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Review Article| Volume 167, ISSUE 1, P138-151, January 2016

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Targeting inflammation in the prevention of cardiovascular disease in patients with inflammatory arthritis

  • Jiayun Shen
    Affiliations
    Department of Medicine and Therapeutics, The Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China
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  • Qing Shang
    Affiliations
    Department of Medicine and Therapeutics, The Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China
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  • Lai-Shan Tam
    Correspondence
    Reprint requests: Lai-Shan Tam, Department of Medicine and Therapeutics, The Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong, China
    Affiliations
    Department of Medicine and Therapeutics, The Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China
    Search for articles by this author
      Patients with inflammatory arthritis have increased risk of cardiovascular diseases (CVDs) compared with the general population. Subclinical carotid atherosclerosis and increased arterial stiffness are also common in these patients, which may serve as surrogate end points for cardiovascular (CV) events in clinical trials. Although exact mechanisms are still unclear, persistent systemic inflammation in patients with inflammatory arthritis may contribute to the development of CVD. Dysregulated innate immunity pathways in these patients may also play a role in accelerating atherosclerosis. During the last decade, effective suppression of inflammation by biological disease-modifying antirheumatic drugs has improved the disease outcome dramatically in patients with inflammatory arthritis. Growing evidence suggests that antitumor necrosis factor (TNF) therapy may prevent CVD in patients with rheumatoid arthritis. Nonetheless, data on non-TNF biologics are limited. Whether anti-TNF therapy may prevent CVD in patients with spondyloarthritis also remained unclear. In this review, we summarized the effect of both anti-TNF and non-TNF biologics on the CV system, including traditional CVD risk factors, endothelial function, arterial stiffness, subclinical atherosclerosis, and clinical CVD in patients with inflammatory arthritis.

      Abbreviations:

      ABA (abatacept), ADA (adalimumab), AIx (augmentation index), AMI (acute myocardial infarction), ANA (anakinra), Apo (apolipoprotein), AS (ankylosing spondylitis), CTZ (certolizumab pegol), CV (cardiovascular), CVD (cardiovascular disease), DMARD (disease-modifying antirheumatic drug), ETN (etanercept), FMD (flow-mediated vasodilation), GOL (golimumab), HDL (high-density lipoprotein), IFX (infliximab), IL (interleukin), IMT (intima-media thickness), LDL (low-density lipoprotein), MACE (major adverse cardiovascular event), MI (myocardial infarction), MMPs (matrix metalloproteinases), MTX (methotrexate), PsA (psoriatic arthritis), PWV (pulse wave velocity), RA (rheumatoid arthritis), RAGE (receptor for advanced glycation end product), RCT (randomized controlled trial), RTX (rituximab), sRAGE (soluble RAGE), TC (total cholesterol), TCZ (tocilizumab), TG (triglyceride), TNF (tumor necrosis factor), TOF (tofacitinib)
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