Tamura K, Fukuda Y, Ishizaki M, Masuda Y, Yamanaka N, Ferrans V J
Department of Pathology, Nippon Medical School, Tokyo, Japan.
Am Heart J. 1995 Jun;129(6):1149-58. doi: 10.1016/0002-8703(95)90397-6.
Histologic, immunohistochemical, and ultrastructural studies were performed on 12 floppy mitral valves, 4 mitral valves showing focal myxomatous changes without prolapse, and 3 normal mitral valves. All floppy mitral valves were thickened by deposits of proteoglycans and also showed diverse structural abnormalities in collagen and elastic fibers. From these observations we conclude that (1) the structure of all major components of connective tissue in floppy mitral valves is abnormal; (2) alterations in collagen and accumulations of proteoglycans are nonspecific changes that may be caused by the abnormal mechanical forces to which floppy mitral valves are subjected because of their excessively large surface area; (3) the presence of excessive amounts of proteoglycans may interfere with the normal assembly of collagen and elastic fibers; (4) abnormalities of elastic fibers resemble those in other conditions characterized by structural dilatation or tissue expansion; and (5) alterations in elastin could result from defective formation, increased degradation, or both.
对12个松弛二尖瓣、4个显示局灶性黏液瘤样改变但无脱垂的二尖瓣以及3个正常二尖瓣进行了组织学、免疫组织化学和超微结构研究。所有松弛二尖瓣均因蛋白聚糖沉积而增厚，并且在胶原纤维和弹性纤维中还显示出多种结构异常。从这些观察结果我们得出结论：（1）松弛二尖瓣中结缔组织所有主要成分的结构均异常；（2）胶原改变和蛋白聚糖积聚是非特异性变化，可能是由于松弛二尖瓣因其过大的表面积而承受的异常机械力所致；（3）过量蛋白聚糖的存在可能会干扰胶原纤维和弹性纤维的正常组装；（4）弹性纤维异常类似于其他以结构扩张或组织膨胀为特征的情况；（5）弹性蛋白的改变可能是由于形成缺陷、降解增加或两者兼而有之。
