Cardiovascular risks in spondyloarthritides

Curr Opin Rheumatol. 2007 Jul;19(4):358-62. doi: 10.1097/BOR.0b013e328133f58e.


Purpose of review: Spondyloarthritides are associated with increased cardiovascular risks, which can only partly be explained by traditional risk factors. It is likely that the chronic inflammatory state is involved. In this review, novel findings regarding cardiac and vascular pathologies and potential overlapping mechanisms will be discussed.

Recent findings: Cardiac pathologies in spondyloarthritides are conduction disturbances and valvular heart diseases. Recent studies have also focused on vascular pathologies and showed impaired endothelial function, suggesting that atherosclerotic alterations could also be involved in increased cardiovascular mortality. Novel findings suggest that chronic systemic inflammation is involved in these cardiac and vascular pathologies. Thus, spondyloarthritides and ankylosing spondylitis are associated with increased levels of circulating inflammatory mediators such as C-reactive protein. Interestingly, ankylosing spondylitis patients may also have an atherogenic lipid profile and disturbances in their T-helper lymphocyte subsets, which may be involved in cardiovascular disease development. The beneficial effects of statin treatment on circulating inflammatory mediators and atherogenic lipid profiles may reveal new therapeutic options for patients with spondyloarthritides.

Summary: Recent studies have highlighted that the chronic, systemic inflammatory condition of patients with spondyloarthritides may be involved in the development of cardiac and vascular pathologies.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Chronic Disease
  • Dyslipidemias / etiology
  • Heart Diseases / etiology*
  • Humans
  • Inflammation / complications*
  • Inflammation / immunology
  • Inflammation Mediators / adverse effects
  • Risk Factors
  • Spondylarthritis / complications*
  • Spondylarthritis / physiopathology
  • Vascular Diseases / etiology*


  • Inflammation Mediators