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Updated: Jul 9, 2025

Sterile Pericarditis in Aachener Minipigs As a Model for Atrial Myopathy and Atrial Fibrillation
Published on: September 24, 2021
Severe iron overload cardiomyopathy manifested as acute myopericarditis: A case report
Paisit Kosum1,2, Nonthikorn Theerasuwipakorn1,3, Aranna Wicheantawatchai1,3
1Division of Cardiovascular Medicine, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Insights
Iron overload cardiomyopathy (IOC) can mimic acute myopericarditis in patients with transfusion-dependent thalassemia and hemochromatosis. Early diagnosis and iron chelation are crucial, though severe cases may be refractory.
Area of Science:
- Cardiology
- Hematology
- Pathology
Background:
- Iron overload cardiomyopathy (IOC) results from iron deposition in the heart, leading to cardiac dysfunction.
- Patients with transfusion-dependent thalassemia (TDT) and secondary hemochromatosis are at high risk for IOC due to chronic iron accumulation.
- Recognizing rare presentations of IOC is critical for timely intervention.
Abstract:
Iron overload cardiomyopathy (IOC) is a condition in which iron deposition in the heart causes cardiac dysfunction. We described a 21-year-old woman who presented with acute chest pain, dyspnea, and fever. The patient had a history of transfusion-dependent thalassemia (TDT) and secondary hemochromatosis with the latest serum ferritin ranging from 8000 to 15,000. Physical examinations revealed signs of anemia and heart failure. Electrocardiography showed diffuse ST-segment elevation with reciprocal ST-segment depression in aVR and complete atrioventricular block. Cardiac markers were markedly elevated. Echocardiography demonstrated the dilated size, impaired systolic function, global wall hypokinesia, restrictive filling pattern of the left ventricle, and a small amount of pericardial effusion. Coronary angiography showed normal coronary arteries. A cardiac magnetic resonance imaging showed multifocal early and late gadolinium enhancement involving mid-wall and subepicardial areas of biventricular myocardium suggestive of diffuse myocardial injury from an inflammatory process. She was provisionally diagnosed with acute myopericarditis. Ibuprofen and loop diuretic were prescribed; however, cardiogenic shock occurred. Thus, an endomyocardial biopsy was done and revealed diffuse myocardial hemosiderin deposition without evidence of inflammatory cell infiltration. Severe IOC mimicking acute myopericarditis was considered based on an endomyocardial biopsy result. An intravenous iron chelating agent was immediately administered. Unfortunately, cardiogenic shock was refractory resulting in death. This case demonstrated a rare manifestation of IOC, which can masquerade as acute myopericarditis, and emphasized that IOC should be differentially diagnosed, particularly in patients with TDT and hemochromatosis.

