Abstract
Rheumatoid arthritis (RA) is one of the most frequent inflammatory rheumatic diseases, having a considerably increased prevalence of mortality and morbidity due to cardiovascular disease (CVD). RA patients have an augmented risk for ischemic and non-ischemic heart disease. Increased cardiovascular (CV) risk is related to disease activity and chronic inflammation. Traditional risk factors and RA-related characteristics participate in vascular involvement, inducing subclinical changes in coronary microcirculation. RA is considered an independent risk factor for coronary artery disease (CAD). Endothelial dysfunction is a precocious marker of atherosclerosis (ATS). Pro-inflammatory cytokines (such as TNFα, IL-1, and IL-6) play an important role in synovial inflammation and ATS progression. Therefore, targeting inflammation is essential to controlling RA and preventing CVD. Present guidelines emphasize the importance of disease control, but studies show that RA- treatment has a different influence on CV risk. Based on the excessive risk for CV events in RA, permanent evaluation of CVD in these patients is critical. CVD risk calculators, designed for the general population, do not use RA-related predictive determinants; also, new scores that take into account RA-derived factors have restricted validity, with none of them encompassing imaging modalities or specific biomarkers involved in RA activity.
Highlights
Rheumatoid arthritis (RA) refers to the most common inflammatory rheumatic disease characterized by synovitis of small- and medium-sized joints, bone erosions, and destruction and loss of joints function
Studies confirm that the prevalence of traditional risk factors in the RA population is higher compared with the general population, with hypertension, hyperlipidemia, diabetes, and smoking representing the most important ones, but the risk profile, in this case, is a lot different; some researchers are even talking about a “risk factor paradox” in patients with RA [39,40]
It is important to mention other autoantibodies correlated with ATS [112], for example, antibodies against heat shock proteins (HSPs) from the surface of endothelial cells exposed to stress or antinuclear antibodies (ANA) found especially in patients with symptomatic angina pectoris [113]
Summary
Rheumatoid arthritis (RA) refers to the most common inflammatory rheumatic disease characterized by synovitis of small- and medium-sized joints, bone erosions, and destruction and loss of joints function. It is known that systemic inflammation is a significant contributing factor for the increased cardiovascular (CV) risk in patients with this disease [2,3] and is connected with arterial stiffness, lipid-salvage processes, and destabilization of atherosclerotic plaques [4,5]. Studies indicate that the prevalence of heart diseases in patients with RA is higher than in the general population and is equivalent to that in patients with type 2 diabetes [8,9]. Arthritis (ATACC-RA) discovered that approximately 49% of CV incidents in RA were caused by traditional CVD risk factors (especially smoking and hypertension) and 30% by RA-related aspects, such as elevated DAS (Disease Activity Score) 28, positive rheumatoid factor (RF) and/or anti-citrullinated protein antibody (ACPA), and raised erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) [12]. CV events explain 42% of total RA-related deaths (representing the leading cause of mortality in RA) [13] and appear early in patients having RA; for that reason, their survival rate is reduced by 5–15 years [14], representing the major cause of mortality in RA [8,9]
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