Abstract 4135360: Eosinophilic Myocarditis: An Atypical Presentation with a Labile Course: A Case Report

Case presentation: A 64-year-old man presented with one day of chest pain. Initial evaluation showed elevated cardiac enzymes (CE) and normal eosinophil count. Electrocardiogram (EKG) was unremarkable. Transthoracic echocardiogram (TTE) showed an ejection fraction (EF) of 40% and a moderate-large pericardial effusion with signs of tamponade. Pericardiocentesis was deferred due to the lack of a safe window. Left and right heart catheterization showed no occlusive disease or chamber pressure equalization. The patient developed worsening shock, raising suspicion for myocarditis and prompting an endomyocardial biopsy (EMB). He was placed on extracorporeal membrane oxygenation (ECMO) on day 3. The EMB resulted as eosinophilic myocarditis (EM), and high dose Methylprednisolone was started. He was decannulated from ECMO on day 10. Intra-operative transesophageal echocardiogram (TEE) post-decannulation showed a normal EF without segmental abnormalities. Three hours later, a rise in CEs was noted, and EKG showed ST elevations inferiorly. TTE showed a reduced EF with multiple segmental abnormalities concerning for myocardial infarction. A repeat coronary angiogram was unremarkable. Due to the residual pericardial effusion, the patient underwent a pericardial window draining 200 cc of serosanguinous fluid. Intra-operative TEE showed an EF of 20% with no improvement after drainage. He had a cardiac arrest during the procedure and was placed back on ECMO. High-dose steroids were resumed along with intravenous immunoglobulin. Despite interventions, the patient continued to deteriorate and he ultimately expired. Discussion: EM has high mortality and a variable course, often requiring EMB for diagnosis. As in our case, about 25% of cases present without peripheral eosinophilia. Pericardial effusion occurs in 34% of cases and tamponade in 6%. A distinct feature of this case is the decompensation associated with ST elevation and segmental abnormalities, thought initially to be myocardial infarction (MI), after an initial response to steroids. While the etiology of such decompensation is unclear, relapsing EM in the setting of tapering steroids is one explanation, as myocarditis and MI can share similar clinical features. Another explanation is cardiac tamponade, which has also been reported to mimic MI and myocarditis. Air embolism from ECMO decannulation is another possibility, though air embolisms may include cerebrovascular pathology, which was not observed.