Pham T D, Wit A L, Hordof A J, Malm J R, Fenoglio J J
Am J Cardiol. 1978 Dec;42(6):973-82. doi: 10.1016/0002-9149(78)90684-7.
Ultrastructural studies were performed on portions of the operatively resected right atrium from six patients with a ventricular septal defect and six patients with an endocardial cushion defect. The six patients with a ventricular septal defect had normal right atrial mean pressure and no evidence of right atrial volume overload. Ultrastructurally, the atrial muscle cells in these patients appeared normal and measured 6 to 12 mu in diameter. The six patients with an endocardial cushion defect had elevated right atrial mean pressure and evidence of right atrial volume overload. Ultrastructurally, the atrial muscle cells in these patients were generally larger than 12 mu in diameter. The cells were irregular and had multiple and occasionally widened intercalated discs. In addition, there were degenerative changes in two patients with markedly increased atrial pressure. These changes included extensive loss of contractile elements, aggregation of small irregular mitochondria and proliferation of tubules of the sarcoplasmic reticulum. The structural changes suggest that hypertrophy of the right atrium may be secondary to volume overload of the atrium, whereas degenerative changes may be secondary to increased right atrial pressure.
对6例室间隔缺损患者和6例心内膜垫缺损患者手术切除的部分右心房进行了超微结构研究。6例室间隔缺损患者右心房平均压力正常，无右心房容量超负荷的证据。在超微结构上，这些患者的心房肌细胞看起来正常，直径为6至12微米。6例心内膜垫缺损患者右心房平均压力升高，有右心房容量超负荷的证据。在超微结构上，这些患者的心房肌细胞直径一般大于12微米。细胞不规则，有多个且偶尔增宽的闰盘。此外，2例心房压力明显升高的患者出现了退行性改变。这些改变包括收缩成分大量丧失、小而不规则的线粒体聚集以及肌浆网小管增生。结构变化表明，右心房肥大可能继发于心房容量超负荷，而退行性改变可能继发于右心房压力升高。
