Rheumatoid arthritis (RA) has long been associated with increased cardiovascular risk, but despite substantial improvements in disease management, mortality remains high. Atherosclerosis is more prevalent in RA than in the general population, and atherosclerotic lesions progress at a faster rate and might be more prone to rupture, causing clinical events. Cells and cytokines implicated in RA pathogenesis are also involved in the development and progression of atherosclerosis, which is generally recognized as an inflammatory condition. The two diseases also share genetic and environmental risk factors, which suggests that patients who develop RA might also be predisposed to developing cardiovascular disease. In RA, inflammation and atherosclerosis are closely linked. Inflammation mediates its effects on atherosclerosis both through modulation of traditional risk factors and by directly affecting the vessel wall. Treatments such as TNF inhibitors might have a beneficial effect on cardiovascular risk. However, whether this benefit is attributable to effective control of inflammation or whether targeting specific cytokines, implicated in atherosclerosis, provides additional risk reduction is unclear. Further knowledge of the predictors of cardiovascular risk, the effects of early control of inflammation and of drug-specific effects are likely to improve the recognition and management of cardiovascular risk in patients with RA.
Rheumatoid arthritis (RA) is associated with a significantly increased risk of cardiovascular mortality, accounted for mainly by increased atherosclerotic disease.1, 2 Although the prevalence of some traditional cardiovascular risk factors is increased in RA, adjustment for these factors does not fully account for the heightened risk, suggesting that RA itself is an independent risk factor for cardiovascular disease (CVD).3 The prevalence of atherosclerosis is increased in RA, even in early disease,4 and chronic inflammation is thought to promote atherosclerosis both by modulation of traditional risk factors and also possibly by direct biological effects on the artery. In this article, we discuss the potential mechanisms that might accelerate atherosclerosis in RA, with a particular focus on inflammation.
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| Figure 2: Development of an atherosclerotic plaque. |
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