title: Clinical recovery from end-stage heart failure using left-ventricular assist device and pharmacological therapy correlates with increased sarcoplasmic reticulum calcium content but not with regression of cellular hypertrophy.
abstract: BACKGROUND
  Left ventricular assist device (LVAD) treatment is known to lead to structural and functional cellular modifications in the heart. The relevance of these changes for clinical recovery is unknown.
  
  
  RESULTS
  We compared properties of cardiomyocytes obtained from tissue taken at explantation of the LVAD in patients with clinical recovery with those obtained from hearts of patients who did not show clinical recovery, thus requiring transplantation. Compared with myocytes taken at implantation, both the recovery and nonrecovery groups showed approximately 50% reduction in cell capacitance, an index of cell size. However, action potential duration shortened, L-type Ca2+ current fast inactivation was more rapid, and sarcoplasmic reticulum Ca2+ content was increased in the recovery compared with the nonrecovery group.
  
  
  CONCLUSIONS
  These results show that specific changes in excitation-contraction coupling, and not regression of cellular hypertrophy, are specifically associated with clinical recovery after LVAD and further identify sarcoplasmic reticulum Ca2+ handling as a key functional determinant in patients with heart failure.
authors.affiliation: Cellular Electrophysiology, Imperial College London, NHLI, Harefield Heart Science Centre, Harefield Hospital, Harefield, Middlesex UB9 6JH, UK. c.terracciano@imperial.ac.uk
authors.forename: C M N
authors.initials: CM
authors.lastname: Terracciano
authors.forename: J
authors.initials: J
authors.lastname: Hardy
authors.forename: E J
authors.initials: EJ
authors.lastname: Birks
authors.forename: A
authors.initials: A
authors.lastname: Khaghani
authors.forename: N R
authors.initials: NR
authors.lastname: Banner
authors.forename: M H
authors.initials: MH
authors.lastname: Yacoub
mesh_terms: D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000032:analysis*; D020746:Calcium Channels, L-Type / Q000378:metabolism; D020013:Calcium Signaling; D002317:Cardiovascular Agents / Q000627:therapeutic use; D048429:Cell Size; D003131:Combined Modality Therapy; D006333:Heart Failure / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology / Q000601:surgery / Q000628:therapy*; D016027:Heart Transplantation; D006352:Heart Ventricles / Q000473:pathology; D006353:Heart-Assist Devices; D006801:Humans; D017136:Ion Transport / Q000187:drug effects; D032383:Myocytes, Cardiac / Q000737:chemistry* / Q000473:pathology; D012074:Remission Induction; D012519:Sarcoplasmic Reticulum / Q000737:chemistry / Q000648:ultrastructure*; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology / Q000628:therapy
chemical_list: D020746:Calcium Channels, L-Type; D002317:Cardiovascular Agents; D002110:Caffeine; D002118:Calcium