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A woman in her 50s with discoid lupus in remission and recent adult-onset asthma presented to the emergency department with 2 weeks of dyspnea on exertion associated with substernal chest pain radiating to her jaw. She noted a 5-kg weight loss in the preceding 3 months. Examination revealed nonreproducible chest tenderness, bibasilar crackles, and no extra heart sounds. A 12-lead electrocardiogram is shown in Figure 1A. Testing revealed leukocytosis (white blood cell count, 16 900 cells/μL [to convert to × 109 cells/L, multiply by 0.001]) with a differential of 6% neutrophils and 59% eosinophils, an elevated N-terminal pro B-type natriuretic peptide of 3963 pg/mL (reference level, <900 pg/mL [to convert to ng/L, multiply by 1.0]), and an elevated initial troponin T of 0.36 ng/mL, which later peaked at 0.41 ng/mL (to convert to micrograms per liter, multiply by 1.0). Her C-reactive protein level was 3.09 mg/dL (normal, <0.5 mg/dL [to convert to milligrams per liter, multiply by 10]). Subsequent plasma flow cytometry demonstrated 65% eosinophils, and a bone marrow biopsy with immunohistochemistry showed eosinophilia without evidence of clonal expansion. Cardiac magnetic resonance imaging was performed (Figure 1B; Video).
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Eosinophilic myopericarditis associated with eosinophilic granulomatosis with polyangiitis
C. Urgent initiation of high-dose steroids, colchicine, and high-dose NSAIDs during hospitalization
The keys to the diagnosis in this case are the elevated biomarkers suggesting cardiac damage, decreased left ventricular ejection fraction, and late gadolinium enhancement on cardiac magnetic resonance imaging, all of which are consistent with myocardial injury. The patient’s peripheral eosinophilia without clonal expansion and history of adult-onset asthma are most suggestive of eosinophilic myopericarditis (EM) associated with eosinophilic granulomatosis with polyangiitis (EGPA), formerly known as Churg-Strauss syndrome.
Eosinophilic myopericarditis is a rare form of myocarditis characterized by eosinophilic infiltration of the myocardium.1 It can present with chest pain, acute heart failure, arrhythmias, and mural thrombus, and it is associated with high mortality, especially when presenting as fulminant myocarditis.2 This case highlights the broad differential diagnosis of EM causative mechanisms, which include primary neoplastic processes, helminthic and parasitic infections, allergic immune response and hypersensitivity, autoimmune diseases, and idiopathic hypereosinophilia.2- 5 A recent meta-analysis found the most common causative mechanism of EM to be idiopathic or undefined (36%), followed by hypersensitivity (34%) and EGPA-associated (13%) causative mechanisms.2 Eosinophilic myopericarditis associated with EGPA is often accompanied by asthma and peripheral eosinophilia, as was the case with this patient.2
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Corresponding Author: David A. McNamara, MD, MPH, Frederik Meijer Heart & Vascular Institute, Spectrum Health, 2900 Bradford St NE, Grand Rapids, MI 49525 (firstname.lastname@example.org).
Published Online: August 12, 2020. doi:10.1001/jamacardio.2020.2808
Conflict of Interest Disclosures: Dr McNamara is supported by the National Heart, Lung, and Blood Institute (grant T32-HL125247). No other disclosures were reported.
Additional Contributions: We thank the patient for granting permission to publish this information.
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