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[Coronary involvement in systemic lupus erythematosus]
1Clinique dermatologique, Hôpital Charles Nicolle, Rouen.
Insights
Coronary artery disease is rare in lupus erythematosus. In patients with lupus and antiphospholipid antibodies, smoking may contribute to coronary artery disease development.
Area of Science:
- Cardiology
- Rheumatology
- Immunology
Background:
- Coronary artery disease (CAD) is infrequently observed in patients with systemic lupus erythematosus (SLE).
- The underlying mechanisms of coronary occlusion in SLE are complex and multifactorial.
- This report details three SLE patients diagnosed with CAD via coronary angiography, who also presented with antiphospholipid antibodies.
Observation:
- Three young SLE patients (21-35 years) developed CAD 3-11 years post-SLE onset.
- All patients tested positive for antiphospholipid antibodies and had received corticosteroid therapy.
- Coronary angiography revealed coronary occlusion in two patients and myocardial microvasculopathy in one; SLE was quiescent at the time of CAD diagnosis.
Findings:
- Antiphospholipid antibodies were present in all three patients with SLE and CAD.
- Smoking was identified as a potential contributing factor in two of the three patients.
- The combination of antiphospholipid antibodies and smoking may play a role in the pathogenesis of CAD in this cohort.
Implications:
- Highlights a potential link between antiphospholipid antibodies, smoking, and CAD in SLE patients.
- Suggests the need for cardiovascular risk assessment in SLE patients with antiphospholipid antibodies, particularly those who smoke.
- Underscores the complex interplay of factors contributing to cardiovascular complications in systemic lupus erythematosus.
Background:
Coronary artery disease is an uncommon event in lupus erythematosus. The mechanisms responsible for coronary occlusion are probably complex and intermixed. We report three patients with lupus erythematosus and antiphospholipid antibodies who had coronary artery disease diagnosed with coronary angiogram.
Observation:
Coronary artery disease occurred in three young patients aged from 21 to 35 years 3 to 11 years after the onset of lupus. They all had antiphospholipid antibodies. They had been treated with corticosteroids for 6 to 36 months. Two of them were smokers. Angiograms showed coronary occlusion two patients while the third one had probable myocardial microvasculopathy. The lupus was quiescent in all cases when coronary artery disease occurred.
Discussion:
Antiphospholipid antibodies associated with smoking may be involved in the pathogenesis of coronary artery disease in these 3 patients.