Flomenbaum M A, Schoen F J
Department of Pathology, Brigham and Women's Hospital, Boston, MA 02115.
J Thorac Cardiovasc Surg. 1993 Jan;105(1):154-64.
Calcification frequently causes failure of porcine aortic valve bioprostheses; changes in collagen configuration induced by high-back-pressure fixation have deleterious effects on porcine aortic valve mechanics. Although modified porcine aortic valve bioprostheses that include the use of lower-pressure fixation and antimineralization treatments are used clinically, the morphologic characteristics of these valves are not known. We evaluated, by light and scanning and transmission electron microscopy, the comparative structural details of clinically processed Hancock Standard (no antimineralization treatment, 80 mm Hg fixation), Hancock II (T-6 antimineralization treatment, fixed initially at 1.5 mm Hg, then 80 mm Hg) and Intact (toluidine blue antimineralization treatment, zero-pressure-fixed [0 mm Hg]) porcine aortic valve bioprostheses as well as true low-pressure (1.5 mm Hg) fixed valves, zero-pressure-fixed porcine aortic valves (with no further treatment), and freshly fixed porcine aortic valve cusps as controls. Commercially processed valves had near-complete loss of endothelium and amorphous extracellular matrix and autolytic changes in the cuspal connective tissue cells. Both 80 and 1.5/80 mm Hg fixed valves, but not zero-pressure-fixed cusps (Intact valves, zero-pressure-fixed porcine aortic valves or immediately fixed porcine aortic valve cusps), had overall flattening and compression with near-complete loss of transverse cuspal ridges and collagen crimp; valves fixed at 1.5 mm Hg had intermediate features. T-6 and toluidine blue treatments induced no definite incremental microscopic changes attributable to the antimineralization treatment. No degenerative changes in collagen were noted in any valves that underwent antimineralization treatment. These studies indicate that valves fixed at zero but not at 80 or 1.5/80 mm Hg pressure retain collagen architecture virtually identical to that of relaxed native porcine aortic valve cusps and that the antimineralization treatments studied do not adversely affect collagen morphology.
钙化常常导致猪主动脉瓣生物假体失效;高背压固定引起的胶原结构变化对猪主动脉瓣力学性能具有有害影响。尽管临床上使用了包括采用较低压力固定和抗矿化处理的改良猪主动脉瓣生物假体,但这些瓣膜的形态学特征尚不清楚。我们通过光学显微镜、扫描电子显微镜和透射电子显微镜,评估了临床处理的汉考克标准型(未进行抗矿化处理,80 mmHg固定)、汉考克二代(T - 6抗矿化处理,最初在1.5 mmHg下固定,然后在80 mmHg下固定)和完整型(甲苯胺蓝抗矿化处理,零压力固定[0 mmHg])猪主动脉瓣生物假体以及真正的低压(1.5 mmHg)固定瓣膜、零压力固定猪主动脉瓣(未进一步处理)和新鲜固定的猪主动脉瓣尖作为对照的比较结构细节。商业化处理的瓣膜内皮几乎完全丧失,细胞外基质呈无定形,瓣尖结缔组织细胞出现自溶变化。80 mmHg和1.5/80 mmHg固定的瓣膜,但零压力固定的瓣尖(完整型瓣膜、零压力固定猪主动脉瓣或立即固定的猪主动脉瓣尖)没有,出现了整体变平和压缩,横向瓣尖嵴和胶原卷曲几乎完全丧失;在1.5 mmHg下固定的瓣膜具有中间特征。T - 6和甲苯胺蓝处理未引起可归因于抗矿化处理的明确的微观变化增加。在任何接受抗矿化处理的瓣膜中均未观察到胶原的退行性变化。这些研究表明,在零压力而非80 mmHg或1.5/80 mmHg压力下固定的瓣膜保留了与松弛的天然猪主动脉瓣尖几乎相同的胶原结构,并且所研究的抗矿化处理不会对胶原形态产生不利影响。