Su X, Sekiguchi M, Endo M
The 1st Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto City, Japan.
Cardiovasc Pathol. 2000 Jan-Feb;9(1):1-8. doi: 10.1016/s1054-8807(99)00025-3.
To elucidate the characteristic myocytic changes in chronic ischemic myocardium, an electronmicroscopic (EM) study was carried out in surgically excised postmyocardial infarction left ventricular aneurysm (LVAN) (n = 15) using semiquantitative (in all 15 cases) and quantitative assessment methods (in 10 cases). The control group, representing normal ultrastructure, included left ventricular endomyocardial biopsy specimens of sick sinus syndrome (SSS) (n = 3), Wolff-Parkinson-White (WPW) Syndrome (n = 1), and intraoperative left ventricular endomyocardial biopsy in mitral stenosis (MS) (n = 3). Myocardial condition was assessed at the ultrastructural level according to the severity of morphologic changes, first semiquantitatively, thereafter with the use of the Image Processor-Analyzer LUZEX III for morphometric analysis. The most marked EM findings were mitochondrial regressive changes, glycogen accumulation, nuclear deformities, increased rough-surfaced endoplasmic reticulum at the perinuclear portion, lysis of myofibrils, and myofibrillar degeneration. The quantitative analysis revealed significant (p < 0.05) increase of glycogen deposition, only at the perinuclear portion in the LVAN group. The myofibril to mitochondria ratio at the intercalated disc (ID) portion of the cardiac myocytes significantly increased (p < 0.01) in the LVAN group as compared with the normal control group. Light microscopically evaluated quantitative analysis, using toluidine-blue stained semithin sections which underwent EM observation, showed that the fractional area of interstitial fibrous tissue was significantly increased in the LVAN group compared to the normal controls (p < 0.01). These results signify that in chronic ischemic myocardium, decreased consumption of glycogen in oxidative phosphorylation occurs in the surviving myocytes, and that hypertrophy of the myocytes appears. The results of this study may lead to the proper ultrastructural interpretation of biopsied human myocardium, regardless of etiology.
为阐明慢性缺血心肌中特征性的心肌细胞变化，我们对手术切除的心肌梗死后左心室室壁瘤（LVAN）（n = 15）进行了电子显微镜（EM）研究，采用了半定量（所有15例）和定量评估方法（10例）。代表正常超微结构的对照组包括病态窦房结综合征（SSS）（n = 3）、预激综合征（WPW）（n = 1）的左心室心内膜活检标本，以及二尖瓣狭窄（MS）术中左心室心内膜活检标本（n = 3）。根据形态学变化的严重程度，在超微结构水平评估心肌状况，首先进行半定量评估，然后使用图像处理器分析仪LUZEX III进行形态计量分析。最显著的EM表现为线粒体退行性变化、糖原积累、核畸形、核周部分粗面内质网增加、肌原纤维溶解和肌原纤维变性。定量分析显示，LVAN组仅在核周部分糖原沉积显著增加（p < 0.05）。与正常对照组相比，LVAN组心肌细胞闰盘（ID）部分的肌原纤维与线粒体比率显著增加（p < 0.01）。使用经EM观察的甲苯胺蓝染色半薄切片进行的光镜评估定量分析表明，与正常对照组相比，LVAN组间质纤维组织的分数面积显著增加（p < 0.01）。这些结果表明，在慢性缺血心肌中，存活的心肌细胞氧化磷酸化过程中糖原消耗减少，并且出现心肌细胞肥大。本研究结果可能有助于对活检的人类心肌进行正确的超微结构解释，而不论其病因如何。
