Abstract Body (Do not enter title and authors here): Eosinophilic myocarditis (EM) is a rare inflammatory myocarditis characterized by eosinophilic infiltration of myocardial tissue. Despite the high mortality rate, EM is frequently underdiagnosed and is often first identified in postmortem studies. We share a case of EM as an early manifestation of newly diagnosed eosinophilic granulomatosis polyangiitis (EGPA). The patient is a 46-year-old female with a past medical history of ulcerative colitis and adult-onset asthma who presented to the emergency department with a 2–3-week history of worsening positional chest pain radiating to the left upper extremity. Associated symptoms include 3 months of fatigue, headaches, right foot neuropathy, urticaria, and B-symptoms. Prior to admission, the patient was started on empiric prednisone for presumed EGPA. Initial lab work on admission was notable for elevated troponin (602 ng/L), hyper-eosinophilia (19.5%), thrombocytosis (680K/uL), and elevated ESR (42 mm/h) that have improved since initiation of prednisone. Transthoracic echocardiogram revealed a newly reduced LVEF of 40% with basal and mid-septal wall motion abnormalities. Cardiac catheterization showed normal coronaries confirming the diagnosis of non-ischemic cardiomyopathy. Late gadolinium enhancement in cardiac MRI was seen in basal to mid segments with patchy pericardial enhancement, meeting the Lake Louise criteria for myocarditis. An endomyocardial biopsy showed substantial myocardial infiltration with lymphocytes, histiocytes and eosinophils, confirming the diagnosis of EM. After multidisciplinary team discussion with cardiology and rheumatology, the patient was started on guideline-directed medical therapy for her HFrEF and pulse dose steroids with a prolonged taper and cyclophosphamide. She is tolerating her treatment well. This case highlights the importance of early recognition, comprehensive assessment and targeted treatment for EM depending on its underlying etiology. In the case of autoimmune dysfunction, it involves a combination of immunosuppressive and symptomatic therapy. Ongoing research is crucial to enhance our understanding and improve clinical outcomes, like arrhythmias and cardiogenic shock, for this complex condition.