Abstract

Rheumatoid arthritis is a chronic, systemic inflammatory disease that carries an increased risk of mortality due to cardiovascular disease. The link between inflammation and atherosclerotic disease is clear; however, recent evidence suggests that inflammation may also play a role in the development of nonischemic heart disease in rheumatoid arthritis (RA) patients. We consider here the link between inflammation and cardiovascular disease in the RA community with a focus on heart failure with preserved ejection fraction. The effect of current anti-inflammatory therapeutics, used to treat RA patients, on cardiovascular disease are discussed as well as whether targeting resolution of inflammation might offer an alternative strategy for tempering inflammation and subsequent inflammation-driven comorbidities in RA.

Highlights

  • The disease is characterised by inflammation within synovial joints, which may lead to bone and cartilage destruction, extra-articular manifestations result in a 1.5-fold higher risk of death than the general population [2]

  • Even with earlier diagnosis and better treatment strategies, there are still patients who do not respond to current therapeutics or who do not remain in remission and cardiovascular disease in the rheumatoid arthritis (RA) population remains a concern in terms of both morbidity and mortality

  • There is still a need for furthering our understanding of the mechanisms linking systemic inflammatory conditions such as RA with cardiovascular disease (CVD), which will lead to new opportunities for the development of new treatments, with regards to heart failure (HF) with preserved ejection fraction (HFpEF), where treatment options are limited irrespective of the comorbidities driving pathogenesis

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Summary

Inflammation

CVD in RA can be divided into that arising from insufficient blood supply (ischemic heart disease) occurring as a consequence of atherosclerotic disease and nonischemic disease, which occurs in the absence of coronary artery disease and is associated with changes in the cells of the cardiac muscle

Ischemic Heart Disease
CVD Risk Factors in the RA Population
The Role of Inflammation
Effect of Current RA Therapies on CVD
Synthetic DMARDs
Biological DMARDs
Is the Heightened Cardiovascular Risk a Result of Failed Resolution Pathways?
Findings
Conclusions
Full Text
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