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[Myocardial infarction in systemic lupus erythematosus. 7 cases in 6 patients]
J J Lanore1, J C Piette, C Chapelon
1Service de Médecine Interne, Groupe Hospitalier Pitié-Salpêtrière, Paris.
Insights
Systemic lupus erythematosus patients on high-dose steroids face increased risk of myocardial infarction, even with quiescent disease. Factors beyond traditional atheroma contribute to coronary artery occlusion in these patients.
Area of Science:
- Cardiology
- Rheumatology
- Immunology
Background:
- Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with diverse clinical manifestations.
- Cardiovascular complications, including myocardial infarction (MI), are a significant concern in SLE patients.
- Long-term management of SLE often involves high-dose corticosteroid therapy.
Observation:
- A study observed 7 myocardial infarctions in 6 SLE patients (4 men, 2 women) between 1974 and 1988.
- Patients' ages at lupus onset ranged from 13 to 44 years (mean 26), with 4 having renal involvement.
- MI occurred 4-19 years after lupus onset, often when the disease was quiescent or mildly active, requiring high-dose steroids (≥1 mg/kg/d prednisone).
Findings:
- Four patients had renal involvement, and MI occurred 4-19 years post-lupus onset.
- Among 5 patients with quiescent or mildly active disease, one had no traditional atheroma risk factors but used steroids for 10 years.
- Coronary angiography revealed occlusion in all 4 assessed patients, with atheroma in only 2. Lupus anticoagulant was present in 3 patients.
Implications:
- Coronary artery occlusion in SLE patients likely results from complex, interacting factors.
- Beyond vasculitis and steroid-induced atheroma, antiphospholipid antibodies and smoking may play crucial thrombogenic roles.
- This highlights the need for comprehensive cardiovascular risk assessment and management in SLE patients, considering non-traditional risk factors.
Abstract:
Between 1974 and 1988, 7 myocardial infarctions occurred in 6 (4 men, 2 women) out of 400 systemic lupus erythematosus patients. Their ages at the onset of lupus ranged from 13 to 44 years (m = 26). Four had renal involvement. Control of lupus in all 6 patients required high-dose steroids (at least 1 mg/kg/d of prednisone). Myocardial infarction occurred 4 to 19 years after the onset of lupus (m = 13). One patient died of cardiogenic shock. When the infarction occurred, only one patient was undergoing a lupus flare, while the disease was quiescent or slightly active in the 5 others. One patient had no risk factors for atheroma but had been taking steroids for 10 years. Among the other 4, one had hypertension, another had hyperlipidemia and 3 were smokers; they had been on steroids for 2, 4, 11 and 13 years. Coronary angiogram showed occlusion in all 4, but atheroma in only 2 patients. Lupus anticoagulant was present in 3 of these 4 patients. The mechanisms responsible for coronary occlusion in lupus patients are probably complex and interwoven. In addition to "classical" factors (i.e., vasculitis or steroid-induced atheroma), other factors, such as antiphospholipid antibodies and/or smoking, may play an important thrombogenic role.