Abstract
Objective: Rheumatoid arthritis (RA) leads not only to joint destruction but also to systemic manifestations, with an increased incidence of cardiovascular events (CVE). Many studies have shown a link between RA severity and CV risk, but the duration of follow-up remains often insufficient to allow a conclusion. The CVE definition was generally reduced to myocardial infarction and stroke, and few studies were conducted in non-Anglo-Saxon countries with low CV incidence. This study aimed to assess the relationship between joint destruction and the occurrence of different types of CVE in a large cohort of French RA patients with a long-term follow-up.Methods: This historical cohort study included 571 RA patients followed between 1992 and 2012 in Lyon, France. The primary endpoint was the first occurrence of a CVE. Logistic regressions were used to identify factors associated with CVE occurrence. Cox proportional hazard models were performed as a separate analysis to take advantage of the long-term follow-up.Results: During a mean follow-up of 16.1 years, 30.3% of patients experienced a CVE, mostly acute arterial events. Joint destruction was associated with an increased risk of CVE [odds ratio = 3.72; 95% confidence interval (CI), 1.09–15.35; p = 0.047] among non-smoker RA patients. A survival analysis revealed that joint destruction was associated with a shorter time to onset of the first CVE only among non-smokers (hazard ratio = 3.44; 95% CI, 1.07–11.04; p = 0.038).Conclusion: Joint destruction is associated with CVE occurrence in RA patients from a population with a lower incidence of CV disease. This study suggests that RA patients, especially those with destruction, merit the institution of precise guidelines to manage this CV risk, and trials are required to evaluate them.
Highlights
Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by joint destruction [1]
A detailed analysis showed the modest contribution of classical CV risk factors, suggesting a direct link between cardiovascular events (CVE) occurrence and chronic inflammation [2,3,4]
Tumor necrosis factor-alpha (TNFα), interleukin (IL)-6, and IL-17 have a direct contribution to joint damage and to the development of accelerated atherosclerosis and premature CVE [4,5,6,7,8,9]
Summary
Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by joint destruction [1]. A detailed analysis showed the modest contribution of classical CV risk factors, suggesting a direct link between CVE occurrence and chronic inflammation [2,3,4]. The exact cause of RA remains unknown, the contribution of pro-inflammatory cytokines is well-established. Tumor necrosis factor-alpha (TNFα), interleukin (IL)-6, and IL-17 have a direct contribution to joint damage and to the development of accelerated atherosclerosis and premature CVE [4,5,6,7,8,9]. The control of inflammation with inhibitors of these cytokines appears to reduce CV risk in RA, and more trials are ongoing [4, 10, 11]
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