3.8 Article

Atherosclerotic Cardiovascular Disease in Rheumatoid Arthritis: Impact of Inflammation and Antirheumatic Treatment

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EUROPEAN CARDIOLOGY REVIEW
卷 16, 期 -, 页码 -

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RADCLIFFE CARDIOLOGY
DOI: 10.15420/ecr.2020.44

关键词

Rheumatoid arthritis; cardiovascular disease; atherosclerosis; inflammation; antirheumatic agents

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Patients with rheumatoid arthritis have a 1.5-fold increased risk of atherosclerotic cardiovascular disease compared to the general population due to a combination of traditional risk factors and systemic inflammation. Treatment of systemic inflammation with antirheumatic medication, along with managing traditional risk factors, is crucial for reducing cardiovascular disease risk in this high-risk patient group. Various antirheumatic drugs have shown potential in reducing cardiovascular disease risk in observational studies, but more randomized controlled trials with hard endpoints are needed. Anti-inflammatory therapies targeting specific pathways may be potential treatments after a cardiovascular event in patients without rheumatic disease.
Patients with rheumatoid arthritis (RA) are at approximately 1.5-fold risk of atherosclerotic cardiovascular disease (CVD) compared with the general population, a phenomenon resulting from combined effects of traditional CVD risk factors and systemic inflammation. Rheumatoid synovitis and unstable atherosclerotic plaques share common inflammatory mechanisms, such as expression of proinflammatory cytokines interleukin (IL)-1, tumour necrosis factor (TNF)-alpha and IL-6. RA patients are undertreated in terms of CVD prevention, and structured CVD prevention programmes are warranted. Alongside management of traditional risk factors, suppressing systemic inflammation with antirheumatic medication is fundamental for the reduction of CVD risk among this high risk patient group. Many antirheumatic drugs, especially methotrexate, INF-alpha inhibitors and IL-6-inhibitors are associated with reduced risk of CVD in observational studies among RA patients, but randomised controlled trials with hard CVD endpoints are lacking. In patients without rheumatic disease, anti-inflammatory therapies targeting nucleotide-binding oligomerisation domain, leucine-rich repeat and pyrin domain-containing protein 3 inflammasome and the IL-1/IL-6 pathway arise as potential therapies after an atherosclerotic CVD event.

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