PMID- 15925562
OWN - NLM
STAT- MEDLINE
DCOM- 20050719
LR  - 20071115
IS  - 0002-9149 (Print)
IS  - 0002-9149 (Linking)
VI  - 95
IP  - 11A
DP  - 2005 Jun 6
TI  - Broad modulation of tissue responses (immune activation) by celacade may 
      favorably influence pathologic processes associated with heart failure 
      progression.
PG  - 30C-37C; discussion 38C-40C
AB  - Immune activation and inflammation contribute to the progression of chronic heart 
      failure (CHF), but therapeutic approaches directed against these processes have 
      been largely unsuccessful. This clinical study evaluated a novel, 
      nonpharmacologic immune modulation therapy, shown experimentally to reduce 
      inflammatory and increase anti-inflammatory cytokines. A total of 75 patients 
      with New York Heart Association (NYHA) functional class III or IV CHF were 
      randomized to receive either Celacade (immune modulation therapy) or placebo (n = 
      38 and n = 37, respectively) in a double-blind trial for 6 months, during which 
      standard therapy for CHF was maintained. Patients were evaluated using the 
      6-minute walk test, changes in NYHA class, cardiac function, and quality-of-life 
      assessments, and were observed for the occurrence of death and hospitalization. 
      There was no between-treatment difference in the 6-minute walk test results, but 
      15 Celacade-treated patients (compared with 9 placebo-treated patients) improved 
      NYHA classification by > or = 1 class (p = 0.140). Kaplan-Meier survival analysis 
      showed that Celacade significantly reduced the risk of death (p = 0.022) and 
      hospitalization (p = 0.008). Analysis of a clinical composite score demonstrated 
      a significant between-group difference (p = 0.006). There was no difference in 
      left ventricular ejection fraction between groups, but there was a trend toward 
      improved quality of life favoring the Celacade-treated group (p = 0.110). These 
      preliminary findings are consistent with the hypothesis that immune activation is 
      important in the pathogenesis of CHF, and they establish the basis for a phase 3 
      trial to define the benefit of Celacade in CHF.
FAU - Torre-Amione, Guillermo
AU  - Torre-Amione G
AD  - Heart Transplant Service, Methodist DeBakey Heart Center, Baylor College of 
      Medicine, Houston, Texas 77030, USA. gtorre@bcm.tmc.edu
FAU - Sestier, Francois
AU  - Sestier F
FAU - Radovancevic, Branislav
AU  - Radovancevic B
FAU - Young, James
AU  - Young J
LA  - eng
PT  - Clinical Trial
PT  - Journal Article
PT  - Multicenter Study
PT  - Randomized Controlled Trial
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am J Cardiol
JT  - The American journal of cardiology
JID - 0207277
SB  - IM
MH  - Aged
MH  - Animals
MH  - Disease Progression
MH  - Double-Blind Method
MH  - Female
MH  - Heart Failure/*drug therapy/*immunology/mortality/pathology
MH  - Humans
MH  - Immunotherapy/*methods
MH  - Male
MH  - Middle Aged
MH  - Quality of Life
MH  - Survival Analysis
MH  - Treatment Outcome
EDAT- 2005/06/01 09:00
MHDA- 2005/07/20 09:00
CRDT- 2005/06/01 09:00
PHST- 2005/06/01 09:00 [pubmed]
PHST- 2005/07/20 09:00 [medline]
PHST- 2005/06/01 09:00 [entrez]
AID - S0002-9149(05)00389-9 [pii]
AID - 10.1016/j.amjcard.2005.03.010 [doi]
PST - ppublish
SO  - Am J Cardiol. 2005 Jun 6;95(11A):30C-37C; discussion 38C-40C. doi: 
      10.1016/j.amjcard.2005.03.010.