PMID- 10484539
OWN - NLM
STAT- MEDLINE
DCOM- 19991006
LR  - 20190623
IS  - 1524-4539 (Electronic)
IS  - 0009-7322 (Linking)
VI  - 100
IP  - 11
DP  - 1999 Sep 14
TI  - Decreased expression of tumor necrosis factor-alpha in failing human myocardium 
      after mechanical circulatory support : A potential mechanism for cardiac 
      recovery.
PG  - 1189-93
AB  - BACKGROUND: An increasing number of observations in patients with end-stage heart 
      failure suggest that chronic ventricular unloading by mechanical circulatory 
      support may lead to recovery of cardiac function. Tumor necrosis factor-alpha 
      (TNF-alpha) is a proinflammatory cytokine capable of producing pulmonary edema, 
      dilated cardiomyopathy, and death. TNF-alpha is produced in the myocardium in 
      response to volume overload; however, the effects of normalizing ventricular 
      loading conditions on myocardial TNF-alpha expression are not known. We 
      hypothesize that chronic ventricular unloading by the placement of a left 
      ventricular assist device (LVAD) may eliminate the stress responsible for 
      persistent TNF-alpha expression in human failing myocardium. METHODS AND RESULTS: 
      Myocardial tissue was obtained from normal hearts and from paired samples of 8 
      patients with nonischemic end-stage cardiomyopathy at the time of LVAD 
      implantation and removal. Tissue sections were stained for TNF-alpha, and 
      quantitative analysis of the stained area was performed. We found that TNF-alpha 
      content decreased significantly after LVAD support. Furthermore, the magnitude of 
      the changes did not correlate with the length of LVAD support, although greater 
      reductions in myocardial TNF-alpha content were found in patients who were 
      successfully weaned off the LVAD who did not require transplantation. 
      CONCLUSIONS: These data show for the first time that chronic mechanical 
      circulatory assistance decreases TNF-alpha content in failing myocardium; 
      furthermore, we suggest that the magnitude of the change may predict which 
      patients will recover cardiac function.
FAU - Torre-Amione, G
AU  - Torre-Amione G
AD  - Department of Medicine, Section of Cardiology, The Winters Center for Heart 
      Failure Research, Baylor College of Medicine and The Methodist Hospital, Houston, 
      Texas, USA.
FAU - Stetson, S J
AU  - Stetson SJ
FAU - Youker, K A
AU  - Youker KA
FAU - Durand, J B
AU  - Durand JB
FAU - Radovancevic, B
AU  - Radovancevic B
FAU - Delgado, R M
AU  - Delgado RM
FAU - Frazier, O H
AU  - Frazier OH
FAU - Entman, M L
AU  - Entman ML
FAU - Noon, G P
AU  - Noon GP
LA  - eng
GR  - HL-42550/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Circulation
JT  - Circulation
JID - 0147763
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Adult
MH  - Female
MH  - Heart/physiopathology
MH  - Heart Failure/*metabolism/physiopathology
MH  - *Heart-Assist Devices
MH  - Histocytochemistry
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Myocardium/*chemistry
MH  - Tumor Necrosis Factor-alpha/*analysis
EDAT- 1999/09/14 00:00
MHDA- 1999/09/14 00:01
CRDT- 1999/09/14 00:00
PHST- 1999/09/14 00:00 [pubmed]
PHST- 1999/09/14 00:01 [medline]
PHST- 1999/09/14 00:00 [entrez]
AID - 10.1161/01.cir.100.11.1189 [doi]
PST - ppublish
SO  - Circulation. 1999 Sep 14;100(11):1189-93. doi: 10.1161/01.cir.100.11.1189.