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Review
. 2024 Jul 19;12(7):1608.
doi: 10.3390/biomedicines12071608.

Treating Cardiovascular Disease in the Inflammatory Setting of Rheumatoid Arthritis: An Ongoing Challenge

Affiliations
Review

Treating Cardiovascular Disease in the Inflammatory Setting of Rheumatoid Arthritis: An Ongoing Challenge

Saloni Godbole et al. Biomedicines. .

Abstract

Despite progress in treating rheumatoid arthritis, this autoimmune disorder confers an increased risk of developing cardiovascular disease (CVD). Widely used screening protocols and current clinical guidelines are inadequate for the early detection of CVD in persons with rheumatoid arthritis. Traditional CVD risk factors alone cannot be applied because they underestimate CVD risk in rheumatoid arthritis, missing the window of opportunity for prompt intervention to decrease morbidity and mortality. The lipid profile is insufficient to assess CVD risk. This review delves into the connection between systemic inflammation in rheumatoid arthritis and the premature onset of CVD. The shared inflammatory and immunologic pathways between the two diseases that result in subclinical atherosclerosis and disrupted cholesterol homeostasis are examined. The treatment armamentarium for rheumatoid arthritis is summarized, with a particular focus on each medication's cardiovascular effect, as well as the mechanism of action, risk-benefit profile, safety, and cost. A clinical approach to CVD screening and treatment for rheumatoid arthritis patients is proposed based on the available evidence. The mortality gap between rheumatoid arthritis and non-rheumatoid arthritis populations due to premature CVD represents an urgent research need in the fields of cardiology and rheumatology. Future research areas, including risk assessment tools and novel immunotherapeutic targets, are highlighted.

Keywords: biological therapy; cardiovascular disease; inflammation; rheumatoid arthritis; statin; therapeutics.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Schematic representation of common mechanisms in the pathogenesis of cardiovascular disease and rheumatoid arthritis. Increased levels of pro-inflammatory cytokines are found in the joint space and the systemic circulation. The combination of pro-inflammatory mediators and reduced levels of atheroprotective nitric oxide and IL-10 trigger endothelial dysfunction. Dysfunctional endothelium, poorly functioning pro-inflammatory HDL, highly atherogenic citrullinated LDL, and an altered blood lipid profile contribute to atherosclerosis and thrombosis, which favor accelerated development of cardiovascular disease in patients with rheumatoid arthritis. ↑ = increases; ↓ = decreases; → = progresses to.
Figure 2
Figure 2
Illustration of the effects of three cytokines, TNF-α, IL-1β, and IFN-γ on the musculoskeletal system (left side) and cardiovascular system (right side).

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