Maron B J, Ferrans V J, Roberts W C
Am J Pathol. 1975 Jun;79(3):387-434.
Degenerated cardiac muscle cells were present in hypertrophied ventricular muscle obtained at operation from 12 (38%) of 32 patients with asymmetric septal hypertrophy (hypertrophic cardiomyopathy) or aortic valvular disease. Degenerated cells demonstrated a wide variety of ultrastructural alterations. Mildly altered cells were normal-sized or hypertrophied and showed focal changes, including preferential loss of thick (myosin) filaments, streaming and clumping of Z band material, and proliferation of the tubules of sarcoplasmic reticulum. Moderately and severely degenerated cells were normal-sized or atrophic and showed additional changes, including extensive myofibrillar lysis and loss of T tubules. The appearance of the most severely degenerated cells usually reflected the cytoplasmic organelle (sarcoplasmic reticulum, glycogen, or mitochondria) which underwent proliferation and filled the myofibril-free areas of these cells. Moderately and severely degenerated cells were present in areas of fibrosis, had thickened basement membranes, and had lost their intercellular connections. These observations suggest that degenerated cardiac muscle cells have poor contractile function and may be responsible for impaired cardiac performance in some patients with chronic ventricular hypertrophy.
在32例不对称性室间隔肥厚（肥厚型心肌病）或主动脉瓣疾病患者手术获取的肥厚心室肌中，12例（38%）存在变性的心肌细胞。变性细胞呈现出多种超微结构改变。轻度改变的细胞大小正常或肥大，表现为局灶性变化，包括粗（肌球蛋白）丝的优先丢失、Z带物质的流注和聚集以及肌浆网小管的增生。中度和重度变性的细胞大小正常或萎缩，并表现出其他变化，包括广泛的肌原纤维溶解和T小管的丢失。最严重变性细胞的外观通常反映了发生增生并填充这些细胞无肌原纤维区域的细胞质细胞器（肌浆网、糖原或线粒体）。中度和重度变性细胞存在于纤维化区域，基底膜增厚，细胞间连接丧失。这些观察结果表明，变性的心肌细胞收缩功能较差，可能是一些慢性心室肥厚患者心脏功能受损的原因。
