We have located links that may give you full text access.
Case Reports
Journal Article
Case report: Systemic lupus erythematosus combined with myocardial hypertrophy.
Immunity, Inflammation and Disease 2024 March
OBJECTIVE: Systemic lupus erythematosus (SLE) is a multisystem-involved, highly heterogeneous autoimmune disease with diverse clinical manifestations. We report an extremely rare case of SLE with severe diffuse myocardial hypertrophy.
METHODS: The patient's echocardiography and cardiac magnetic resonance imaging (CMR) results indicated diffuse myocardial hypertrophy. After excluding coronary atherosclerosis, hypertensive cardiomyopathy, drug toxicity, and other causes, the patient was diagnosed with SLE-specific cardiomyopathy. Medications such as hormones, antimalarials, immunosuppressants, and biologics were administered.
RESULTS: Ancillary test results were as follows: hs-cTnI: 0.054 ng/mL (0-0.016); NTproBNP: 1594.0 pg/mL (<150); A contrast-enhanced CMR revealed the diffuse thickening of the left ventricular wall with multiple abnormal enhancements, reduced left ventricular systolic and diastolic function, and moderate amount of pericardial effusion. Endomyocardial myocardial biopsy was performed, showing cardiomyocyte hypertrophy and degeneration, and no changes in myocarditis or amyloidosis. The pathology viewed by electron microscopy showed increased intracellular glycogen in the myocardium, and no hydroxychloroquine-associated damage in the myocardium. The 24-h ambulatory blood pressure and contrast-enhanced computed tomography of coronary arteries were normal. The diagnosis of SLE-specific cardiomyopathy was clear. The myocardial hypertrophy showed reversible alleviation following treatment with high-dose corticosteroids. CMR results before and after treatment were as follows: interventricular septum, pretreatment (28) versus post-treatment (22) mm; left ventricular inferior wall, pretreatment (18-21) versus post-treatment (12-14) mm; left ventricular lateral wall, pretreatment (17-18) versus post-treatment (10-12) mm; pericardial effusion (left ventricular lateral wall), pretreatment (25) versus post-treatment (12) mm; left ventricular ejection fraction, pretreatment (38.9%) versus post-treatment (66%).
CONCLUSION: Myocardial hypertrophy may be an important sign of active and prognostic assessment in SLE diagnosis and management. Similarly, when encountering cases of myocardial hypertrophy, the possibility of autoimmune disease should be considered in addition to common causes.
METHODS: The patient's echocardiography and cardiac magnetic resonance imaging (CMR) results indicated diffuse myocardial hypertrophy. After excluding coronary atherosclerosis, hypertensive cardiomyopathy, drug toxicity, and other causes, the patient was diagnosed with SLE-specific cardiomyopathy. Medications such as hormones, antimalarials, immunosuppressants, and biologics were administered.
RESULTS: Ancillary test results were as follows: hs-cTnI: 0.054 ng/mL (0-0.016); NTproBNP: 1594.0 pg/mL (<150); A contrast-enhanced CMR revealed the diffuse thickening of the left ventricular wall with multiple abnormal enhancements, reduced left ventricular systolic and diastolic function, and moderate amount of pericardial effusion. Endomyocardial myocardial biopsy was performed, showing cardiomyocyte hypertrophy and degeneration, and no changes in myocarditis or amyloidosis. The pathology viewed by electron microscopy showed increased intracellular glycogen in the myocardium, and no hydroxychloroquine-associated damage in the myocardium. The 24-h ambulatory blood pressure and contrast-enhanced computed tomography of coronary arteries were normal. The diagnosis of SLE-specific cardiomyopathy was clear. The myocardial hypertrophy showed reversible alleviation following treatment with high-dose corticosteroids. CMR results before and after treatment were as follows: interventricular septum, pretreatment (28) versus post-treatment (22) mm; left ventricular inferior wall, pretreatment (18-21) versus post-treatment (12-14) mm; left ventricular lateral wall, pretreatment (17-18) versus post-treatment (10-12) mm; pericardial effusion (left ventricular lateral wall), pretreatment (25) versus post-treatment (12) mm; left ventricular ejection fraction, pretreatment (38.9%) versus post-treatment (66%).
CONCLUSION: Myocardial hypertrophy may be an important sign of active and prognostic assessment in SLE diagnosis and management. Similarly, when encountering cases of myocardial hypertrophy, the possibility of autoimmune disease should be considered in addition to common causes.
Full text links
Related Resources
Trending Papers
A Guide to the Use of Vasopressors and Inotropes for Patients in Shock.Journal of Intensive Care Medicine 2024 April 14
British Society for Rheumatology guideline on management of adult and juvenile onset Sjögren disease.Rheumatology 2024 April 17
Albumin: a comprehensive review and practical guideline for clinical use.European Journal of Clinical Pharmacology 2024 April 13
Renin-Angiotensin-Aldosterone System: From History to Practice of a Secular Topic.International Journal of Molecular Sciences 2024 April 5
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app