Abstract

Systemic autoimmune diseases (SADs) are associated with significantly enhanced cardiovascular (CV) morbidity and mortality due to a cluster of risk factors. Among them we find traditional markers of CV risk but also specific risk factors principally related to inflammation and autoimmunity. Therefore, CV involvement assessment in those diseases is more and more important and several authors have been studying for the last years that phenomenon. The most important goal for all of them is CV prevention and follow-up of subjects with such abnormalities; in particular, CV burden is mainly due to atherosclerosis (ATS). So, in order to achieve the best CV prevention program a very early diagnose of ATS in these patients (pts) is fundamental, especially in those phases of disease in which no symptoms are present and clinical manifestations are not clearly visible. In this review, our aim was to find the best marker for identifying early ATS in systemic autoimmune diseases (SADs) by starting our long experience in this field.

Highlights

  • Systemic autoimmune diseases (SADs) are quite widespread syndromes with an incidence of 0.13-0.16 in general population [1]

  • Analyzing the markers used for ATS evaluation we can observe that aymmetric dymethilarginine (ADMA) values are always very important as indicator of ATS and/or endothelial dysfunction in the large spectrum of systemic autoimmune diseases (SADs): rheumatoid arthritis (RA), psoriatic arthritis (PsA), systemic sclerosis (SSc) and s syndrome (SS)

  • In comparison with controls’ groups of healthy subjects, we have ADMA plasma values above the normal ranges in RA (OR=3.89; 95% CI 1.99-5.69), in PsA (OR=2.49; 95% CI 1.16-3.21), in SSc (OR=1.96; 95% CI 1.08-2.31) and in SS (1.13; 95% CI 0.99-2.06) (Table 1)

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Summary

Introduction

Systemic autoimmune diseases (SADs) are quite widespread syndromes with an incidence of 0.13-0.16 in general population [1] They are characterized by an important inflammatory response associated with a much or less large grade of autoimmunity mechanisms [2]. They consist of a multi-organ involvement including cardiovascular (CV) system [3,4]. We may imagine our important interference in the travel that brings us from endothelial dysfunction to ATS towards inflammation [8]. It is our goal, our hopefulness: we would like to manage ATS more and more better in the future

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