Mönninghoff W, Themann H, Grosse-Heitmeyer W, Dittrich H
Erich-Schütz-Forschungsinstitut des Staatsbades Salzuflen, Universität Münster.
Herz. 1987 Oct;12(5):354-8.
Surgically-obtained tissue specimens from 41 patients with ventricular aneurysm were studied electron microscopically. The tissue from the resected aneurysms showed substantially varied morphological differences. In some, there were extensive regions of scar containing increased fibrotic material and few cells, in others there were also larger contiguous regions of myocardium with an essentially normal appearance. In the preserved myocardial regions, the cardiac cells showed moderate hypertrophy. There was an increase in contractile substance in parallel with an increase in mitochondria and enlargement of the nucleus with frequent waves and invaginations in the cell membrane. The cells at the marginal regions between fibrous tissue and preserved myocardium were frequently isolated from adjacent cells. In particular, when the isolated cells were completely surrounded by fibrous tissue, clear degeneration was apparent. These cells showed mainly a fibrillolysis with dissolution of the cross-bands and loss of the entire contractile apparatus. In compensation, occasionally there was proliferation of other cell structures, especially the free sarcoplasmatic reticulum. The hypertrophy of the still intact myocardial cells is considered compensatory for the infarct-incurred loss of tissue. The degenerative appearance is mainly attributable to fibrous tissue invasion. The diminished oxygen supply, compromised or abolished impulse conduction, loss of function and passive stretch during systole may be regarded as causes of the degeneration.
对41例心室动脉瘤患者手术获取的组织标本进行了电子显微镜研究。切除的动脉瘤组织呈现出显著不同的形态学差异。在一些标本中,存在广泛的瘢痕区域,其中纤维化物质增多且细胞稀少;在另一些标本中,也有较大的连续心肌区域,外观基本正常。在保留的心肌区域,心肌细胞显示出中度肥大。收缩物质增加,同时线粒体增多,细胞核增大,细胞膜频繁出现波浪状和内陷。纤维组织与保留的心肌之间边缘区域的细胞常常与相邻细胞分离。特别是当分离的细胞完全被纤维组织包围时,明显的变性就很明显。这些细胞主要表现为肌原纤维溶解,横纹溶解,整个收缩装置丧失。作为代偿,偶尔会有其他细胞结构的增生,尤其是游离的肌浆网。仍完整的心肌细胞肥大被认为是对梗死导致的组织损失的代偿。变性表现主要归因于纤维组织的侵入。氧气供应减少、冲动传导受损或中断、功能丧失以及收缩期的被动牵拉可被视为变性的原因。