Schwarz F, Kittstein D, Winkler B, Schaper J
Basic Res Cardiol. 1980 Jan-Feb;75(1):109-17. doi: 10.1007/BF02001402.
Light and electron microscopic morphometry was carried out in tissue samples which were obtained from the left ventricular free wall in 29 patients with chronic aortic valve disease during open-heart surgery. 6 patients had aortic stenosis, 9 had aortic insufficiency and 14 had a mixed aortic valve lesion. Hemodynamics were studied before operation. Patients with mixed aortic valve disease had a higher left ventricular mass, a lower ejection fraction and mean circumferential fiber shortening rate than patients with aortic stenosis. Peak systolic wall stress was comparable between groups. The intracellular content of contractile material was lower and the sarcoplasmic volume was higher in mixed aortic valve disease than in aortic stenosis. Mitochondrial volume and interstitial fibrosis were not different between groups. Patients with aortic insufficiency showed no significant difference of parameters as compared to both other groups. We conclude that an intracellular deficiency of myofibrils causes lack of contractility in advanced hypertrophy due to mixed aortic valve disease.
对29例慢性主动脉瓣疾病患者在心脏直视手术期间取自左心室游离壁的组织样本进行了光镜和电镜形态计量学研究。6例患者有主动脉瓣狭窄，9例有主动脉瓣关闭不全，14例有主动脉瓣混合病变。术前研究了血流动力学。与主动脉瓣狭窄患者相比，主动脉瓣混合病变患者的左心室质量更高，射血分数和平均圆周纤维缩短率更低。各组间的收缩期峰值壁应力相当。与主动脉瓣狭窄相比，主动脉瓣混合病变时收缩物质的细胞内含量较低，肌浆容积较高。各组间线粒体容积和间质纤维化无差异。与其他两组相比，主动脉瓣关闭不全患者的参数无显著差异。我们得出结论，由于主动脉瓣混合病变导致的晚期肥厚中，肌原纤维的细胞内缺乏导致收缩力不足。
