Abstract
There is abundant evidence that rheumatoid arthritis (RA), a chronic inflammatory disorder, is associated with an increased risk for cardiovascular (CV) disease. While there may be several mechanisms contributing to a higher CV risk in RA patients, inflammation is considered to be the main cause explaining the excess CV burden. Inflammatory processes appear pivotal to the atherothrombotic process and are linked to endothelial dysfunction, fatty streak initiation and progression, deterioration of fatty streaks into (unstable) plaques, and plaque rupture. Moreover, systemic inflammation, through tumor necrosis factor (TNF) or related cytokines, appears to accelerate atherothrombosis either directly or via effects on conventional and novel CV risk factors, such as lipids and lipoproteins, blood pressure, haemostatic factors, and insulin resistance. New and highly specific therapeutic agents (TNF inhibitors) may significantly lower CV risk in RA. This review summarizes the evidence base supporting the notion that TNF inhibitors confer benefit CV disease risk in RA.
Keywords: Rheumatoid arthritis, cardiovascular disease, inflammation, TNF inhibitors, endothelial dysfunction, plaque rupture, cytokines, atherothrombosis, lipoproteins, insulin resistance
Current Pharmaceutical Design
Title: The Effects of Tumor Necrosis Factor Inhibitors on Cardiovascular Risk in Rheumatoid Arthritis
Volume: 18 Issue: 11
Author(s): Mike J.L. Peters, Alper M. van Sijl, Alexandre E. Voskuyl, Naveed Sattar, Yvo M. Smulders and Michael T. Nurmohamed
Affiliation:
Keywords: Rheumatoid arthritis, cardiovascular disease, inflammation, TNF inhibitors, endothelial dysfunction, plaque rupture, cytokines, atherothrombosis, lipoproteins, insulin resistance
Abstract: There is abundant evidence that rheumatoid arthritis (RA), a chronic inflammatory disorder, is associated with an increased risk for cardiovascular (CV) disease. While there may be several mechanisms contributing to a higher CV risk in RA patients, inflammation is considered to be the main cause explaining the excess CV burden. Inflammatory processes appear pivotal to the atherothrombotic process and are linked to endothelial dysfunction, fatty streak initiation and progression, deterioration of fatty streaks into (unstable) plaques, and plaque rupture. Moreover, systemic inflammation, through tumor necrosis factor (TNF) or related cytokines, appears to accelerate atherothrombosis either directly or via effects on conventional and novel CV risk factors, such as lipids and lipoproteins, blood pressure, haemostatic factors, and insulin resistance. New and highly specific therapeutic agents (TNF inhibitors) may significantly lower CV risk in RA. This review summarizes the evidence base supporting the notion that TNF inhibitors confer benefit CV disease risk in RA.
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Cite this article as:
J.L. Peters Mike, M. van Sijl Alper, E. Voskuyl Alexandre, Sattar Naveed, M. Smulders Yvo and T. Nurmohamed Michael, The Effects of Tumor Necrosis Factor Inhibitors on Cardiovascular Risk in Rheumatoid Arthritis, Current Pharmaceutical Design 2012; 18 (11) . https://dx.doi.org/10.2174/138161212799504786
DOI https://dx.doi.org/10.2174/138161212799504786 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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