title: Biventricular assist device-induced right ventricular reverse structural and functional remodeling.
abstract: BACKGROUND
  Support with a left ventricular assist device (LVAD) induces LV reverse structural and functional remodeling, evidenced by normalization of passive end-diastolic pressure-volume relationships (EDPVRs) and cardiomyocyte function. These changes are not evident in the right ventricle (RV), which remains dilated during LVAD support. However, studies on whether RV reverse remodeling could be induced by RV or biventricular assist support (BiVAD) have not been published.
  
  
  METHODS
  Whole hearts from 16 patients with end-stage congestive heart failure (CHF) at the time of cardiac transplantation without LVAD support, 16 patients with LVAD support, and 3 patients with BiVAD support were used to study RV EDPVRs, with estimation of chamber stiffness. Perfused isolated myocardial trabeculae were used for functional studies. Furthermore, RV free wall samples were used for histology and collagen determination by hydroxyproline.
  
  
  RESULTS
  The RV size, calculated from the ex vivo RV EDPVRs, RV mass, and myocyte diameter were significantly smaller in BiVAD-supported hearts than in non-supported or LVAD-supported hearts (p < 0.05) and reached normal levels. Furthermore, cardiomyocyte function demonstrated a normalized response to increased stimulation frequency and after perfusion with isoproterenol following BiVAD support. In addition, myocardial collagen content and chamber stiffness increased tremendously after BiVAD support (p < 0.05 vs CHF and LVAD).
  
  
  CONCLUSIONS
  BiVAD-induced hemodynamic unloading support resulted in significant reverse structural and functional remodeling of the right chamber. The lack of these findings during LVAD support alone provides additional support that diastolic pressure and volume unloading is an important mechanism underlying the process of reverse remodeling.
authors.affiliation: Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.
authors.forename: Stefan
authors.initials: S
authors.lastname: Klotz
authors.forename: Yoshifumni
authors.initials: Y
authors.lastname: Naka
authors.forename: Mehmet C
authors.initials: MC
authors.lastname: Oz
authors.forename: Daniel
authors.initials: D
authors.lastname: Burkhoff
mesh_terms: D000328:Adult; D001794:Blood Pressure / Q000502:physiology; D048429:Cell Size; D005260:Female; D006333:Heart Failure / Q000503:physiopathology*; D016027:Heart Transplantation; D006353:Heart-Assist Devices; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000166:cytology*; D032383:Myocytes, Cardiac / Q000502:physiology*; D011652:Pulmonary Circulation / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology*; D016278:Ventricular Function, Right / Q000502:physiology*; D020257:Ventricular Remodeling / Q000502:physiology