Mechanisms of bioprosthetic heart valve failure: fatigue causes collagen denaturation and glycosaminoglycan loss.
Mechanisms of bioprosthetic heart valve failure: fatigue causes collagen denaturation and glycosaminoglycan loss.
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DOI：
10.1002/(sici)1097-4636(199907)46:1
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发表时间：
1999-07
期刊：
影响因子：
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通讯作者：
N. Vyavahare;M. Ogle;F. Schoen;R. Zand;D. Gloeckner;M. Sacks;R. Levy
中科院分区：
文献类型：
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作者：
N. Vyavahare;M. Ogle;F. Schoen;R. Zand;D. Gloeckner;M. Sacks;R. Levy
生物假体心脏瓣膜（BPHV）变性以细胞外基质恶化、重塑和钙化为特征，是一个重要的临床问题，每年导致数千例手术。在这里，我们首次报道，在一系列使用戊二醛固定猪主动脉瓣生物假体的体外加速疲劳研究（5-5亿次循环）中，通过傅里叶变换红外光谱（FTIR）评估，心脏瓣膜尖瓣的机械功能对 I 型胶原蛋白的分子结构造成了渐进性损伤。循环疲劳导致生物假体尖端胶原蛋白的螺旋性逐渐丧失，这从酰胺 I 羰基拉伸区域的 FTIR 光谱变化中可以明显看出。此外，这些研究中的心脏瓣膜疲劳还导致尖部细胞外基质中糖胺聚糖（GAG）的损失。戊二醛交联的猪主动脉瓣尖瓣中的GAG水平对于对照为65.2+/-8.66微克糖醛酸/10毫克干重，对于10-3亿个循环尖瓣而言为7.91+/-1.1微克糖醛酸/10毫克干重。总之，这些分子变化导致尖端弯曲强度显着逐渐降低，如测量三点变形的生物力学弯曲测定中所记录的那样。我们得出的结论是，疲劳引起的 I 型胶原损伤和 GAG 损失是生物假体心脏瓣膜材料退化的主要影响因素。
Bioprosthetic heart valve (BPHV) degeneration, characterized by extracellular matrix deterioration, remodeling, and calcification, is an important clinical problem accounting for thousands of surgeries annually. Here we report for the first time, in a series of in vitro accelerated fatigue studies (5-500 million cycles) with glutaraldehyde fixed porcine aortic valve bioprostheses, that the mechanical function of cardiac valve cusps caused progressive damage to the molecular structure of type I collagen as assessed by Fourier transform IR spectroscopy (FTIR). The cyclic fatigue caused a progressive loss of helicity of the bioprosthetic cuspal collagen, which was evident from FTIR spectral changes in the amide I carbonyl stretching region. Furthermore, cardiac valve fatigue in these studies also led to loss of glycosaminoglycans (GAGs) from the cuspal extracellular matrix. The GAG levels in glutaraldehyde crosslinked porcine aortic valve cusps were 65.2 +/- 8.66 microg uronic acid/10 mg of dry weight for control and 7.91 +/- 1.1 microg uronic acid/10 mg of dry weight for 10-300 million cycled cusps. Together, these molecular changes contribute to a significant gradual decrease in cuspal bending strength as documented in a biomechanical bending assay measuring three point deformation. We conclude that fatigue-induced damage to type I collagen and loss of GAGs are major contributing factors to material degeneration in bioprosthetic cardiac valve deterioration.