Heart 2009;95:1471-1472
Editorials
Disease-modifying anti-rheumatic drugs: do they reduce cardiac complications of RA?
Cardiovascular Sciences, Bywaters Center for Vascular Inflammation, National Heart and Lung Institute, Imperial College London, Hammersmith Hospital, London, UK
Correspondence to Dr Justin Mason, Cardiovascular Sciences, Bywaters Center for Vascular Inflammation, Imperial College, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK; justin.mason@imperial.ac.uk
| The first 150 words of the full text of this article appear below. |
Our understanding of the pathogenesis of atherosclerosis has evolved from a lipid deposition disorder to a focal, chronic inflammatory disease of medium-large arteries characterised by inflammatory plaques susceptible to rupture and thrombosis. Atherogenesis shares certain pathogenic features with other inflammatory diseases including the autoimmune disease rheumatoid arthritis (RA). These include macrophage-activating cytokines such as tumour necrosis factor 
(TNF), interleukin-1 (IL-1) and interleukin-6 (IL-6), the presence of CD4+CD28– regulatory T-cells, raised inflammatory markers including C-reactive protein (CRP) and enhanced expression of endothelial adhesion molecules including VCAM-1.1 However, the association between atherosclerosis and RA extends beyond common pathogenic mechanisms. Standardised mortality ratios for cardiovascular disease in RA range from 1.2 to 5, and cardiovascular death accounts for up to 50% of mortality with life expectancy reduced by 10–15 years.2 A similar alarming trend is observed in systemic lupus erythematosus (SLE), with a marked increase in stroke and myocardial infarction (MI)
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Heart 2009 95: 1502-1507.[Abstract] [Full Text] [PDF]
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