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Systemic lupus erythematosus cardiomyopathy—a case series demonstrating a reversible form of left ventricular
Insights
Systemic lupus erythematosus (SLE) can cause cardiomyopathy. This study found that left ventricular dysfunction in SLE patients often improves rapidly, suggesting stress cardiomyopathy rather than myocarditis.
Area of Science:
- Cardiology
- Rheumatology
- Internal Medicine
Background:
- Myocarditis is a known postmortem finding in systemic lupus erythematosus (SLE).
- However, endomyocardial biopsies in SLE cardiomyopathy (CM) cases rarely show evidence of myocarditis.
- The etiology of LV dysfunction in SLE remains unclear.
Purpose of the Study:
- To characterize the nature, course, and reversibility of left ventricular (LV) dysfunction in patients with SLE.
- To differentiate between myocarditis and other potential causes of cardiomyopathy in SLE patients.
Main Methods:
- Retrospective review of 526 SLE patient records.
- Inclusion criteria: ≥4 American College of Rheumatology criteria for SLE, ESR and hs-CRP testing, and echocardiogram showing LVEF <50%.
- Analysis of echocardiographic findings, clinical course, and outcomes.
Main Results:
- 14 SLE patients met the criteria; mean LVEF was 33.1 ± 9%.
- Generalized hypokinesis was the predominant echocardiographic pattern.
- 12 patients (86%) showed LVEF reversal within 1 week (mean improvement 21.0 ± 7%); 4 (29%) improved within 3 days.
- Coronary angiography and cardiac biopsy ruled out obstructive coronary disease and myocarditis, respectively, in a subset of patients.
Conclusions:
- The observed pattern of wall-motion abnormalities and rapid reversibility in SLE patients suggests stress cardiomyopathy.
- The findings challenge the traditional view of myocarditis as the primary cause of cardiomyopathy in SLE.
- Further research is needed to elucidate the precise mechanisms of cardiac dysfunction in SLE.
Objective:
Myocarditis is reported to be a common postmortem finding of systemic lupus erythematosus (SLE). However, most case reports on SLE cardiomyopathy (CM) have not found evidence of myocarditis upon biopsy. Our aim was to characterize the nature, course, and reversibility of left ventricular (LV) dysfunction in patients with SLE.
Methods:
The records of 526 SLE patients were reviewed. Patients were included if: (1) at least 4 of 11 American College of Rheumatology criteria for SLE were met, (2) testing for erythrocyte sedimentation rate and hs-CRP were performed during hospitalization, and (3) echocardiogram demonstrated left ventricular ejection function (LVEF) <50%.
Results:
We identified 14 patients meeting study criteria. Mean LVEF was 33.1 ± 9% upon presentation. The main echocardiographic pattern observed was generalized hypokinesis. Twelve patients demonstrated reversal of cardiomyopathy within 1 week, showing a mean improvement in LVEF of 21.0 ± 7%. Of these, 2 patients underwent coronary angiography demonstrating no evidence of obstructive coronary disease, and 1 underwent cardiac biopsy with no evidence of myocarditis. Four patients (29%) demonstrated improvement within 3 days. Two of the 14 patients died due to their underlying medical illness and did not have a repeat echocardiogram.
Conclusion:
The pattern of wall-motion abnormalities and reversibility demonstrated in the majority of these patients with SLE suggests an etiology more consistent with stress cardiomyopathy rather than myocarditis.
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