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ABSTRACT
Introduction: Cardiovascular disease is a leading comorbidity in rheumatoid arthritis. Timely introduction of biologic therapies in a treat-to-target approach has optimized disease-related outcomes and attenuated accrual of comorbidities, including cardiovascular risk.
Areas covered: A literature search in MEDLINE (via PubMed) was performed between January 2009 and November 2020. This manuscript explores recent developments in atherosclerotic cardiovascular risk in RA compared with non-RA individuals; it synopsizes differences in vascular function and inflammation, prevalence, burden, vulnerability, and progression of atherosclerotic plaque and their underlying cellular and molecular mechanisms. Finally, it reviews the recent literature on cardioprotective benefits of biologics and draws mechanistic links with inhibition of new plaque formation, stabilization of high-risk lesions and improvement in endothelial function, arterial stiffness, lipid metabolism, and traditional cardiac risk factors.
Expert opinion: Increasing evidence points to a solid cardioprotective influence of earlier, longer, and ongoing use of biologic treatments in RA. Nevertheless, the precise mechanistic effects of plaque progression and remodeling, vascular stiffness, endothelial dysfunction, lipid metabolism, and traditional cardiac risk factors are less rigorously characterized.
Article highlights
• Cardiovascular disease is a leading comorbidity in rheumatoid arthritis. Interactions between traditional cardiac risk factors and inflammation promote cardiovascular risk.
• Earlier implementation of effective RA therapies in a treat-to-target approach and cardiovascular risk stratification has significantly reduced morbidity and mortality in the past decade. However, the risk for incident or recurrent acute coronary syndrome remains higher in RA patients compared to non-rheumatic disease controls.
• RA-related proinflammatory cytokines, cellular, and humoral immune responses closely resemble mechanisms operative in the atherosclerotic process. RA and atherosclerosis share genetic and environmental risk factors, with inflammation as a common effector pathway for tissue damage and morbidity.
• All stages of atherogenesis are accelerated in RA, including endothelial dysfunction, arterial stiffness, vessel wall inflammation, plaque formation, remodeling, and destabilization. Emerging data suggests that surrogate measures of the outcomes predict enhanced cardiovascular risk.
• A large body of evidence indicates that biologic DMARDs effectively control RA inflammation in conventional DMARD inadequate responders and attenuate cardiovascular risk. In earlier implementations, longer and continuous use seems to convey better outcomes. Whether the cardioprotective benefits of biologics reflects more effective control of inflammation or a class-specific influence on the atherosclerotic process itself, remains elusive.
• The nature and duration of the effects of various biologic classes on endothelial function, arterial stiffness, plaque progression, and remodeling are less clear and a topic of interest and future research.
• The impact of various biologic classes on lipid levels and function, body composition, insulin sensitivity, and blood pressure control is an area of active investigation.
Declaration of interest
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.