title: Hibernating myocardium: an incomplete adaptation to ischemia.
abstract: BACKGROUND
  We tested the hypothesis that hibernating myocardium represents an incomplete adaptation to a reduced myocardial oxygen supply.
  
  
  RESULTS
  In 38 patients, areas of hibernating myocardium were identified by angiography, multigated radionuclide ventriculography, thallium scintigraphy with reinjection, and low-dose dobutamine echocardiography. Biopsies removed at cardiac surgery showed structural degeneration characterized by a reduced protein and mRNA expression and disorganization of the contractile and cytoskeletal proteins myosin, actin, desmin, titin, alpha-actinin, and vinculin by electron microscopy, immunohistochemistry, and in situ hybridization. Additionally, an increased amount of extracellular matrix proteins resulting in a significant degree of reparative fibrosis was present. Dedifferentiation, ie, expression of fetal proteins, was absent. Apoptosis indicating suicidal cell death was found by the terminal deoxynucleotidyl transferase end-labeling method and electron microscopy. Radionuclide ventriculography showed improvement of regional function at 3 months postoperatively compared with preoperative values (mean values, 23.5% and 48%, respectively), and the echocardiographic wall-motion score index decreased from 3.4 to 1.8. The degree of severity of the morphological changes (three stages) correlated well with the extent of postoperative functional recovery: more advanced clinical improvement was observed in patients with slight and moderate morphological degeneration (stages 1 and 2), but recovery was only partial in severe degeneration (stage 3).
  
  
  CONCLUSIONS
  Cellular degeneration rather than adaptation is present in hibernating myocardium. The consequence is progressive diminution of the chance for complete structural and functional recovery after restoration of blood flow. The practical consequence from this study should be early revascularization in patients showing areas of hibernating myocardium.
authors.affiliation: Department of Cardiology, Max Planck Institute, Bad Nauheim, Germany.
authors.forename: A
authors.initials: A
authors.lastname: Elsässer
authors.forename: M
authors.initials: M
authors.lastname: Schlepper
authors.forename: W P
authors.initials: WP
authors.lastname: Klövekorn
authors.forename: W J
authors.initials: WJ
authors.lastname: Cai
authors.forename: R
authors.initials: R
authors.lastname: Zimmermann
authors.forename: K D
authors.initials: KD
authors.lastname: Müller
authors.forename: R
authors.initials: R
authors.lastname: Strasser
authors.forename: S
authors.initials: S
authors.lastname: Kostin
authors.forename: C
authors.initials: C
authors.lastname: Gagel
authors.forename: B
authors.initials: B
authors.lastname: Münkel
authors.forename: W
authors.initials: W
authors.lastname: Schaper
authors.forename: J
authors.initials: J
authors.lastname: Schaper
mesh_terms: D000222:Adaptation, Physiological; D000328:Adult; D000368:Aged; D017209:Apoptosis; D004280:Dobutamine; D004452:Echocardiography; D005260:Female; D006801:Humans; D017403:In Situ Hybridization; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000503:physiopathology*; D009204:Myocardial Revascularization; D017682:Myocardial Stunning / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D013794:Thallium Radioisotopes
chemical_list: D013794:Thallium Radioisotopes; D004280:Dobutamine