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Destruction of bone and soft tissue in rheumatoid arthritis (RA) occurs as a result of unchecked systemic inflammation. While swollen and deformed joints are easy to see, less obvious to the naked eye is the impact of this same inflammatory process on the cardiovascular (CV) system. Cardiovascular disease (CVD) is the leading cause of death in patients with RA. The mortality rate from CVD in RA is approximately 1.5 times that of individuals from the general population with the same age, sex and CV risk factors.1 The excess CV risk has been attributed to inflammation; however, the pathways and mechanisms linking inflammation to CV events are less clear. Lipids, specifically low-density lipoprotein cholesterol (LDL-C), are considered part of the causal pathway for atherosclerosis and CVD in the general population. However, the established relationships between LDL-C and CV risk are altered in RA. As expected, elevated levels of LDL-C are associated with increased CV risk in RA; however, low LDL-C is also associated with increased CV risk.2 Subjects with RA who experience a reduction in inflammation, considered beneficial for CV risk, have concomitant increases in LDL-C,3 suggesting the opposite effect of increased CV risk. Post hoc studies of lipids from randomised controlled trials of RA therapies have shown that increases in LDL-C occur across different classes of RA therapies.4 Together, these data demonstrate that the relationship between LDL-C, inflammation and increased CV risk, observed in the general population, becomes uncoupled in RA. A similar uncoupling was observed with total cholesterol (TC). Interestingly, the departure from established relationships was not as apparent when examining high-density lipoprotein (HDL-C) levels and CV risk in RA.
Recent studies have highlighted that HDL function is an independent predictor of incident CV events, even after adjusting for HDL-C levels.5 This HDL function, …
Contributors KPL drafted the editorial and takes full responsibility for its content.
Funding KPL is funded by the K08 AR 060257, R01 HL127118, and the Harold and Duval Bowen Fund.
Competing interests None declared.
Provenance and peer review Commissioned; externally peer reviewed.
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