlodipine, nifedipine, Ni2+, or La3+, revealing an uninhibitable calcium leak during atherogenesis. In culture, cholesterol enrichment increased SMC proliferation, collagen synthesis, and the secretion of a soluble SMC mitogen, which were inhibited by amlodipine (10(-9) M). Finally, in SMC membranes, amlodipine uniquely restored the cholesterol-expanded membrane bilayer width without any effect on membrane fluidity. This study establishes a causal role between serum HC and the development of spontaneous and angioplasty-induced lesions and the ability of amlodipine to disrupt this action by a novel remodelling action on the SMC membrane.