title: Evidence of improved right ventricular structure after LVAD support in patients with end-stage cardiomyopathy.
abstract: BACKGROUND
  Although many reports demonstrate the hemodynamic benefits of left ventricular assist devices (LVAD) in right-sided circulation, it is not known whether the right ventricular myocardium goes through reverse remodeling after left ventricular mechanical circulatory support. Accordingly, the purposes of our studies were 1). to investigate the right ventricular changes that occur in fibrosis, in cellular hypertrophy, and in intra-myocardial tumor necrosis factor alpha (TNF-alpha) levels in patients receiving LVAD support; and 2). to determine whether the type of LVAD used influences right ventricular myocardial changes.
  
  
  RESULTS
  We measured myocyte size, total collagen content, and TNF-alpha levels using semi-quantitative immunohistochemical analysis of myocardial samples from the right and left ventricles of control and failing myocardia, either supported by 1 of 2 distinct forms of LVADs or without support. We found that when compared with control, although myocyte size was not increased in the right ventricle of failing myocardia (p = not significant), total collagen content and myocardial TNF-alpha levels were decreased in the right ventricle compared with controls (p < 0.01 and p < 0.001, respectively).
  
  
  CONCLUSIONS
  These data demonstrate that chronic left ventricular unloading with either pulsatile or continuous-flow devices decreases right ventricular total collagen and myocardial TNF-alpha content. We suggest that the decreased fibrosis and normalization of cytokine milieu observed may in part contribute to the recovery of right-sided cardiac function associated with chronic mechanical circulatory support.
authors.affiliation: M E DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas 77030, USA.
authors.forename: Seref A
authors.initials: SA
authors.lastname: Küçüker
authors.forename: Sonny J
authors.initials: SJ
authors.lastname: Stetson
authors.forename: Katy A
authors.initials: KA
authors.lastname: Becker
authors.forename: Ahmet
authors.initials: A
authors.lastname: Akgül
authors.forename: Matthias
authors.initials: M
authors.lastname: Loebe
authors.forename: Javier A
authors.initials: JA
authors.lastname: Lafuente
authors.forename: George P
authors.initials: GP
authors.lastname: Noon
authors.forename: Michael M
authors.initials: MM
authors.lastname: Koerner
authors.forename: Mark L
authors.initials: ML
authors.lastname: Entman
authors.forename: Guillermo
authors.initials: G
authors.lastname: Torre-Amione
mesh_terms: D002311:Cardiomyopathy, Dilated / Q000473:pathology*; D048429:Cell Size; D003094:Collagen / Q000032:analysis; D005260:Female; D006353:Heart-Assist Devices; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D016277:Ventricular Function, Left / Q000502:physiology; D016278:Ventricular Function, Right / Q000502:physiology*; D020257:Ventricular Remodeling
chemical_list: D014409:Tumor Necrosis Factor-alpha; D003094:Collagen