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TOWARDS A MECHANISM FOR BIOPROSTHETIC VALVE FAILURE

机译:朝着生物假杆瓣膜破坏的机制

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Porcine bioprosthetic valves are commonly used to replace the native cardiac valves when they become diseased and dysfunctional. One class of bioprosthesis consists of whole pig aortic valves, tanned in glutaraldehyde and mounted on plastic or wire frames. These devices work very well in the short term (<5 years) but eventually begin to fail gradually and typically do not last more than 15 years (1). Many have tried to elucidate a mechanism of bioprosthetic valve failure, but little progress has been made, until recently. Historically, calcification has been thought to be the primary mechanism of bioprosthetic valve failure (2). Recently, however, it has become recognized that mechanical damage to bioprosthetic valves can occur independently from calcification (3). This shift in opinion has been supported by a number of observations. For example, Purinya et. al. (4) have shown that after four years of implantation, bioprosthetic valve explants have lower failure stresses and fail at greater strains than fresh porcine bioprostheses. Similar observations have been made in valves fatigued in vitro (5). Others have shown that these mechanical changes are accompanied by biochemical changes in the collagen fibers (6). We have shown previously in preliminary studies that glycosaminoglycans (GAGs) are lost from implanted bioprosthetic valves (7). Since GAGs are responsible for maintaining tissue viscoelasticity, loss of GAGs would have detrimental effects on tissue mechanics. In separate studies, we have demonstrated that damage to elastin can also have detrimental effects on tissue mechanics, and on valve durability as a whole (8). The objectives of the current study were to relate these previous findings to a more detailed survey of the mechanical properties of explanted bioprosthetic valves, in order to better clarify the likely mechanisms of bioprosthetic valve failure. We were specifically interested in determining how the mechanical changes could be explained by changes in valve tissue chemistry, particularly, the GAG content.
机译:猪生物假体瓣膜通常用于在患病和功能失调时更换天然心阀。一类生物假期由整个猪主动脉瓣组成,鞣制在戊二醛鞣制,并安装在塑料或电线框架上。这些设备在短期内工作非常好(<5年),但最终开始逐步失败,通常不会超过15年(1)。许多人试图阐明生物保护阀失效的机制,但在最近的进展情况下已经很少。从历史上看,已经认为钙化是生物假体瓣膜破坏的主要机制(2)。然而,最近,已经认识到,对生物保护阀的机械损伤可以独立于钙化(3)。这一转变已经得到了许多观察结果。例如,Purinya等。 al。 (4)表明,经过四年的植入后,生物假体瓣膜外植体具有较低的衰竭应力,并且比新鲜的猪生物原植更大的菌株。在体外疲劳(5)的阀门中已经进行了类似的观察结果。其他人表明,这些机械变化伴随着胶原纤维(6)的生化变化。我们之前在初步研究中显示,糖胺聚糖(GAG)损失植入的生物假体瓣膜(7)。由于GAG负责维持组织粘弹性,因此GAG的丧失对组织力学产生不利影响。在单独的研究中,我们已经证明,对弹性蛋白的损害也可能对组织力学的有害影响以及整体(8)的阀门耐久性。目前研究的目的是将这些先前的发现与进出型生物假体阀的机械性能进行了更详细的调查,以便更好地阐明了生物抑制瓣膜破坏的可能机制。我们专门对确定机械变化如何通过瓣膜组织化学的变化来解释机械变化,特别是GAG含量。

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