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[Critical myocardial ischemia in systemic lupus erythematosus. Case report]
E Astorri1, E Ridolo, P P Dall'Aglio
1Cattedra di Cardiologia, Università degli Studi di Parma.
Insights
Systemic lupus erythematosus can cause coronary artery vasculitis, leading to heart disease and angina. Prompt immunosuppressive treatment improved symptoms and cardiac perfusion in a young woman.
Area of Science:
- Cardiology
- Rheumatology
- Immunology
Background:
- Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with diverse clinical manifestations.
- Cardiac involvement in SLE can range from pericarditis to myocarditis and valvulitis.
- Coronary artery disease is less commonly reported in SLE patients, particularly at a young age.
Observation:
- A 26-year-old woman with a 15-year history of SLE presented with new-onset angina pectoris on mild exertion.
- Diagnostic tests revealed significant anteroseptal and apical perfusion defects on Thallium-201 exercise testing.
- Echocardiography showed anteroseptal hypokinesis, and ECG indicated a new Q wave in lead V4.
Findings:
- The patient's presentation suggested acute coronary syndrome, likely secondary to an autoimmune process.
- A diagnosis of coronary artery vasculitis, possibly linked to early atherosclerosis, was hypothesized.
- Following intensified corticosteroid and immunosuppressive therapy, angina symptoms resolved, and perfusion defects normalized within months.
Implications:
- This case highlights the potential for SLE to manifest as premature coronary artery disease via vasculitis.
- Early recognition and aggressive immunosuppressive treatment are crucial for managing cardiac complications in SLE.
- Coronary artery vasculitis should be considered in young SLE patients presenting with ischemic heart disease symptoms.
Abstract:
We present the clinical case of a 26-year-old woman, suffering systemic lupus erythematosus for 15 years, who suddenly had coronary heart disease with angina pectoris on mild effort. Thallium 201 exercise test demonstrated clearcut anteroseptal and apical perfusion defects, whereas repeated echocardiography showed a hypokinetic anteroseptal segment; ECG also reported new Q wave in lead V4. After stronger corticosteroid and immunosuppressive treatment, angina pectoris attenuated and perfusion defects disappeared within few months. We hypothesize a coronary artery vasculitis in the course of systemic lupus erythematosus, probably associated with early coronary artery atherosclerosis.