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Chronic arthritis and cardiovascular disease: Altered blood parameters give rise to a prothrombotic propensity

Journal

SEMINARS IN ARTHRITIS AND RHEUMATISM
Volume 44, Issue 3, Pages 345-352

Publisher

W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.semarthrit.2014.06.006

Keywords

Rheumatoid arthritis; Ankylosing spondylitis; Psoriatic arthritis; Platelets; Coagulation; Cardiovascular disease; TNF-alpha

Categories

Funding

  1. Center for Translational Molecular Medicine (INCOAG)
  2. Netherlands Heart Foundation [2011T6]
  3. ZonMW [MKMD 114021004]

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Objective: Rheumatoid arthritis, and to a lesser extent ankylosing spondylitis and psoriatic arthritis, associates with increased morbidity and mortality due to cardiovascular complications. We hypothesized that the increased risk of cardiovascular disease is reflected by changes in blood parameters that are compatible with a prothrombotic propensity. To substantiate this notion, we performed an extensive literature search identifying such parameters. Methods: A search through PubMed (1970-2013) was done to find primary articles with the following search terms: rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis or synovial fluid. These were combined with keywords reflecting processes of atherothrombosis: atherosclerosis, cardiovascular disease, coagulation, endothelial, fibrinolysis, mean platelet volume, microparticle, platelet, platelet count and mass, thrombosis, and thrombus. Results: The published studies point to a multitude of blood-related processes that can contribute to a prothrombotic propensity in chronic inflammatory diseases. These include an increase in platelet mass; low-level platelet activation, enforced by interaction with leukocytes and the formation of proinflammatory cytokines; a locally activated endothelium; and an increased coagulant activity. Patient treatment with methotrexate or TNF-alpha blockers appears to result in normalization of several of these prothrombotic parameters. Conclusion: This analysis provides a first identification of the mechanisms by which inflammatory arthritis can aggravate cardiovascular disease. (C) 2014 Elsevier Inc. All rights reserved.

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