Abstract:BackgroundAccording to recent national and EULAR recommendation cardiovascular risk (CVR) in pts with RA should be evaluated using modified SCORE system. But a lot of investigations and real clinical data demonstrate that this system commonly down-estimates CVR in RA pts.ObjectivesAim of our study was to compare standard CVR assessment and additional CVR evaluation on the basis of specific disease-associated risk factors (RF) and CV system investigations in long standing RA.Methods118 pts (96 female, 22 male) … Show more
“…3 Although the prevalence of some traditional CVD risk factors is increased in patients with RA, extending the general population approach to CVD risk estimation in the RA population is flawed. 4,5 For example, the most commonly used clinical instruments for estimating CVD risk scores, such as the Framingham Risk Score and the European SCORE system, underestimate CVD risk in RA by as much as 2-fold. 2 The main reason for this discrepancy is related to the presence of novel CVD risk factors uniquely associated with RA progression and their synergy with traditional factors in elevating CVD risk.…”
Objective: To scope the current published evidence on cardiovascular risk factors in rheumatoid arthritis (RA) focusing on the role of autoantibodies and the effect of antirheumatic agents. Methods: Two reviews were conducted in parallel: A targeted literature review (TLR) describing the risk factors associated with cardiovascular disease (CVD) in RA patients; and a systematic literature review (SLR) identifying and characterizing the association between autoantibody status and CVD risk in RA. A narrative synthesis of the evidence was carried out. Results: A total of 69 publications (49 in the TLR and 20 in the SLR) were included in the qualitative evidence synthesis. The most prevalent topic related to CVD risks in RA was inflammation as a shared mechanism behind both RA morbidity and atherosclerotic processes. Published evidence indicated that most of RA patients already had significant CV pathologies at the time of diagnosis, suggesting subclinical CVD may be developing before patients become symptomatic. Four types of autoantibodies (rheumatoid factor, anti-citrullinated peptide antibodies, anti-phospholipid autoantibodies, anti-lipoprotein autoantibodies) showed increased risk of specific cardiovascular events, such as higher risk of cardiovascular death in rheumatoid factor positive patients and higher risk of thrombosis in anti-phospholipid autoantibody positive patients. Conclusion: Autoantibodies appear to increase CVD risk; however, the magnitude of the increase and the types of CVD outcomes affected are still unclear. Prospective studies with larger populations are required to further understand and quantify the association, including the causal pathway, between specific risk factors and CVD outcomes in RA patients.
“…3 Although the prevalence of some traditional CVD risk factors is increased in patients with RA, extending the general population approach to CVD risk estimation in the RA population is flawed. 4,5 For example, the most commonly used clinical instruments for estimating CVD risk scores, such as the Framingham Risk Score and the European SCORE system, underestimate CVD risk in RA by as much as 2-fold. 2 The main reason for this discrepancy is related to the presence of novel CVD risk factors uniquely associated with RA progression and their synergy with traditional factors in elevating CVD risk.…”
Objective: To scope the current published evidence on cardiovascular risk factors in rheumatoid arthritis (RA) focusing on the role of autoantibodies and the effect of antirheumatic agents. Methods: Two reviews were conducted in parallel: A targeted literature review (TLR) describing the risk factors associated with cardiovascular disease (CVD) in RA patients; and a systematic literature review (SLR) identifying and characterizing the association between autoantibody status and CVD risk in RA. A narrative synthesis of the evidence was carried out. Results: A total of 69 publications (49 in the TLR and 20 in the SLR) were included in the qualitative evidence synthesis. The most prevalent topic related to CVD risks in RA was inflammation as a shared mechanism behind both RA morbidity and atherosclerotic processes. Published evidence indicated that most of RA patients already had significant CV pathologies at the time of diagnosis, suggesting subclinical CVD may be developing before patients become symptomatic. Four types of autoantibodies (rheumatoid factor, anti-citrullinated peptide antibodies, anti-phospholipid autoantibodies, anti-lipoprotein autoantibodies) showed increased risk of specific cardiovascular events, such as higher risk of cardiovascular death in rheumatoid factor positive patients and higher risk of thrombosis in anti-phospholipid autoantibody positive patients. Conclusion: Autoantibodies appear to increase CVD risk; however, the magnitude of the increase and the types of CVD outcomes affected are still unclear. Prospective studies with larger populations are required to further understand and quantify the association, including the causal pathway, between specific risk factors and CVD outcomes in RA patients.
The article presents an analysis of the current view of comorbidity problem in rheumatology from the perspective of inflammatory disorders of the joints and spine combination with the most common diseases of the internal organs and endocrine system. The data gained from recent sources regarding the frequency and structure of concomitant disorders in patients with rheumatoid arthritis (RA) and spondylarthritis (ankylosing spondylitis [AS] and psoriatic arthritis [PsA]) are presented. It has been shown that the most common comorbidity in patients with RA, AS, PsA are diseases of the gastrointestinal tract and cardiovascular diseases. The authors present the results of their own research on the study of comorbidity in RA, AS and PsA, which are consistent with modern literature data. It is noted that there are specific disease-associated factors, as well as the negative effect of anti-inflammatory drugs in the development and manifestation of comorbid pathology.
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