REVIEW

What effects might anti-TNF treatment be expected to have on cardiovascular morbidity and mortality in rheumatoid arthritis? A review of the role of TNF in cardiovascular pathophysiology

W G Dixon, D P M Symmons

ARC Epidemiology Unit, University of Manchester, Manchester, UK

Correspondence to:
Professor Deborah P M Symmons
ARC Epidemiology Unit, Stopford Building, University of Manchester, Manchester M13 9PT, UK; deborah.symmons{at}manchester.ac.uk

Patients with rheumatoid arthritis (RA) have an increased burden of atherosclerotic cardiovascular disease which cannot be explained by an increased prevalence of traditional cardiovascular risk factors alone. Atherosclerosis is now being viewed as an inflammatory condition and the cumulative inflammation experienced in RA may contribute to accelerated atherosclerosis. It has been hypothesised that treatment with anti-tumour necrosis factor (TNF) in RA may reduce both intra-articular inflammation and the inflammation associated with atherosclerosis. Thus, TNF blockade may reduce the cardiovascular morbidity and mortality associated with RA. This review examines the pathophysiological role of TNF in atherosclerosis and the evidence to date that anti-TNF treatment modifies this process in RA.

Abbreviations: CHF, chronic heart failure; CVD, cardiovascular disease; DMARD, disease modifying anti-rheumatic drug; ESR, erythrocyte sedimentation rate; HDL, high-density lipoprotein; hsCRP, high-sensitivity C-reactive protein; IL, interleukin; LDL, low-density lipoprotein; MI, myocardial infarction; IMT, intima media thickness; RA, rheumatoid arthritis; TNF, tumour necrosis factor

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