title: Relevance of apoptosis in influencing recovery of hibernating myocardium.
abstract: BACKGROUND
  Hibernating myocardium (HM) is viable but dysfunctional myocardium which can recover following revascularization. Myocyte necrosis is virtually absent in HM; however, cellular loss may take place by apoptosis, although this is controversial.
  
  
  OBJECTIVE
  To assess the presence of apoptosis and its relevance in HM.
  
  
  METHODS
  During coronary artery by-pass surgery (CABG), 21 patients underwent transmural biopsy in the dysfunctional left anterior descending artery tributary area of the left ventricle (LV), with kinetic recovery at follow-up, thus fulfilling the HM criteria. All patients underwent echocardiographic follow-up at 12 months. All biopsies were evaluated by light microscopy, electron microscopy (EM), and molecular analysis.
  
  
  RESULTS
  All biopsies were structurally altered, showing increased fibrosis and myocytes with variable size. Myocyte dedifferentiation was not detected by immunohistochemistry or EM. On stepwise linear regression, 1 year LVEF was predicted by the apoptotic index (beta=-0.973, p=0.002), the normotrophic cell percentage (beta=0.449, p=0.038), and mean fibrosis (beta=-0.412, p=0.51).
  
  
  CONCLUSIONS
  Our biopsy study detected a wide range of morphological substrate heterogeneity in HM with degenerative features. We have demonstrated for the first time in humans that myocyte apoptosis is an important phenomenon in HM, negatively influencing LV functional recovery after CABG.
authors.affiliation: Department of Pathological Anatomy, University of Padua, Via Gabelli, 61, 35121 Padova, and Department of Non-invasive Diagnostic Cardiology, San Raffaele Foundation Institute and University Hospital, Milan, Italy. annalisa.angelini@unipd.it
authors.forename: Annalisa
authors.initials: A
authors.lastname: Angelini
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Maiolino
authors.forename: Giovanni
authors.initials: G
authors.lastname: La Canna
authors.forename: Claudio
authors.initials: C
authors.lastname: Ceconi
authors.forename: Fiorella
authors.initials: F
authors.lastname: Calabrese
authors.forename: Elena
authors.initials: E
authors.lastname: Pettenazzo
authors.forename: Marialuisa
authors.initials: M
authors.lastname: Valente
authors.forename: Ottavio
authors.initials: O
authors.lastname: Alfieri
authors.forename: Gaetano
authors.initials: G
authors.lastname: Thiene
authors.forename: Roberto
authors.initials: R
authors.lastname: Ferrari
mesh_terms: D017209:Apoptosis; D009202:Cardiomyopathies / Q000000981:diagnostic imaging / Q000503:physiopathology*; D005260:Female; D005355:Fibrosis / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology*; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D032342:Muscle Cells; D009206:Myocardium / Q000166:cytology / Q000473:pathology*; D009336:Necrosis; D011446:Prospective Studies; D013318:Stroke Volume; D014463:Ultrasonography