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[A case of myocardial infarction in a young man with systemic lupus erythematosus]
Y Asakura1, S Nakamoto, Y Nishikawa
1Department of Internal Medicine, School of Medicine, Keio University.
Insights
Systemic lupus erythematosus (SLE) can cause acute myocardial infarction in young adults due to coronary artery thrombosis, not atherosclerosis. Anticardiolipin antibodies likely contribute to this rare but serious complication in SLE patients.
Area of Science:
- Cardiology
- Rheumatology
- Immunology
Background:
- Coronary artery disease (CAD) incidence is rising in systemic lupus erythematosus (SLE) patients, often linked to corticosteroid treatment and atherosclerosis.
- Acute myocardial infarction (AMI) is uncommon in young, untreated SLE patients without traditional risk factors.
Observation:
- A 21-year-old male with latent, untreated SLE experienced AMI.
- Coronary arteriography revealed a transient proximal right coronary artery stenosis.
- The patient had no conventional coronary risk factors but presented with SLE markers and lymphocytopenia.
Findings:
- The transient coronary stenosis was attributed to thrombus formation, excluding atherosclerosis, arteritis, or embolus.
- Laboratory results confirmed SLE, including positive antinuclear antibody and LE cell tests.
- Elevated antibodies to cardiolipin were detected, suggesting a thrombogenic role.
Implications:
- This case highlights a potential mechanism for AMI in SLE via anticardiolipin antibody-mediated coronary thrombosis.
- It underscores the importance of considering thrombotic events in young SLE patients presenting with cardiac symptoms.
- Further research into the role of antiphospholipid antibodies in SLE-related cardiovascular complications is warranted.
Abstract:
Apparently the incidence of coronary artery disease in systemic lupus erythematosus (SLE) has been increasing. However, most of the cases had been treated with corticosteroids, and had atherosclerotic lesions in the coronary arterial tree. A 21-year-old man with latent and untreated SLE had an attack of acute myocardial infarction. Coronary arteriography showed eccentric stenotic lesion at the proximal segment of the right coronary artery. One week later, in the 2nd coronary arteriography, this stenotic lesion was not able to be recognized. We supposed that the coronary artery occlusion was due to thrombus formation, and was not related to atherosclerosis, arteritis and embolus. He had no coronary risk factors. Laboratory data showed lymphocytopenia, proteinuria, positive antinuclear antibody, and positive LE cell, and the case was diagnosed as SLE. Subsequent investigations showed the presence of antibodies to cardiolipin. It was suggested that anticardiolipin antibody and other thrombogenic factors were the causes of the coronary occlusive thrombosis in this patient with SLE.