title: Cellular and hemodynamics responses of failing myocardium to continuous flow mechanical circulatory support using the DeBakey-Noon left ventricular assist device: a comparative analysis with pulsatile-type devices.
abstract: BACKGROUND
  An increasing number of continuous flow pumps are currently under clinical studies, however very little data exist on the hemodynamic and cellular responses of the failing heart to continuous flow support. The purpose of this investigation was to characterize the response of the failing myocardium to continuous flow support.
  
  
  METHODS
  We compared echocardiographic and cellular markers of failing myocardium at the time of left ventricular assist device (LVAD) implantation and explantation in 20 consecutive patients (12 pulsatile flow [Novacor] and 8 continuous flow [DeBakey-Noon]).
  
  
  RESULTS
  The use of mechanical support with both continuous- or pulsatile-type LVADs resulted in a reduction of left ventricular end-diastolic dimension (LVEDD), end-diastolic volume (EDV), end-systolic volume (ESV) and left atrial volume (LAV), as well as a decrease in mitral E/A ratio, tricuspid regurgitation velocity (TRV) and pulmonary valve acceleration time (PVAT). Comparative analyses for patients treated with a continuous- vs pulsatile-type LVAD support showed a greater degree of unloading with the latter type, as shown by the effect on LVEDD (-13.7% vs -33.7%, p = 0.0.004), EDV (-23.5% vs -41.2%, p = 0.015), ESV (-25.6% vs -57.6%, p = 0.001) and LAV (-25.2% vs -40.4%, p = 0.071). The hemodynamic effects of continuous vs pulsatile LVAD support were similar, as shown by their effect on mitral E/A ratio (-23.9% vs -39.9%, p = NS), TRV (-26.4% vs -23.8%, p = NS) and PVAT (28.5% vs 38.5%, p = NS). Only pulsatile support demonstrated a statistically significant percent change in mass (-6.3% vs -20.6%, p = 0.038). Continuous and pulsatile forms of mechanical support demonstrated equivalent reductions in myocardial tumor necrosis factor-alpha (TNF-alpha), total collagen and mycocyte size.
  
  
  CONCLUSIONS
  Our findings show that, although there are differences between these 2 devices in magnitude of unloading, both forms of support effectively normalize cellular markers of the failing phenotype.
authors.affiliation: Department of Medicine, Thoracic and Cardiovascular Surgery, Section of Cardiology, Methodist DeBakey Heart Center, The Winters Center for Heart Failure Research, Baylor College of Medicine and the Methodist Hospital, Houston 77030, USA.
authors.forename: Vinay
authors.initials: V
authors.lastname: Thohan
authors.forename: Sonny J
authors.initials: SJ
authors.lastname: Stetson
authors.forename: Sherif F
authors.initials: SF
authors.lastname: Nagueh
authors.forename: Carlos
authors.initials: C
authors.lastname: Rivas-Gotz
authors.forename: Michael M
authors.initials: MM
authors.lastname: Koerner
authors.forename: Javier A
authors.initials: JA
authors.lastname: Lafuente
authors.forename: Matthias
authors.initials: M
authors.lastname: Loebe
authors.forename: George P
authors.initials: GP
authors.lastname: Noon
authors.forename: Guillermo
authors.initials: G
authors.lastname: Torre-Amione
mesh_terms: D000328:Adult; D015331:Cohort Studies; D004452:Echocardiography; D005260:Female; D006331:Heart Diseases / Q000601:surgery; D006333:Heart Failure / Q000503:physiopathology / Q000601:surgery*; D006353:Heart-Assist Devices; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D011673:Pulsatile Flow / Q000502:physiology