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This report describes the case of a 51-year-old man with myocardial ischemia resulting from in-stent restenosis of the left anterior descending coronary artery who underwent a minimally invasive direct coronary artery bypass using thoracic epidural analgesia while awake, without general endotracheal anesthesia.

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The intraluminal elastase perfusion model has been proven to be potentially effective in producing abdominal aortic aneurysms (AAA) in rodents, yet has produced unpredictable results in larger animals. The purpose of this study was to explore different variations to an existing elastase perfusion model in the dog in the hopes of producing a consistent AAA for endovascular graft validation. The elastase perfusion canine model was modified as follows: (1) inflation of a balloon catheter in the infrarenal aorta (IA) of 3 dogs following elastase perfusion with doses of 2800 U for 40 min; (2) perfusion of the IA of 5 dogs with various elastase doses ranging from 2800 U to 8400 U for 2 h; and (3) perfusion of the IA of 2 dogs with elastase and collagenase for 2 h. The dogs were sacrificed at 4, 7, and 29 weeks. Prior to sacrifice, the treated aortic segments were either examined in vivo by x-ray angiography or by ultrasonography to measure aneurysmal dilation. The aortas were examined macroscopically postmortem to assess the luminal surface characteristics, and under light microscopy and scanning electron microscopy to reveal any pathological injuries induced by the various treatments on the aortic wall. Perfusion of the aorta with 2800 U elastase for 40 min followed by balloon catheter inflation either immediately or 3 weeks after perfusion produced no dilation. Perfusion for 2 h with either elastase alone or in combination with collagenase showed an increased aortic diameter averaging 65.6+/-20.8%, with an irregular dilation of the aortic wall. Histological examination revealed partially digested elastic network of the intima, media, and adventitia, as well as a reduction in the number of smooth muscle cells. An intimal hyperplasic reaction was observed in some of the dogs. Located sparingly within the intima were extravasated erythrocytes associated with recent hemorrhages, intramural thrombi in reorganization, and occasional necrotic lesions. The various modifications brought to the elastase perfusion model failed to produced an aneurysmal dilation with enough expansion to make it a reliable model for endovascular graft validation.

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OBJECTIVE: To assess the short- and long-term outcomes of vena cava filter (VCF) placement for prophylaxis against pulmonary embolism in patients at high risk due to trauma. DESIGN AND SETTING: Case series at a level I trauma center. PATIENTS: Patients were considered for prophylactic VCF placement if they met 1 of the injury criteria--spinal cord injuries with neurologic deficit, severe fractures of the pelvis or long bone (or both), and severe head injury--and had a contraindication to anticoagulation. INTERVENTION: Vena cava filters were placed percutaneously by the interventional radiologists when the acute trauma condition was stabilized following admission. MAIN OUTCOME MEASURES: Filter tilt of 14 degrees or more, strut malposition, insertion-related deep vein thrombosis, pulmonary embolism, or inferior vena cava patency. RESULTS: There were 132 prophylactic VCFs placed. A 3.1% rate of insertion-related deep vein thrombosis occurred, all of which were asymptomatic. Filter tilt occurred in 5.5% of patients and strut malposition in 38%. Three cases of pulmonary embolism (1 fatal) occurred in a prophylactic VCF, and all patients had either filter tilt or strut malposition. The risk of pulmonary embolism developing was higher in those patients with filter tilt or strut malposition than in those who did not have these complications (6.3% vs 0%; P=.05; Fisher exact test). The 1-, 2-, and 3-year inferior vena cava patency rates (+/-SD) were 97%+/-3%. CONCLUSIONS: Prophylactic VCF can be placed safely with an acceptable rate of insertion-related deep vein thrombosis and long-term inferior vena cava patency. Patients with prophylactic VCF remain at risk for pulmonary embolism if the filter is tilted 14 degrees or more or has strut malposition. In such patients, consideration should be given to placing a second filter.

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PURPOSE: Inflammation has been implicated as a contributing factor in the expansion of abdominal aortic aneurysms (AAA). To test this hypothesis, we examined the effects of a monoclonal antibody (MAB) to the leukocyte CD18 adhesion molecule on the expansion of experimental AAA. METHODS: Aneurysms were induced by perfusion of an isolated segment of the infrarenal aorta with elastase in 22 normotensive (WKY) and 17 genetically hypertensive (WKHT) rats. Animals of both strains were randomly allocated to control or MAB-treated groups (MAB, 5 microgram/100 gm body weight intraperitoneally, daily, beginning on the operative day for a total of four doses). The activity of the MAB against rat leukocytes had first been determined by in vitro immunofluorescence flow cytometry. Aortic size was directly measured initially and on day 14. At that time, a segment of aorta was stained with hematoxylin and eosin and mononuclear leukocytes and neutrophils were counted in each of 10 microscopic fields (400X). RESULTS: The initial aortic size in all animals was 1.11+/-0.15 mm. All groups developed aneurysms significantly larger than the initial aortic size (p<0.01). However, the MAB-treated animals had significantly smaller aneurysms than the untreated controls (mm): WKY: 3.63+/-1.26, WKY-MAB: 2.08+/-0.30, WKHT: 4.54+/-1.86, WKHT-MAB: 2.37+/-0.40, p<0.0001. There also were significantly fewer monocytes in the MAB-treated normotensive rats: WKY:35.5+/-29.9, WKHT:40.6+/-28.8, WKY-MAB: 8.9+/-8.5, WKHT-MAB: 32.3+/-25.7, p=0.03. Neutrophil counts did not differ significantly between the groups. CONCLUSIONS: Treatment with anti-CD18 monoclonal antibody slows the expansion of AAA in this experimental model. The associated inflammatory process at day 14, as indicated by monocyte infiltration, is reduced, but this effect may be opposed by the presence of hypertension. Further evaluation of the role of leukocytes and adhesion molecules in the expansion of AAA is warranted.

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To examine the role of peptide in alloreactive class II MHC-restricted responses, we transfected I-A molecules into the Ag-processing defective mutant cell line, T2. Consistent with their defective Ag-processing phenotype, the T2 transfectants predominantly express SDS-unstable I-A molecules on their surface. These cells and phenotypically normal APCs were used to study primary and secondary alloreactive T cell responses in limiting dilution assays. The results demonstrate that the majority of CD4 T cells that participate in primary alloresponses and essentially all the CD4 T cells that participate in secondary alloresponses recognize I-A conformers that depend on the presence of peptide and do not recognize the SDS-unstable I-A expressed by T2 transfectants. To further investigate the requirement for peptide in these responses, we incubated the T2 transfectants with E alpha 52-68 peptide and generated SDS-stable I-A-peptide complexes on the cell surface. The I-Ab-E alpha peptide complexes expressed on T2 cells are stimulatory in secondary alloresponses if the T cells were exposed to the same I-A peptide complex during the priming step. These studies demonstrate that peptide-containing class II MHC is the relevant ligand for alloreactive T cells, and identify an alloreactive response to a peptide (E alpha 52-68) derived from a highly expressed cell surface "self" Ag, the I-E molecule.

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