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Cardiovascular risk in rheumatoid arthritis: recent advances in the understanding of the pivotal role of inflammation, risk predictors and the impact of treatment

Journal

RHEUMATOLOGY
Volume 53, Issue 12, Pages 2143-2154

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/keu224

Keywords

rheumatoid arthritis; cardiovascular disease; inflammation; atherosclerosis; dyslipidaemias; anti-rheumatic agents

Categories

Funding

  1. F. Hoffman-La Roche Chugai Pharma
  2. UCB
  3. Pfizer
  4. MSD
  5. AbbVie
  6. BMS
  7. Abbott Laboratories
  8. Boehringer Ingelheim
  9. Daiichi Sankyo
  10. Eli Lilly
  11. ISIS
  12. MedImmune
  13. Synovate
  14. Ferring Pharmacuetical
  15. GSK
  16. Jazz Pharmaceuticals
  17. Merck/Schering-Plough
  18. Abbott
  19. Pfizer/Wyeth
  20. F. Hoffman-La Roche
  21. Raagholtstiftelsen
  22. Norwegian Extra Foundation for Health and Rehabilitation
  23. South Eastern Regional Health Authority of Norway

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Risk of cardiovascular (CV) disease is increased among RA patients. High inflammatory burden associated with RA appears to be a key driver of the increased cardiovascular risk. Inflammation is linked with accelerated atherosclerosis and associated with a paradoxical inversion of the relationship between CV risk and lipid levels in patients with untreated RA, recently coined the lipid paradox. Furthermore, the inflammatory burden is also associated with qualitative as well as quantitative changes in lipoproteins, with the anti-inflammatory and atheroprotective roles associated with high-density lipoprotein cholesterol significantly altered. RA therapies can increase lipid levels, which may reflect the normalization of lipids due to their inflammatory-dampening effects. However, these confounding influences of inflammation and RA therapies on lipid profiles pose challenges for assessing CV risk in RA patients and interpretation of traditional CV risk scores. In this review we examine the relationship between the increased inflammatory burden in RA and CV risk, exploring how inflammation influences lipid profiles, the impact of RA therapies and strategies for identifying and monitoring CV risk in RA patients aimed at improving CV outcomes.

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