PMID- 16168288
OWN - NLM
STAT- MEDLINE
DCOM- 20051222
LR  - 20171116
IS  - 1558-3597 (Electronic)
IS  - 0735-1097 (Linking)
VI  - 46
IP  - 6
DP  - 2005 Sep 20
TI  - Myocardial expression of fas and recovery of left ventricular function in 
      patients with recent-onset cardiomyopathy.
PG  - 1036-42
AB  - OBJECTIVES: This study aimed to evaluate the role of gene expression for 
      predicting myocardial recovery in recent-onset cardiomyopathy. BACKGROUND: 
      Apoptosis may limit ventricular recovery. We examined the myocardial expression 
      of Fas, Fas ligand (FasL), tumor necrosis factor (TNF)-alpha, and TNF receptor 1 
      (TNFR1), and myocardial recovery in patients from the multicenter Intervention in 
      Myocarditis and Acute Cardiomyopathy (IMAC) study. METHODS: Endomyocardial biopsy 
      samples were obtained in 20 patients with recent-onset (<6 months) idiopathic 
      dilated cardiomyopathy (left ventricular ejection fraction [LVEF] < or =0.40). 
      The LVEF was assessed at baseline and at 6 and 12 months by nuclear scans. 
      Myocardial expression was assessed by ribonuclease (RNase) protection, normalized 
      to a constitutively active gene (glyceraldehydes 3-phosphate dehydrogenase 
      [GAPDH]) and reported as percent GAPDH expression. The change in LVEF at 6 and 12 
      months was compared by tertiles of expression. RESULTS: For all patients (14 men, 
      6 women; age 46.5 +/- 10.7 years), the mean LVEF was 0.28 +/- 0.05 at baseline 
      and 0.40 +/- 0.14 at six months. Patients in the highest tertile of Fas 
      expression had minimal improvement at six months (DeltaEF = 0.03 +/- 0.05) when 
      compared with the intermediate (DeltaEF = 0.10 +/- 0.13) and lowest tertiles 
      (DeltaEF = 0.21 +/- 0.11, change in LVEF by tertile, p = 0.006). A similar 
      relationship was seen with TNFR1 expression (highest tertile, DeltaEF = 0.06 +/- 
      0.07; lowest tertile, DeltaEF = 0.21 +/- 0.11, p = 0.02). In contrast with Fas 
      and TNFR1, expression of TNF-alpha and FasL did not predict recovery of LV 
      function. CONCLUSIONS: In cardiomyopathy of recent onset, increased expression of 
      Fas and TNFR1 was associated with minimal recovery of LV function. Apoptosis 
      limits myocardial recovery, and represents a potential target for therapeutic 
      intervention.
FAU - Sheppard, Richard
AU  - Sheppard R
AD  - McGill University, Sir Mortimer B. Davis-Jewish General Hospital, Montreal, 
      Canada.
FAU - Bedi, Maninder
AU  - Bedi M
FAU - Kubota, Toru
AU  - Kubota T
FAU - Semigran, Marc J
AU  - Semigran MJ
FAU - Dec, William
AU  - Dec W
FAU - Holubkov, Richard
AU  - Holubkov R
FAU - Feldman, Arthur M
AU  - Feldman AM
FAU - Rosenblum, Warren D
AU  - Rosenblum WD
FAU - McTiernan, Charles F
AU  - McTiernan CF
FAU - McNamara, Dennis M
AU  - McNamara DM
CN  - IMAC Investigators
LA  - eng
GR  - K24 HL69912/HL/NHLBI NIH HHS/United States
GR  - R01 HL75038/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Am Coll Cardiol
JT  - Journal of the American College of Cardiology
JID - 8301365
RN  - 0 (FASLG protein, human)
RN  - 0 (Fas Ligand Protein)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Tumor Necrosis Factors)
RN  - 0 (fas Receptor)
SB  - IM
CIN - J Am Coll Cardiol. 2005 Sep 20;46(6):1043-4. PMID: 16168289
MH  - Adult
MH  - Cardiomyopathies/drug therapy/*metabolism/*physiopathology
MH  - Fas Ligand Protein
MH  - Female
MH  - Humans
MH  - Male
MH  - Membrane Glycoproteins/*biosynthesis
MH  - Middle Aged
MH  - Receptors, Tumor Necrosis Factor, Type I/*biosynthesis
MH  - Recovery of Function
MH  - Time Factors
MH  - Tumor Necrosis Factor-alpha/*biosynthesis
MH  - Tumor Necrosis Factors/*biosynthesis
MH  - *Ventricular Function, Left
MH  - fas Receptor/*biosynthesis
EDAT- 2005/09/20 09:00
MHDA- 2005/12/24 09:00
CRDT- 2005/09/20 09:00
PHST- 2005/03/04 00:00 [received]
PHST- 2005/04/27 00:00 [revised]
PHST- 2005/05/03 00:00 [accepted]
PHST- 2005/09/20 09:00 [pubmed]
PHST- 2005/12/24 09:00 [medline]
PHST- 2005/09/20 09:00 [entrez]
AID - S0735-1097(05)01392-6 [pii]
AID - 10.1016/j.jacc.2005.05.067 [doi]
PST - ppublish
SO  - J Am Coll Cardiol. 2005 Sep 20;46(6):1036-42. doi: 10.1016/j.jacc.2005.05.067.