J Avouac1, Y Allanore. 1. Paris Descartes University, Medical Faculty, Department of Rheumatology A, Cochin Hospital, AP-HP, Paris, France.
Abstract
BACKGROUND: Patients with rheumatoid arthritis (RA) have an increased risk of atherosclerotic cardiovascular disease which cannot be explained by traditional cardiovascular risk factors alone. Atherosclerosis is considered an inflammatory condition and inflammation experienced in RA may contribute to accelerated atherosclerosis. Thus, it should be hypothesized that treatment with antitumor necrosis factor alpha (anti-TNF-alpha), TNF-alpha being a pivotal component of the inflammatory cascade, may decrease concomitantly intra-articular inflammation and vessel inflammation. OBJECTIVE: The purpose of this review is to examine the data regarding cardiovascular mortality and morbidity in RA and the evidence available to date evaluating the influence of anti-TNF-alpha treatments in RA on the occurrence of cardiovascular events, on surrogate markers of atherosclerosis and classical cardiovascular risk factors. METHODS: Clinical trials, original studies and review articles were identified from a Medline search (1998 - December 2007). Articles in English were reviewed, with emphasis on those containing assessments of cardiovascular effects (i.e., biological, structural, clinical) of anti-TNF-alpha drug. CONCLUSION: The suppression of systemic inflammation favoring atherosclerosis may lead to an improvement in cardiovascular prognosis in inflammatory disorders. Thus, reduction of inflammatory joint disease in RA with anti-TNF-alpha therapy, as probably with any powerful disease-modifying antirheumatic drugs, seems to be, at least in part, associated with concomitant reduction of the risk of cardiovascular events.
BACKGROUND:Patients with rheumatoid arthritis (RA) have an increased risk of atherosclerotic cardiovascular disease which cannot be explained by traditional cardiovascular risk factors alone. Atherosclerosis is considered an inflammatory condition and inflammation experienced in RA may contribute to accelerated atherosclerosis. Thus, it should be hypothesized that treatment with antitumor necrosis factor alpha (anti-TNF-alpha), TNF-alpha being a pivotal component of the inflammatory cascade, may decrease concomitantly intra-articular inflammation and vessel inflammation. OBJECTIVE: The purpose of this review is to examine the data regarding cardiovascular mortality and morbidity in RA and the evidence available to date evaluating the influence of anti-TNF-alpha treatments in RA on the occurrence of cardiovascular events, on surrogate markers of atherosclerosis and classical cardiovascular risk factors. METHODS: Clinical trials, original studies and review articles were identified from a Medline search (1998 - December 2007). Articles in English were reviewed, with emphasis on those containing assessments of cardiovascular effects (i.e., biological, structural, clinical) of anti-TNF-alpha drug. CONCLUSION: The suppression of systemic inflammation favoring atherosclerosis may lead to an improvement in cardiovascular prognosis in inflammatory disorders. Thus, reduction of inflammatory joint disease in RA with anti-TNF-alpha therapy, as probably with any powerful disease-modifying antirheumatic drugs, seems to be, at least in part, associated with concomitant reduction of the risk of cardiovascular events.
Authors: Chun Li; X R Wang; H J Ji; X Y Zhang; X F Li; L Z Wang; C H Wang; Y F Wang; Rong Yang; G C Wang; Xin Lu; Ping Zhu; L N Chen; H T Jin; J T Liu; X Y Liu; Lin Sun; H Y Chen; Ping Wei; J X Wang; L F Cui; Rong Shu; B L Liu; Z L Zhang; G T Li; Z B Li; Jing Yang; J F Li; Bin Jia; F X Zhang; J M Tao; S L Han; J Y Lin; M Q Wei; X M Liu; Dan Ke; S X Hu; Cong Ye; X Y Yang; Hao Li; C B Huang; Ming Gao; Bei Lai; X F Li; L J Song; Yi Wang; X Y Wang; Y D Tang; Yin Su; Rong Mu; Z G Li Journal: Clin Rheumatol Date: 2017-03-24 Impact factor: 2.980
Authors: George S Metsios; Antonios Stavropoulos-Kalinoglou; Aamer Sandoo; Jet J C S Veldhuijzen van Zanten; Tracey E Toms; Holly John; George D Kitas Journal: Open Cardiovasc Med J Date: 2010-02-23