Polyvinylidene fluoride (PVDF) represents an attractive alternative to polypropylene as a monofilament vascular suture because of its satisfactory physicochemical properties, it ease of handling, and its good biocompatibility. However, the polymer's ability to remain mechanically and chemically stable when exposed to a mild hydrolytic environment over the long term has yet to be demonstrated. One in vitro study involved the comparison of the long-term relative resistance of PVDF and polypropylene sutures to hydrolysis for a period of 9 years. The PVDF suture showed major molecular rearrangements from the original ratio of three crystalline structures to the single beta crystalline phase. The observation of some surface oxidation and water inhibition did not significantly modify the tensile strength of the PVDF suture, which retained 92.5% of its original value. In contrast, the polypropylene sample did not undergo any recrystallization but was associated with more oxidation byproducts and more water molecules near the surface, which contributed to a 46.6% loss in initial tensile strength. An in vivo study confirmed that PVDF sutures are biocompatible and are able to maintain satisfactory biostability when used to anastomose thoracic aortic allografts for a period of 6 months in the dog. The cellular reaction of fresh allografts as well as the control autografts to PVDF sutures was minimal. In other allografts that had been preserved in a supplemented medium for 1 week prior to implantation, the PVDF sutures healed satisfactorily with the formation of neocollagen and few macrophages surrounding the monofilament. No evidence of instability at the allograft-host artery junction was observed, confirming that the PVDF sutures were able to ensure a secure anastomosis in the thoracic aorta. PVDF sutures have demonstrated superior long-term biostability in vitro and minimal tissue response in vivo. These are two essential requirements when evaluating the use of a suture for vascular surgery in general and thoracic aortic surgery in particular.
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.
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