The effect of tumor necrosis factor-α antagonists on arterial stiffness in rheumatoid arthritis: a literature review

Semin Arthritis Rheum. 2012 Aug;42(1):1-8. doi: 10.1016/j.semarthrit.2012.02.002. Epub 2012 Apr 3.

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.

Search strategy: 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.

Findings: 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.

Publication types

  • Review

MeSH terms

  • Adalimumab
  • Antibodies, Monoclonal / therapeutic use*
  • Antibodies, Monoclonal, Humanized / therapeutic use
  • Antirheumatic Agents / therapeutic use*
  • Arteriosclerosis / complications
  • Arteriosclerosis / drug therapy*
  • Arteriosclerosis / physiopathology
  • Arthritis, Rheumatoid / complications
  • Arthritis, Rheumatoid / drug therapy*
  • Arthritis, Rheumatoid / physiopathology
  • Databases, Bibliographic
  • Endothelium, Vascular / drug effects
  • Etanercept
  • Humans
  • Immunoglobulin G / therapeutic use
  • Infliximab
  • Pulse Wave Analysis
  • Receptors, Tumor Necrosis Factor / therapeutic use
  • Treatment Outcome
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*
  • Vascular Resistance / drug effects
  • Vascular Stiffness / drug effects*
  • Vascular Stiffness / physiology
  • Vasodilation / drug effects

Substances

  • Antibodies, Monoclonal
  • Antibodies, Monoclonal, Humanized
  • Antirheumatic Agents
  • Immunoglobulin G
  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha
  • Infliximab
  • Adalimumab
  • Etanercept