title: The effect of tumor necrosis factor-α antagonists on arterial stiffness in rheumatoid arthritis: a literature review.
abstract: BACKGROUND
  There is evidence that patients with rheumatoid arthritis (RA) have a higher arterial stiffness than their age-matched healthy counterparts and thus have a higher cardiovascular risk. Under National Institute for Clinical Excellence guidelines, tumor necrosis factor-α (TNF-α) antagonists are indicated clinically in patients with severe active rheumatoid disease. TNF-α antagonists have been found to reduce inflammatory markers in RA; however, it is debatable if they have favorable effects on the cardiovascular system. This review evaluates the effect of TNF-α antagonists on arterial stiffness, a predictor of cardiovascular disease, in RA patients.
  
  
  METHODS
  A search of Ovid MEDLINE and ISI Web of Knowledge databases was conducted to identify studies into the effect of TNF-α antagonists on arterial stiffness in RA patients. Eight studies matching the search criteria were included for analysis.
  
  
  RESULTS
  Two methods were used to assess arterial stiffness: pulse wave velocity and augmentation index. Despite inconsistencies in augmentation index values, aortic pulse wave velocity in all but one study was significantly reduced following TNF-α antagonist treatment. Most studies had methodological limitations, including inadequate sample size, nonblinding of those involved in the measurements, and inadequate inclusion/exclusion criteria. Variation in results could be due to the use of different TNF-α antagonists, different outcome measures being used, and differences in follow-up.
  
  
  CONCLUSIONS
  The balance of evidence suggests that TNF-α antagonists may have a beneficial effect on arterial stiffness and therefore cardiovascular risk. However, larger more robust longer term studies are warranted to confirm recent findings.
authors.affiliation: Centre for Sports and Exercise Medicine, Barts, and The London School of Medicine and Dentistry, Mile End Hospital, London, UK.
authors.forename: Rajdip
authors.initials: R
authors.lastname: Dulai
authors.forename: Mark
authors.initials: M
authors.lastname: Perry
authors.forename: Richard
authors.initials: R
authors.lastname: Twycross-Lewis
authors.forename: Dylan
authors.initials: D
authors.lastname: Morrissey
authors.forename: Fabiola
authors.initials: F
authors.lastname: Atzeni
authors.forename: Stephen
authors.initials: S
authors.lastname: Greenwald
mesh_terms: D000068879:Adalimumab; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001161:Arteriosclerosis / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D001172:Arthritis, Rheumatoid / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D016206:Databases, Bibliographic; D004730:Endothelium, Vascular / Q000187:drug effects; D000068800:Etanercept; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use; D000069285:Infliximab; D063177:Pulse Wave Analysis; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D014655:Vascular Resistance / Q000187:drug effects; D059289:Vascular Stiffness / Q000187:drug effects* / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept