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I10 Cardiovascular disease burden and biomarkers in SLE
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  1. Elisabet Svenungsson
  1. Karolinska Institutet, Dept. of Medicine Solna, Karolinska University Hospital, Stockholm, Sweden

Abstract

Background Premature vascular disease is a major major clinical problem and the major cause of the shortened life expectancy observed among patients with SLE in modern societies. Both ischemic heart disease (IHD) and ischemic cerebrovascular disease (ICVD), is common in SLE, 10% and 12% respectively in our cross-sectional Swedish study. The risk estimates for VD in SLE are comparable to diabetes and premenopausal women are at particularly high relative risk. Only a minor part of the vascular risk in SLE is explained by abundance of traditional cardiovascular risk factors Thus, the major reasons for SLE related VD is associated with autoimmunity and SLE per se.

Methods This presentation will review current literature with focus on confirmed and recent findings which can explain why patients with SLE are so commonly affected by VD. Special focus will be given to biomarkers which are associated with the occurrence of VD, and which can serve to select patients in need of preventive treatment.

Results The focus of this presentation will be on SLE related vascular risk factors, but also on vascular outcomes and the temporal relationship between disease onset and VD.

Risk factors seem to differ between various hard vascular outcomes e.g. myocardial infarction, stroke and venous thromboembolism. Many studies use subclinical atherosclerosis or other measures of vascular vulnerability as outcomes, these are important to study but they should be distinctly separated from hard vascular events.

The following patient subgroups/biomarkers will be discussed in the context of SLE related VD: 1) Nephritis and impaired renal function, 2) Antiphospholipid antibodies 3) Complement activation, 4) Systemic inflammation 5) Genetic predisposition. In the clinic there is an interaction between all these factors and also traditional cardiovascular risk factors, which result in high risk for VD. Another approach is to subgroup SLE patients depending on autoantibodies and thus identify subgroups of patients with high risk for VD.

Conclusions Through early mapping and recognition of vascular risk factors in patients with SLE, it should in the future be possible to tailor preventive treatments to individual patients. The goal is to reduce and eventually prevent the heavy burden of vascular disease among patients with SLE.

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