PMID- 11489774
OWN - NLM
STAT- MEDLINE
DCOM- 20010913
LR  - 20190623
IS  - 1524-4539 (Electronic)
IS  - 0009-7322 (Linking)
VI  - 104
IP  - 6
DP  - 2001 Aug 7
TI  - Cardiac hypertrophy after transplantation is associated with persistent 
      expression of tumor necrosis factor-alpha.
PG  - 676-81
AB  - BACKGROUND: The mechanisms that contribute to cardiac allograft hypertrophy are 
      not known; however, the rapid progression and severity of hypertrophy suggest 
      that nonhemodynamic factors may play a contributory role. Tumor necrosis 
      factor-alpha (TNF-alpha) is a cytokine produced in cardiac allografts and capable 
      of producing hypertrophy and fibrosis; therefore, we suggest that TNF-alpha may 
      play a contributory role. Accordingly, the aims of our study were to define the 
      role of systemic hypertension in the development of hypertrophy, characterize the 
      histological determinants of hypertrophy, and characterize the expression of 
      myocardial TNF-alpha after heart transplantation. METHODS AND RESULTS: To 
      separate the effect of hypertension from immune injury in the development of 
      cardiac allograft hypertrophy, we measured the gain in left ventricular mass by 
      2D echocardiography in heart transplant recipients and lung transplant recipients 
      who developed similar rates of systemic hypertension. The gain in left 
      ventricular mass was 73% in heart transplant recipients and 7% in lung transplant 
      recipients (P<0.0001). By comparing myocardial samples obtained during the first 
      week after transplant and at 1 year, we found that there was a significant 
      increase in total collagen content (P<0.0001), collagen I (P<0.0001), collagen 
      III (P<0.0001), and myocyte size (P<0.0001). These changes were associated with 
      persistent myocardial TNF-alpha expression. CONCLUSIONS: We suggest that the 
      contribution of hypertension to cardiac allograft hypertrophy is minimal and that 
      persistent intracardiac expression of TNF-alpha may contribute to the development 
      of cardiac allograft hypertrophy.
FAU - Stetson, S J
AU  - Stetson SJ
AD  - Department of Medicine, The DeBakey Heart Center, The Winters Center for Heart 
      Failure Research, Baylor College of Medicine, Houston, Texas, USA.
FAU - Perez-Verdia, A
AU  - Perez-Verdia A
FAU - Mazur, W
AU  - Mazur W
FAU - Farmer, J A
AU  - Farmer JA
FAU - Koerner, M M
AU  - Koerner MM
FAU - Weilbaecher, D G
AU  - Weilbaecher DG
FAU - Entman, M L
AU  - Entman ML
FAU - Quinones, M A
AU  - Quinones MA
FAU - Noon, G P
AU  - Noon GP
FAU - Torre-Amione, G
AU  - Torre-Amione G
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)
RN  - 9007-34-5 (Collagen)
SB  - IM
MH  - Cardiomegaly/*metabolism/pathology
MH  - Collagen/metabolism
MH  - Female
MH  - Graft Rejection/metabolism/pathology
MH  - *Heart Transplantation
MH  - Heart Ventricles/chemistry/pathology/physiopathology
MH  - Humans
MH  - Hypertension/physiopathology
MH  - Immunohistochemistry
MH  - Male
MH  - Middle Aged
MH  - Organ Size
MH  - Systole/physiology
MH  - Time Factors
MH  - Tumor Necrosis Factor-alpha/*biosynthesis
EDAT- 2001/08/08 10:00
MHDA- 2001/09/14 10:01
CRDT- 2001/08/08 10:00
PHST- 2001/08/08 10:00 [pubmed]
PHST- 2001/09/14 10:01 [medline]
PHST- 2001/08/08 10:00 [entrez]
AID - 10.1161/hc3101.093765 [doi]
PST - ppublish
SO  - Circulation. 2001 Aug 7;104(6):676-81. doi: 10.1161/hc3101.093765.