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

Abstract 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 pa...

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Bibliographic Details
Published in:Seminars in arthritis and rheumatism 2014-12, Vol.44 (3), p.345-352
Main Authors: Beinsberger, Jilke, MSc, Heemskerk, Johan W.M., PhD, Cosemans, Judith M.E.M., PhD
Format: Article
Language:English
Subjects:
Ankylosing spondylitis
Arthritis - blood
Arthritis - complications
Arthritis - physiopathology
Blood Coagulation - physiology
Cardiovascular disease
Cardiovascular Diseases - epidemiology
Cardiovascular Diseases - physiopathology
Coagulation
Humans
Mean Platelet Volume
Platelet Activation - physiology
Platelet Count
Platelets
Psoriatic arthritis
Rheumatoid arthritis
Rheumatology
Risk Factors
Thrombosis - epidemiology
Thrombosis - physiopathology
TNF-α
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Summary:Abstract 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-α 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.
ISSN:0049-0172
1532-866X
DOI:10.1016/j.semarthrit.2014.06.006