Cardiovascular outcomes and tumour necrosis factor antagonists in chronic inflammatory rheumatic disease: a focus on rheumatoid arthritis

Expert Opin Drug Saf. 2016 Dec;15(sup1):55-61. doi: 10.1080/14740338.2016.1218469.

Abstract

Many chronic rheumatic diseases have an inflammatory etiology, leading to accelerated atherosclerosis and increased occurrence of vascular diseases. In rheumatoid arthritis (RA), a reduction in cardiovascular (CV) events has been reported under treatments reducing systemic inflammation. Areas covered: Given the central role of tumour necrosis factor alpha (TNFα) in chronic inflammatory conditions and in atherosclerosis, it has been suggested that TNFα-antagonists may reduce CV risk and mortality. Although there are no randomized controlled or head-to-head trials investigating the effect of specific anti-TNF-agents on CV outcomes, observational cohort studies, national registry data, and meta-analyses in RA have reported improved CV outcomes with anti-TNF therapy. Expert opinion: It is unclear whether this is due to reduced systemic inflammation or a specific anti-TNF effect at the atherosclerotic plaque level. Observed CV benefits appear to correlate with anti-TNF response. Conversely, although inconsistently, anti-TNF agents have also been linked with increased incidence/worsening of heart failure. Additional CV adverse events with anti-TNFs include vasculitis and venous thromboembolic events. We provide an overview of the likely effects of anti-TNF therapy on CV risk and adverse events, and evaluated differences in CV outcomes among different anti-TNF-agents.

Keywords: Anti-TNF agents; TNF-alpha; cardiovascular outcomes; chronic inflammation; rheumatic disease.

Publication types

  • Review

MeSH terms

  • Antirheumatic Agents / administration & dosage*
  • Antirheumatic Agents / adverse effects
  • Antirheumatic Agents / pharmacology
  • Arthritis, Rheumatoid / drug therapy
  • Cardiovascular Diseases / epidemiology
  • Cardiovascular Diseases / etiology*
  • Cardiovascular Diseases / prevention & control
  • Heart Failure / chemically induced
  • Heart Failure / epidemiology
  • Humans
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*
  • Vasculitis / chemically induced
  • Vasculitis / epidemiology
  • Venous Thromboembolism / chemically induced
  • Venous Thromboembolism / epidemiology

Substances

  • Antirheumatic Agents
  • Tumor Necrosis Factor-alpha