Why the study?
Patients with rheumatoid arthritis are at increased risk of atherosclerotic cardiovascular disease and undertreated in terms of prevention, but randomized controlled trials of antirheumatic drugs with hard cardiovascular endpoints are lacking.
Does antirheumatic treatment reduce the risk of atherosclerotic cardiovascular disease in patients with rheumatoid arthritis?
Does antirheumatic treatment reduce the risk of atherosclerotic cardiovascular disease in patients with rheumatoid arthritis?
Suppressing systemic inflammation with antirheumatic medication is fundamental for reducing the elevated CVD risk in rheumatoid arthritis patients, though RCTs are needed to confirm observational findings.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for antirheumatic drugs lowering CVD risk in RA; RCTs with hard endpoints required before practice change.
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)-α 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, TNF-α-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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Kerola et al. (2021) studied this question.
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