title: Tumor necrosis factor-alpha, biologic agents and cardiovascular risk.
abstract: 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-alpha (TNF-alpha). TNF-alpha 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-alpha may play a role in the triggering and perpetuation of atherosclerosis. Treatment with biologic agents directed against TNF-alpha 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-alpha in CVD may have various explanations. However, the effects of TNF-alpha 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-alpha 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.
authors.affiliation: Rheumatology Unit, L Sacco University Hospital, Milan, Italy. sarzi@tiscali.it
authors.forename: P
authors.initials: P
authors.lastname: Sarzi-Puttini
authors.forename: F
authors.initials: F
authors.lastname: Atzeni
authors.forename: A
authors.initials: A
authors.lastname: Doria
authors.forename: L
authors.initials: L
authors.lastname: Iaccarino
authors.forename: M
authors.initials: M
authors.lastname: Turiel
mesh_terms: D000818:Animals; D001172:Arthritis, Rheumatoid / Q000503:physiopathology; D050197:Atherosclerosis / Q000276:immunology / Q000503:physiopathology; D001327:Autoimmune Diseases / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000276:immunology* / Q000503:physiopathology; D050171:Dyslipidemias / Q000188:drug therapy / Q000276:immunology; D006333:Heart Failure / Q000188:drug therapy / Q000276:immunology / Q000503:physiopathology; D006801:Humans; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000378:metabolism*
chemical_list: D014409:Tumor Necrosis Factor-alpha