title: Will antirheumatic treatment improve cardiovascular outcomes in patients with rheumatoid arthritis?
abstract: In recent years, the scientific community has gained significant insight into the complex interaction between inflammation and the cardiovascular system in patients with rheumatoid arthritis (RA), which leads to increased cardiovascular (CV) morbidity and mortality in these patients. Our common understanding of this association is that persistent inflammation contributes to the development of premature atherosclerosis. Consequently, the question arises whether control of inflammation with antirheumatic treatment will be able to improve CV outcome. While there are a lot of data that demonstrate improvement of numerous CV surrogate markers in patients treated with virtually all antirheumatic drug classes, there is much less information about the possible translation of these beneficial effects into improved CV outcome. In summary, the published evidence suggests that tumor necrosis factor (TNF) alpha inhibitors may improve CV outcome. The same is true for methotrexate (MTX). However, it is not clear whether MTX works via suppression of inflammation or through drug specific mechanisms. For other traditional disease-modifying antirheumatic drugs and biologic therapies, there are no convincing data for improved CV outcome. Only a few drugs (glucocorticoids and NSAIDs) have been associated with increased CV risk. Treating RA aggressively, as recommended by current guidelines, is likely to have a beneficial effect on CV outcomes.
authors.forename: Herwig
authors.initials: H
authors.lastname: Pieringer
authors.forename: Max
authors.initials: M
authors.lastname: Pichler
authors.forename: Erich
authors.initials: E
authors.lastname: Pohanka
authors.affiliation: Academic Research Unit, 2nd Department of Medicine, General Hospital Linz, Krankenhausstr. 9, A-4020 Linz, Austria. herwigpi@yahoo.com.
authors.forename: Uta C
authors.initials: UC
authors.lastname: Hoppe
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000009:adverse effects / Q000627:therapeutic use*; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000276:immunology / Q000503:physiopathology; D050197:Atherosclerosis / Q000209:etiology / Q000517:prevention & control; D002317:Cardiovascular Agents / Q000009:adverse effects / Q000627:therapeutic use*; D002318:Cardiovascular Diseases / Q000209:etiology / Q000517:prevention & control*; D019317:Evidence-Based Medicine; D006801:Humans; D007166:Immunosuppressive Agents / Q000009:adverse effects / Q000627:therapeutic use; D058990:Molecular Targeted Therapy / Q000009:adverse effects*; D056653:Rheumatoid Vasculitis / Q000209:etiology / Q000517:prevention & control; D016896:Treatment Outcome
chemical_list: D000893:Anti-Inflammatory Agents; D000894:Anti-Inflammatory Agents, Non-Steroidal; D018501:Antirheumatic Agents; D002317:Cardiovascular Agents; D007166:Immunosuppressive Agents