Inflammation: The classic double-edged sword

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Presentation transcript:

Inflammation: The classic double-edged sword Paul Kurlansky, MD The Journal of Thoracic and Cardiovascular Surgery Volume 149, Issue 3, Pages 866-868 (March 2015) DOI: 10.1016/j.jtcvs.2014.11.070 Copyright © 2015 The American Association for Thoracic Surgery Terms and Conditions

Figure 1 Pathogenesis of atherosclerosis in inflammatory rheumatic diseases. Traditional risk factors play an important role in premature atherosclerosis and are typically more prevalent in patients with inflammatory rheumatic diseases. Both shared and disease-specific pathogenic mechanisms also contribute to accelerated atherogenesis, with rheumatoid arthritis, systemic lupus erythematosus, and the vasculitides shown as examples. Ab, Antibody; ANCA, antineutrophil cytoplasmic antibody; dsDNA, double-stranded DNA; CCP, cyclic citrullinated peptide; EC, endothelial cells; IFN, interferon; FcγR, Fc gamma receptor; HOCL, hypochlorite; MPO, myeloperoxidase; ROS, reactive oxygen species; T reg, regulatory T lymphocytes lymphocytes. Reprinted from Mason JC, Libby P. Cardiovascular disease in patients with chronic inflammation: mechanisms underlying premature cardiovascular events in rheumatologic conditions Eur Heart J. November 28, 2014 [Epub ahead of print]. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2014. For permissions please E-mail: journals.permissions@oup.com. The Journal of Thoracic and Cardiovascular Surgery 2015 149, 866-868DOI: (10.1016/j.jtcvs.2014.11.070) Copyright © 2015 The American Association for Thoracic Surgery Terms and Conditions