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Atherosclerosis and connective tissue diseases
1Rheumatology Department, Hôpital Bichat, Paris, France. olivier.meyer@bch.ap-hop-paris.fr
Insights
Patients with systemic lupus erythematosus (SLE), antiphospholipid syndrome (APLS), and rheumatoid arthritis (RA) face significantly higher risks of premature atherosclerosis and cardiovascular events. Early intervention targeting inflammation and traditional risk factors is crucial for managing these conditions and preventing heart disease.
Area of Science:
- Cardiovascular Medicine
- Rheumatology
- Immunology
Background:
- Systemic lupus erythematosus (SLE), antiphospholipid syndrome (APLS), and rheumatoid arthritis (RA) are associated with substantially increased mortality from premature atherosclerosis, including coronary artery disease and stroke.
- Studies indicate elevated risks, such as a 5-fold increased risk of myocardial infarction and a 6- to 10-fold increased risk of stroke in SLE patients, and a 3.6-fold increased risk of cardiovascular deaths in RA patients.
Purpose of the Study:
- To identify and summarize the risk factors contributing to accelerated atherosclerosis in patients with SLE, APLS, and RA.
- To explore the pathogenic mechanisms underlying inflammation-driven atherosclerosis in these autoimmune diseases.
Main Methods:
- Review of epidemiological studies and clinical data on cardiovascular risk in patients with SLE, APLS, and RA.
- Analysis of established and disease-specific risk factors for atherosclerosis.
- Examination of the proposed inflammatory and immunological pathways involved in atherogenesis.
Main Results:
- Key risk factors include traditional ones (age, high cholesterol, hypertension, diabetes, obesity) and disease-specific factors (prolonged glucocorticoid therapy, long disease duration, postmenopausal status, heart failure).
- Systemic lupus erythematosus (SLE) is identified as an independent risk factor for atherosclerosis.
- Pathogenesis involves inflammatory responses, autoantibodies, immune complexes, activated T cells, and immune responses to heat shock proteins (HSPs).
Conclusions:
- Effective management of connective tissue diseases requires early intervention for risk factors and robust control of inflammation.
- Proactive strategies are essential to mitigate the heightened risk of atherosclerosis and cardiovascular events in patients with SLE, APLS, and RA.
Abstract:
Large increases in mortality related to premature atherosclerosis with coronary artery disease and stroke have been reported in patients with systemic lupus erythematosus (SLE), antiphospholipid syndrome (APLS), or rheumatoid arthritis (RA). Studies found relative risks of 5 for myocardial infarction, 6 to 10 for stroke in SLE patients, and 3.6 for cardiovascular deaths in RA patients. The main risk factors for atherosclerosis included not only the classic factors identified in epidemiological studies such as the Framingham study (advanced age, high cholesterol levels, hypertension, diabetes mellitus, and obesity), but also prolonged glucocorticoid therapy, long duration of SLE, postmenopausal status, and heart failure. SLE per se is an independent risk factor. The current pathogenic hypothesis for atherosclerosis involves an inflammatory response (erythrocyte sedimentation rate, C-reactive protein, and fibrin), autoantibodies, immune complexes (containing antibodies to phospholipids, to oxidized LDLs, and to endothelial cells), cytokine-producing activated T cells, and bacterial or viral infections responsible for an immune response against heat shock proteins (endogenous HSP60 and its equivalent, bacterial HSP65). Early risk factor intervention and effective control of inflammation should be incorporated into the management of connective tissue disease with the goal of protecting patients against atherosclerosis.