Cardiac Sarcoidosis With Elevated Cardiac Troponin Mimicking Acute Myocardial Ischemia: A Case Report
Bruce C Casipit1, Hussein Al-Sudani2, Aman Amanullah3
1Internal Medicine, Einstein Medical Center Philadelphia, Philadelphia, USA.
Insights
Cardiac sarcoidosis (CS) can present unusually, mimicking heart attacks with elevated troponin levels. Early diagnosis and treatment of this rare heart condition are crucial for patient outcomes.
Area of Science:
- Cardiology
- Immunology
- Oncology
Background:
- Cardiac sarcoidosis (CS) is a rare granulomatous disease affecting the heart, leading to significant morbidity and mortality.
- Diagnosis is often challenging due to variable presentations and potential mimicry of other cardiac conditions.
Observation:
- A 48-year-old female presented with presyncope, bifascicular block, and elevated troponin I, suggestive of myocardial infarction.
- Cardiac imaging revealed left ventricular systolic dysfunction and conduction abnormalities, while coronary angiography excluded significant epicardial coronary artery disease.
Findings:
- Fluorodeoxyglucose-positron emission tomography and cardiac magnetic resonance imaging indicated active myocardial inflammation consistent with CS.
- The patient showed clinical improvement after treatment with corticosteroids and methotrexate for CS.
Implications:
- This case highlights the diagnostic complexity of CS, particularly when troponin elevation mimics acute ischemic events.
- Effective treatment strategies for CS are essential to prevent long-term cardiac damage, though optimal pharmacological regimens require further research.
Abstract:
Cardiac sarcoidosis (CS) is a disease entity with variable presentation causing significant morbidity and mortality. Concurrent signs of myocardial injury as evidenced by troponin elevation add to the complexity of an already challenging diagnosis. We present an unusual case of CS with elevated troponin I mimicking an acute ischemic cardiac event. A 48-year-old female presented with a two-month history of presyncope. Electrocardiogram showed a bifascicular block with concomitant significant troponin I elevation. Two-dimensional echocardiography showed new-onset left ventricular systolic dysfunction with an ejection fraction of 40-45%. A heparin drip was initiated for possible non-ST-elevation myocardial infarction. Coronary angiography showed no evidence of epicardial coronary artery disease but did show an anomalous right coronary artery; however, CT angiography did not reveal any significant stenosis. Further, the telemetry monitor captured intermittent complete atrioventricular blocks. Due to concerns for an infiltrative cardiac disease, a cardiac magnetic resonance was done showing findings consistent with possible CS. CT scan of the chest showed no radiographic evidence of pulmonary sarcoidosis. Fluorodeoxyglucose-positron emission tomography scan showed findings of active inflammation in the myocardium consistent with possible CS. The patient was treated for clinical CS with systemic corticosteroids and methotrexate. Follow-up six weeks later showed clinical improvement of symptoms. Our clinical case encompasses the unique variable presentation of CS including cardiac conduction abnormalities and left ventricular systolic dysfunction. Concomitant troponin I elevation can mimic myocardial ischemia, making the diagnosis more challenging. Treatment strategies aim to mitigate the long-term effects of CS on the heart; however, there is a paucity of data for appropriate pharmacological regimens.
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