Prediction and management of cardiovascular outcomes in systemic lupus erythematosus

Abstract

Atherosclerosis is the major cause of cardiovascular disease (CVD), which represents the major cause of death. During recent years, it has become clear that atherosclerosis is a chronic inflammatory condition where immunity could play an important role. Usually, it is when atherosclerotic plaques rupture that CVD follows, but some cases of CVD can occur without apparent atherosclerosis. In systemic lupus erythematosus, the risk of CVD is very high and the prevalence of atherosclerotic plaques, including vulnerable ones, is increased. A combination of traditional and non-traditional risk factors is implicated for the prediction of CVD in systemic lupus erythematosus. Traditional risk factors include hypertension, dyslipidemia, smoking and diabetes, though the exact importance of each of these in systemic lupus erythematosus is not clear. Anti-phospholipid antibodies, systemic inflammation and low levels of natural antibodies such as those against phosphorylcholine (anti-PC) are examples of non-traditional risk factors. Control of disease activity and disease manifestations and of established risk factors is important.

Keywords:

• antibodies
• atherosclerosis
• cardiovascular disease
• inflammation
• risk factors
• systemic lupus erythematosus

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.

Key issues

• The risk of cardiovascular disease (CVD) is very high in systemic lupus erythematosus (SLE).

• Atherosclerosis (prevalence of atherosclerotic plaques) is also increased in SLE and associated with CVD in SLE.

• It is possible that some patients develop CVD in SLE without apparent atherosclerosis.

• Traditional risk factors such as hypertension, dyslipidemia, smoking and diabetes contribute to the increased risk, especially the two first ones.

• Non-traditional risk markers include inflammation, disease activity, antiphospholipid antibodies and other factors, one example being low levels of some natural antibodies.

• Traditional risk factors should be treated appropriately.

• Statins should be used according to guidelines, but there is no consensus that statins should be more in SLE than in the general population.

• Novel therapies can hopefully be developed which target the causes of inflammation and immune activation in CVD.