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Published on: June 16, 2020
Systemic lupus erythematosus and cardiovascular disease
1Section of Immunology and Chronic Disease, Karolinska Institutet, Stockholm, Sweden.
Insights
Systemic lupus erythematosus (SLE) patients face higher cardiovascular disease (CVD) risks due to atherosclerosis and antiphospholipid antibodies (aPL). Managing traditional and non-traditional risk factors is crucial for better CVD outcomes in SLE.
Area of Science:
- Rheumatology
- Cardiology
- Immunology
Background:
- Cardiovascular disease (CVD) remains a significant challenge in systemic lupus erythematosus (SLE) despite improved overall prognosis.
- The risk of CVD is substantially elevated in SLE patients compared to the general population.
- Atherosclerosis, a key driver of CVD, is more prevalent in SLE, characterized by inflammatory processes and immune system dysregulation.
Purpose of the Study:
- To elucidate the multifaceted mechanisms contributing to the increased CVD risk in SLE.
- To identify both traditional and non-traditional risk factors implicated in SLE-related cardiovascular complications.
- To emphasize the importance of comprehensive risk factor management in SLE patients.
Main Methods:
- Review and synthesis of existing literature on CVD in SLE.
- Analysis of the roles of atherosclerosis, antiphospholipid antibodies (aPL), and inflammation in SLE pathogenesis.
- Examination of the impact of traditional risk factors (hypertension, dyslipidemia) and non-traditional factors (aPL, anti-PC antibodies) on CVD risk.
Main Results:
- Atherosclerosis, driven by inflammation and immune factors like oxidized LDL and impaired cellular debris clearance, is a primary contributor to CVD in SLE.
- Antiphospholipid antibodies (aPL) promote thrombosis and endothelial dysfunction, significantly increasing arterial and venous risks.
- Low levels of antibodies against phosphorylcholine (anti-PC) are associated with higher CVD and atherosclerosis risk in SLE patients.
Conclusions:
- The elevated CVD risk in SLE is a complex interplay of traditional factors (hypertension, dyslipidemia) and non-traditional factors, notably aPL and inflammation.
- Specific immune markers, such as antiphospholipid antibodies (aPL) and anti-phosphorylcholine (anti-PC) antibodies, play critical roles.
- Close monitoring and management of both traditional and non-traditional risk factors, alongside SLE disease activity, are essential for mitigating CVD in affected individuals.
Abstract:
The prognosis in systemic lupus erythematosus (SLE) has improved due to better treatment and care, but cardiovascular disease (CVD) still remains an important clinical problem, since the risk of CVD in SLE is much higher than among controls. Atherosclerosis is the main cause of CVD in the general population, and in SLE, increased atherosclerosis, especially the prevalence of atherosclerotic plaques, has been demonstrated. Atherosclerosis is an inflammatory condition, where immunity plays an important role. Interestingly, oxidized low-density lipoprotein, defective clearance of dead cells, and inflammation, with a pro-inflammatory T-cell profile are characteristics of both atherosclerosis and SLE. In addition to atherosclerosis as an underlying cause of CVD in SLE, there are also other non-mutually exclusive mechanisms, and the most important of these are antiphospholipid antibodies (aPL) leading to the antiphospholipid antibody syndrome with both arterial and venous thrombosis. aPL can cause direct pro-inflammatory and prothrombotic effects on endothelial and other cells and also interfere with the coagulation, for example, by inhibiting annexin A5 from its antithrombotic and protective effects. Antibodies against phosphorylcholine (anti-PC) and other small lipid-related epitopes, sometimes called natural antibodies, are negatively associated with CVD and atherosclerosis in SLE. Taken together, a combination of traditional risk factors such as hypertension and dyslipidemia, and nontraditional ones, especially aPL, inflammation, and low anti-PC are implicated in the increased risk of CVD in SLE. Close monitoring of both traditional risk factors and nontraditional ones, including treatment of disease manifestations, not lest renal disease in SLE, is warranted.
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