An ultrastructural study of cardiac myocytes in postmyocardial infarction ventricular aneurysm representative of chronic ischemic myocardium using semiquantitative and quantitative assessment.
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.
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The 1st Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto City, Japan.
Sekiguchi
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Endo
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D000328:Adult; D000368:Aged; D002467:Cell Nucleus / Q000648:ultrastructure; D002908:Chronic Disease; D006003:Glycogen / Q000648:ultrastructure; D006322:Heart Aneurysm / Q000209:etiology / Q000473:pathology* / Q000601:surgery; D006352:Heart Ventricles / Q000601:surgery / Q000648:ultrastructure*; D006801:Humans; D007091:Image Processing, Computer-Assisted; D008297:Male; D008875:Middle Aged; D008946:Mitral Valve Stenosis / Q000473:pathology; D009203:Myocardial Infarction / Q000150:complications / Q000473:pathology* / Q000601:surgery; D009206:Myocardium / Q000648:ultrastructure*; D009210:Myofibrils / Q000648:ultrastructure; D015388:Organelles / Q000648:ultrastructure; D012804:Sick Sinus Syndrome / Q000473:pathology; D014927:Wolff-Parkinson-White Syndrome / Q000473:pathology
D006003:Glycogen