title: Apoptosis in dilated cardiomyopathy.
abstract: OBJECTIVE
  Cardiomyopathy, a popular diagnosis that always obscures more than it reveals, nevertheless has several characteristic histological features. These prominently include widespread focal myocardial fibrosis and associated hypertrophy of surviving cardiac myocyte. In fact, focal noninflammatory degeneration (not necrosis) has been demonstrated as a feature of many forms of cardiac hypertrophy. We hypothesized that this loss of myocardial cells in dilated cardiomyopathy (DCMP) may result from cell death by apoptosis.
  
  
  METHODS
  Endomyocardial biopsy specimens from the right ventricles of six patients who suffered from DCMP were studied, and myocardial specimens from two persons who died in motor vehicle accidents were used as negative controls. For identification of apoptosis, immunohistochemistry with terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end-labeling was performed. In addition, apoptosis was confirmed morphologically by confocal laser scanning microscopy with propidium iodide.
  
  
  RESULTS
  Apoptosis, that was represented by an apoptotic index ranging from 19.8 to 25.4%, could be extensively seen in myocytes and also rarely in non-myocytes of interstitium and vascular endothelium. Morphologically, there were a lot of nuclei with clumps of condensed chromatin, suggestive of apoptosis.
  
  
  CONCLUSIONS
  The present study demonstrated that myocyte loss in DCMP might be mainly due to the apoptosis of myocytes and interstitial cells, rather than inflammation or cell necrosis.
authors.affiliation: Cardiology Division, Yonsei Cardiovascular Center, Yonsei University College of Medicine, Seoul, Korea.
authors.forename: B K
authors.initials: BK
authors.lastname: Hong
authors.forename: H M
authors.initials: HM
authors.lastname: Kwon
authors.forename: K H
authors.initials: KH
authors.lastname: Byun
authors.forename: D
authors.initials: D
authors.lastname: Kim
authors.forename: E Y
authors.initials: EY
authors.lastname: Choi
authors.forename: T S
authors.initials: TS
authors.lastname: Kang
authors.forename: S M
authors.initials: SM
authors.lastname: Kang
authors.forename: K J
authors.initials: KJ
authors.lastname: Chun
authors.forename: Y
authors.initials: Y
authors.lastname: Jang
authors.forename: H S
authors.initials: HS
authors.lastname: Kim
authors.forename: M
authors.initials: M
authors.lastname: Kim
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D017209:Apoptosis / Q000502:physiology*; D001707:Biopsy, Needle; D002311:Cardiomyopathy, Dilated / Q000473:pathology* / Q000503:physiopathology; D053148:Caspase 3; D020169:Caspases / Q000032:analysis; D004792:Enzyme Precursors / Q000032:analysis; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D008297:Male; D018613:Microscopy, Confocal; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology*; D012016:Reference Values; D018709:Statistics, Nonparametric
chemical_list: D004792:Enzyme Precursors; C505407:CASP3 protein, human; D053148:Caspase 3; D020169:Caspases