Abstract Body (Do not enter title and authors here): We present a perplexing case of a 33-year-old male with no prior cardiac history who presented to the emergency department with a 5-day history of worsening pleuritic chest pain and dyspnea. The patient had recently returned from El Salvador, where he resided near the beach. Notably, his chest pain worsened with inspiration but was not positional. He denied fevers, chills, or family history of cardiac disease, but reported recreational marijuana use.

Initial evaluation revealed normal vital signs and electrocardiogram, but marked eosinophilia (12%) and mildly elevated C-reactive protein. High-sensitivity troponin levels peaked at 8400 ng/L, raising suspicion for myocardial injury. Echocardiography demonstrated preserved left ventricular ejection fraction but revealed a moderate pericardial effusion. Pericardial fluid analysis showed benign reactive mesothelial cells.

Given the patient's travel history and eosinophilia, a broad differential diagnosis was considered, including parasitic etiologies such as Chagas disease. However, serological testing for Chagas was negative. Interestingly, IgG antibodies for Strongyloides stercoralis were positive, implicating strongyloidiasis as the underlying cause of the eosinophilic myopericarditis.

The patient was treated with non-steroidal anti-inflammatory drugs, colchicine, and empiric ivermectin therapy. A cardiac magnetic resonance imaging study was ordered to further characterize the myocardial involvement, but the patient was unfortunately lost to follow-up.

This case highlights the importance of maintaining a broad differential diagnosis and considering travel-related exposures in patients presenting with eosinophilic myopericarditis. Strongyloidiasis, though uncommon, can manifest with cardiac involvement and should be considered in at-risk populations, particularly those with eosinophilia and a compatible travel history.

It is also important to have a high clinical suspcision for stronglodies induced myopericarditis in high risk patinets such as ours as typical treatment with steroids could result in furthur desemination of strongyloidias infection leading to fulminant eosinophillic myocarditis.