This short-term in vivo study of a nitinol-polyester self-expanding endograft demonstrated the effective exclusion of thoracic aneurysms with a satisfactory healing response and no excessive tissue or inflammatory reactions.
The intraluminal elastase perfusion model has been proved to be potentially effective in producing abdominal aortic aneurysm in rodents, but it produced unpredictable results in larger animals. The purpose of this study was to explore the potential ability of such a model to produce experimental aneurysm consistently in the Yucatán miniature swine. Six Yucatán miniature swine received infusion with porcine elastase into an isolated segment of the infrarenal aorta. The excised arterial segments were examined macroscopically to assess the luminal surface characteristics and histologically to describe the different pathologic injuries induced by the elastase treatment on the intima, media, and adventitia of the arterial wall. Histologic examination revealed that the elastic network of the media was destroyed. In the first week after perfusion, altered smooth muscle cells were located in the intima and innermost layer of the media in juxtaposition with the occlusive thrombus. Infiltration of inflammatory cells was observed in these regions of elastic network and smooth muscle cell alterations. In the arterial segments of swine sustained for 3 weeks, a reduction of smooth muscle cells was noted in some areas. An important number of necrotic lesions was observed, and they were associated with the development of calcium deposits. Significant intimal hyperplasic reaction was identified at day 19 and again at day 21. However, no aneurysmal development was observed. This study constituted the first experiment with infusion of porcine elastase in the Yucatán miniature swine infrarenal aorta. The present experimental protocol induced important elastic network and smooth muscle cell alterations leading to severe necrotic lesions associated with calcium deposition, but it produced no aneurysmal dilatation. This model requires further testing to obtain a more complete degradation of the elastic network in both the media and adventitia and more significant collagenolysis without early thrombotic events.
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.
Purpose: Recent advances in magnetic resonance imaging (MRI) technology may provide a safer and more sensitive monitoring modality than X-ray imaging for endovascular surgical procedures. The purpose of this study was to investigate the feasibility of using MRI to monitor the insertion of endoprostheses. Methods: The endoprostheses we studied were composed of a nitinol stent encased in a polyester sheath. These were characterized with four different MRI techniques: the fast spin-echo; spin-echo; gradient-recalled echo; and the spoiled gradient-recalled echo. The deployment of the endoprosthesis into an artery was simulated in an in vitro model and viewed using a fast spin-echo MRI technique. Results: Image artifacts produced by the nitinol framework in these endoprostheses were minimal when fast spin-echo or spin-echo imaging techniques were used, improving the visibility of the device. In in vitro tests, the catheters and endoprostheses were visualized by MRI with sufficient clarity to guide the placement of a device in the model artery. Conclusions: Insertion of this type of endoprosthesis under interventional MRI guidance is feasible. The convenience and improved safety provided by interventional MR systems and “real-time” imaging capabilities are expected to make this technology an attractive alternative to X-ray imaging techniques.
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