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Tumor necrosis factor-a, biologic agents and cardiovascular risk

Rheumatology Unit, L. Sacco University Hospital, Milan, Italy, sarzi{at}tiscali.it

F Atzeni

Rheumatology Unit, L. Sacco University Hospital, Milan, Italy

A Doria

Division of Rheumatology, University of Padua, Rheumatology Unit

L Iaccarino

Division of Rheumatology, University of Padua, Rheumatology Unit

M Turiel

Department of Cardiology, Istituto Ortopedico Galeazzi, University of Milan, Milan, Italy

The increased risk of premature cardiovascular disease (CVD) in rheumatoid arthritis (RA) patients may depend on traditional risk factors but may also be attributable to RA-specific risk factors such as disease-related dyslipidemia, or cytokines such as tumor necrosis factor-a (TNF-a). TNF-a is a proinflammatory cytokine that can produce widespread deleterious effects when expressed in large amounts. It is produced in the heart by both cardiac myocytes and resident macrophages under conditions of cardiac stress, and is thought to be responsible for many of the untoward manifestations of cardiac disease. TNF-a may play a role in the triggering and perpetuation of atherosclerosis. Treatment with biologic agents directed against TNF-a has significant clinical benefits in inflammatory diseases such as RA and may be able to reduce cardiovascular risk. The disappointing results of the recent studies to antagonize TNF-a in CVD may have various explanations. However, the effects of TNF-a blockers on incident cases of congestive heart failure (CHF) in RA remains controversial. Due to the lack of evidence of a beneficial effect of anti-TNF-a agents in treatment of CHF, they should not be used to treat patients with New York Heart Association (NYHA) class III or IV heart failure.

Key Words: atherosclerosis • biologic agents • cardiovascular disease • rheumatoid arthritis • tumor necrosis factor-a

Lupus, Vol. 14, No. 9, 780-784 (2005)
DOI: 10.1191/0961203305lu2220oa


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