title: Myocardial tumor necrosis factor-alpha expression does not correlate with clinical indices of heart failure in patients on left ventricular assist device support.
abstract: BACKGROUND
  Mechanical unloading with a left ventricular assist device (LVAD) can improve clinical indices of heart failure and alter myocardial tumor necrosis factor-alpha (TNFalpha) expression, but a correlation between clinical and molecular indices has not been established.
  
  
  METHODS
  We enrolled 14 patients with end-stage heart failure treated with drugs and mechanical unloading in a protocol including the collection of myocardial tissue samples at LVAD implantation and explantation. Ten nonfailing donor hearts served as controls. TNFalpha expression was measured by quantitative reverse transcription polymerase chain reaction. Clinical indices of heart failure were retrospectively analyzed and correlated with myocardial TNFalpha expression.
  
  
  RESULTS
  Left ventricular end-diastolic dimension decreased (p < 0.01) and cardiac index (p < 0.001) increased with unloading. Abnormal values of serum sodium, creatinine, blood urea nitrogen, glutamic-oxaloacetic transaminase, glutamic-pyruvic transaminase, and albumin showed a trend toward normalization with mechanical unloading. TNFalpha expression was increased in 5 of 14 patients and decreased with mechanical unloading in 4 of them. Surprisingly, there was no correlation between mRNA levels of TNFalpha and any of the clinical indices studied.
  
  
  CONCLUSIONS
  Although clinical indices of heart failure improve and elevated levels of myocardial TNFalpha expression decrease with mechanical unloading, there is no correlation between the two. Thus, clinical and molecular indices of heart failure in LVAD-supported patients do not always correlate.
authors.affiliation: Division of Cardiology, The University of Texas-Houston Medical School, 77030, USA.
authors.forename: P
authors.initials: P
authors.lastname: Razeghi
authors.forename: M
authors.initials: M
authors.lastname: Mukhopadhyay
authors.forename: T J
authors.initials: TJ
authors.lastname: Myers
authors.forename: J N
authors.initials: JN
authors.lastname: Williams
authors.forename: C S
authors.initials: CS
authors.lastname: Moravec
authors.forename: O H
authors.initials: OH
authors.lastname: Frazier
authors.forename: H
authors.initials: H
authors.lastname: Taegtmeyer
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D009202:Cardiomyopathies / Q000175:diagnosis / Q000473:pathology / Q000601:surgery; D015331:Cohort Studies; D005260:Female; D015870:Gene Expression / Q000502:physiology; D006333:Heart Failure / Q000175:diagnosis / Q000473:pathology / Q000601:surgery*; D006353:Heart-Assist Devices; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology*; D012333:RNA, Messenger / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013318:Stroke Volume / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics*; D016277:Ventricular Function, Left / Q000502:physiology
chemical_list: D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha