PMID- 15823501
OWN - NLM
STAT- MEDLINE
DCOM- 20050809
LR  - 20220413
IS  - 1568-9972 (Print)
IS  - 1568-9972 (Linking)
VI  - 4
IP  - 3
DP  - 2005 Mar
TI  - TNF-alpha, rheumatoid arthritis, and heart failure: a rheumatological dilemma.
PG  - 153-61
AB  - Cardiovascular disease (CVD) is responsible for 35-50% of rheumatoid arthritis 
      (RA) deaths, whereas, in the general UK adult population, coronary heart disease 
      is responsible for 1/4 deaths in males and 1/5 deaths in female. This increased 
      risk may be attributable to RA-specific risk factors such as 
      hyperhomocysteinemia, disease-related dyslipidemia or vascular inflammation, or 
      to morbidity related to medications and high levels of tumor necrosis 
      factor-alpha (TNF-alpha). The possible roles of TNF-alpha in the development of 
      atherosclerosis include the recruitment of inflammatory cells to the site of 
      injury or the promotion of adverse vascular smooth muscle cell remodelling. 
      TNF-alpha may also act as a proinflammatory factor in plaque rupture. 
      Anticytokine therapy could prove beneficial in the treatment of patients with 
      heart failure. While early studies supported this hypothesis, anti-TNF strategies 
      have not demonstrated salutary benefits in large multicenter randomized and 
      placebo-controlled clinical trials in patients with symptomatic heart failure. 
      There is a variety of possible explanations for the failure of anti-TNF therapy: 
      (1) TNF antagonism has untoward effects in the setting of heart failure; (2) the 
      biological agents used in the trials were intrinsically toxic; (3) sex and race 
      may have important implications in the outcome after anticytokine therapy; (4) 
      the TNF-alpha protein contains a polymorphism, and, in fact, genoma plays a role 
      in modifying the pharmacologic response to anticytokines; (5) anti-TNF-alpha 
      approaches could have had pharmacodynamic interactions with other heart failure 
      medications; and (6) the patients in these trials may have been inappropriately 
      selected. These disappointing results may determine controversial attitude in the 
      long-term treatment with anti-TNF agents in RA or Crohn's disease. The effects of 
      TNF-alpha blockers on incident cases of congestive heart failure (CHF) in RA are 
      controversial. The available published data suggest the following: (a) RA 
      patients with history of CHF and a concomitant indication for the use of 
      TNF-alpha blockers do not need a baseline cardiac evaluation to screen for heart 
      failure; (b) patients with well-compensated mild CHF New York Heart Association 
      (NYHA) classes I and II and a concomitant indication for the use of TNF-alpha 
      blockers should be evaluated at baseline and then be closely monitored for any 
      clinical signs of worsening heart failure; and (c) patients with (NYHA) class III 
      or IV heart failure should not be treated with TNF-alpha blockers in any case.
FAU - Sarzi-Puttini, Piercarlo
AU  - Sarzi-Puttini P
AD  - Rheumatology Unit, University Hospital L. Sacco, Via GB Grassi 74, 20157 Milan, 
      Italy. sarzi@tiscali.it
FAU - Atzeni, Fabiola
AU  - Atzeni F
FAU - Shoenfeld, Yehuda
AU  - Shoenfeld Y
FAU - Ferraccioli, Gianfranco
AU  - Ferraccioli G
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Netherlands
TA  - Autoimmun Rev
JT  - Autoimmunity reviews
JID - 101128967
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - 0 (Antirheumatic Agents)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - B72HH48FLU (Infliximab)
RN  - FYS6T7F842 (Adalimumab)
RN  - OP401G7OJC (Etanercept)
SB  - IM
MH  - Adalimumab
MH  - Antibodies, Monoclonal/therapeutic use
MH  - Antibodies, Monoclonal, Humanized
MH  - Antirheumatic Agents/*therapeutic use
MH  - Arthritis, Rheumatoid/*complications/drug therapy
MH  - Etanercept
MH  - Female
MH  - Heart Failure/*complications/drug therapy
MH  - Humans
MH  - Immunoglobulin G/therapeutic use
MH  - Infliximab
MH  - Male
MH  - Receptors, Tumor Necrosis Factor/therapeutic use
MH  - Risk Factors
MH  - Tumor Necrosis Factor-alpha/antagonists & inhibitors/*metabolism
RF  - 40
EDAT- 2005/04/13 09:00
MHDA- 2005/08/10 09:00
CRDT- 2005/04/13 09:00
PHST- 2004/08/02 00:00 [received]
PHST- 2004/09/17 00:00 [accepted]
PHST- 2005/04/13 09:00 [pubmed]
PHST- 2005/08/10 09:00 [medline]
PHST- 2005/04/13 09:00 [entrez]
AID - S1568-9972(04)00198-3 [pii]
AID - 10.1016/j.autrev.2004.09.004 [doi]
PST - ppublish
SO  - Autoimmun Rev. 2005 Mar;4(3):153-61. doi: 10.1016/j.autrev.2004.09.004.